Ma `lumot

Kimyoviy sinapslarda kuchlanishli ionli kanallarning o'rni

Kimyoviy sinapslarda kuchlanishli ionli kanallarning o'rni


We are searching data for your request:

Forums and discussions:
Manuals and reference books:
Data from registers:
Wait the end of the search in all databases.
Upon completion, a link will appear to access the found materials.

Men hujayra darajasida harakat potentsialini yaratish mexanizmlarini tushunishga harakat qilaman.

Odatda, urg'u bor Kuchlanishi-membrana potentsialining tegishli o'zgarishiga olib keladigan kaliy (K+) va natriy (Na+) kanallarining o'tkazuvchanligi o'zgarishi.

Odatda, miyadagi sinapslar kimyoviy sinapslardir (elektr sinapslarning kichik qismidan farqli o'laroq, masalan, signal uzatish uchun bo'shliq birikmalaridan foydalanadigan gipokampda).

Mening chalkashligim endi shunday: kimyoviy sinapslar o'tkazuvchanlik o'zgarishlarini boshlash uchun neyrotransmitterlarga bog'liq. Harakat potentsiallarining kanonik izohi havola bilan amalga oshiriladi kuchlanish bilan qoplangan kanallar -- bu ikki narsa qanday qilib birga keladi?


6.5 IB biologiyasi - neyronlar va sinapslar

Axon: boshqa neyronlar va effektorlar bilan aloqa qilish uchun elektr signallarini terminal hududlarga uzatuvchi cho'zilgan tola.

natriy kaliy pompasi natriy va kaliy ionlarini faol ravishda almashinadigan faol nasosdir.

har 2 ta K+ ioni uchun 3 Na+ ionini chiqaradi.

Bu elektrokimyoviy gradiyentni hosil qiladi, bunda hujayra ichi hujayradan tashqari muhitga nisbatan nisbatan salbiy bo'ladi.

Na+ ionlari membranadan tashqarida ko'proq to'planganligi sababli, natriy kanallarining ochilishi natriy ionlarining passiv oqimini hosil qiladi.

K+ ionlari membrana ichida ko'proq to'planganligi sababli, kaliy kanallarining ochilishi kaliy ionlarining passiv oqimini keltirib chiqaradi.

akson uzunligini egallagan ion kanallari kuchlanish bilan bog'langan (membrana potentsiallarining o'zgarishiga javob sifatida ochiq)

Demak, aksonning bir nuqtasida depolarizatsiya aksonning keyingi segmentida ion kanallarining ochilishiga olib keladi.

Oddiy dam olish holatida natriy kanallari asosan neyron tashqarisida va asosan kaliy ionlarida bo'ladi.

Depolarizatsiyadan (natriy oqimi) va repolarizatsiyadan (kaliy oqimi) so'ng, bu ionli taqsimot asosan qaytariladi.

Dendritlardan qo'shma stimulyatsiya minimal depolarizatsiya darajasidan oshib ketganda, chegara potentsiallari ishga tushiriladi.

Sinaptik yoriq: neyrotransmitterlar chiqariladi va sinaptik yoriqni kesib o'tishga harakat qiladi.

Kaltsiy 2+ ionlari hujayra ichiga tarqaladi va hujayra membranasi bilan neyrotransmitterlari bo'lgan pufakchalarning birlashishiga yordam beradi.

neyrotransmitterlar akson terminalidan ekzotsitoz orqali chiqariladi va sinaptik yoriqni kesib o'tadi.

neyrotransmitterlar post-sinaptik membranadagi maxsus retseptorlarga va ochiq ligandli kanalli kanallarga bog'lanadi.

Ion kanallarining ochilishi sinaptikdan keyingi signalni tarqatuvchi elektr impulsini hosil qiladi.


Sinaps yoki &ldquogap&rdquo - ma'lumot bir neyrondan ikkinchisiga uzatiladigan joy. Sinapslar odatda akson terminallari va dendritik tikanlar o'rtasida hosil bo'ladi, ammo bu hamma uchun to'g'ri emas. Bundan tashqari, akson-akson, dendrit-dendrit va akson-hujayrali tana sinapslari mavjud. Signalni uzatuvchi neyron presinaptik neyron, signalni qabul qiluvchi neyron esa postsinaptik neyron deb ataladi. E'tibor bering, bu belgilar ma'lum bir sinapsga tegishli va mdashmost neyronlar ham presinaptik, ham postsinaptik. Sinapslarning ikki turi mavjud: kimyoviy va elektr.

Kimyoviy sinapslar

Harakat potentsiali akson terminaliga yetganda, u membranani depolarizatsiya qiladi va kuchlanishli ( ce>) kanallari. (ce> ) ionlari hujayra ichiga kirib, presinaptik membranani depolarizatsiya qiladi. Bu depolarizatsiya kuchlanishli ( ce> ) kanallarni ochish. Hujayra ichiga kirgan kaltsiy ionlari sinaptik pufakchalar deb ataladigan, neyrotransmitter molekulalarini presinaptik membrana bilan birlashishiga olib keladigan kichik membrana bilan bog'langan pufakchalarga olib keladigan signal kaskadini ishga tushiradi. Sinaptik pufakchalar 7.18 -rasmda ko'rsatilgan, bu skanerlovchi elektron mikroskopdan olingan tasvir.

7.18 -rasm. Elektron mikroskop yordamida olingan soxta tasvir neyron ichidagi sinaptik pufakchalarni (ko'k va to'q sariq) ochish uchun ochilgan akson terminalini ko'rsatadi. (Kredit: Tina Karvalyoning ishini o'zgartirish, Mett Rasseldan NIH-NIGMS shkalasi ma'lumotlari)

Vesikulaning presinaptik membrana bilan birlashishi, neyrotransmitterning sinaptik yoriqqa, presinaptik va postsinaptik membranalar orasidagi hujayradan tashqari bo'shliqqa chiqarilishiga olib keladi. 7.19-rasm. Neyrotransmitter sinaptik yoriq bo'ylab tarqaladi va postsinaptik membranadagi retseptor oqsillari bilan bog'lanadi.

7.19-rasm. Kimyoviy sinapslardagi aloqa neyrotransmitterlarning chiqarilishini talab qiladi. Presinaptik membrana depolarizatsiya qilinganda, kuchlanish bilan o'ralgan Ca2 + kanallari ochiladi va Ca2 + hujayra ichiga kirishiga imkon beradi. Kaltsiyning kirishi sinaptik pufakchalarning membrana bilan birlashishiga va neyrotransmitter molekulalarini sinaptik yoriqqa chiqarishiga olib keladi. Neyrotransmitter sinaptik yoriq bo'ylab tarqaladi va postsinaptik membranadagi ligandli kanalli ion kanallari bilan bog'lanadi, natijada postsinaptik neyron lokal depolarizatsiya yoki giperpolyarizatsiyaga olib keladi.

Muayyan neyrotransmitterning bog'lanishi postsinaptik membranada ma'lum ion kanallarini, bu holda ligand bilan o'ralgan kanallarni ochishga olib keladi. Neyrotransmitterlar postsinaptik membranaga qo'zg'atuvchi yoki inhibitiv ta'sir ko'rsatishi mumkin, bu 7.2 -jadvalda keltirilgan. Misol uchun, atsetilxolin nerv va mushak o'rtasidagi sinapsda (neyromuskulyar birikma deb ataladi) presinaptik neyron tomonidan chiqarilsa, bu postsinaptik Na+ kanallarining ochilishiga olib keladi. Na+ postsinaptik hujayra ichiga kirib, postsinaptik membranani depolarizatsiyaga olib keladi. Bu depolarizatsiya an deb nomlanadi qo'zg'atuvchi postsinaptik potentsial (EPSP) va postsinaptik neyronning harakat potentsialini yoqish ehtimolini oshiradi. Neyrotransmitterning inhibitiv sinapslarda chiqishi sabab bo'ladi postsinaptik inhibitiv potentsiallar (IPSP), presinaptik membrananing giperpolyarizatsiyasi. Masalan, GABA neyrotransmitteri (gamma-aminobutirik kislota) presinaptik neyrondan chiqarilganda, u Cl&ndash kanallari bilan bog'lanadi va ochiladi. Cl & ndash ionlari hujayraga kiradi va membranani giperpolyarizatsiya qiladi, bu neyronning harakat potentsialini yoqish ehtimolini kamaytiradi.

Neyrotransmisyon sodir bo'lgandan so'ng, neyrotransmitterni sinaptik yoriqdan olib tashlash kerak, shunda postsinaptik membrana "rdquo" o'rnatadi va boshqa signalni qabul qilishga tayyor bo'ladi. Buni uchta usulda amalga oshirish mumkin: neyrotransmitter sinaptik yoriqdan uzoqlashishi mumkin, uni sinaptik yoriqdagi fermentlar parchalanishi mumkin yoki uni presinaptik neyron tomonidan qayta ishlanishi mumkin (ba'zida qaytarib olish deyiladi). Neyrotransmissiyaning bu bosqichida bir nechta dorilar harakat qiladi. Masalan, Altsgeymer bilan og'rigan bemorlarga beriladigan ba'zi dorilar atsetilxolinni parchalovchi ferment atsetilxolinesterazasini inhibe qilish orqali ishlaydi. Fermentning bunday inhibisyonu atsetilxolin chiqaradigan sinapslarda neyrotransmissiyani sezilarli darajada oshiradi. Chiqarilgandan so'ng, atsetilxolin yoriqda qoladi va doimiy ravishda postsinaptik retseptorlarni bog'lashi va ajratishi mumkin.

7 -jadval: Neyrotransmitterning vazifasi va joylashuvi
Neyrotransmitter Misol Manzil
Asetilkolin &mdash CNS va/yoki PNS
Biogen amin Dopamin, serotonin, norepinefrin CNS va/yoki PNS
Aminokislota Glitsin, glutamat, aspartat, gamma-aminobutirik kislota CNS
Neyropeptid P moddasi, endorfinlar CNS va/yoki PNS

Sinapsdagi voqealarni loyihalash va/yoki ijro etish! Ko'rib chiqish faoliyatingizni loyihalashda yordam beradigan ba'zi maslahatlar:

  • Qancha tengdoshlar ishtirok etishi kerakligi haqida o'ylashingiz kerak bo'ladi.
  • Kim qaysi tuzilishga ega bo'ladi?
  • Sizning tengdoshlaringiz va siz bir -biringizga nisbatan qanday harakat qilasiz?
  • Siz yaratgan har bir harakatning umumiy maqsadi nima (har bir strukturaning vazifasi nima)?

Elektr sinapslari

Elektr sinapslari kimyoviy sinapslarga qaraganda kamroq bo'lsa -da, ular barcha asab tizimlarida uchraydi va muhim va o'ziga xos rol o'ynaydi. Elektr sinapslarda neyrotranslyatsiya usuli kimyoviy sinapslardan farq qiladi. Elektr sinapsida presinaptik va postsinaptik membranalar bir -biriga juda yaqin joylashgan va ular bo'shliq birikmalarini tashkil etuvchi kanal oqsillari bilan jismonan bog'langan. Bo'shliqlar tokni to'g'ridan -to'g'ri bir hujayradan ikkinchisiga o'tkazishga imkon beradi. Bu tokni o'tkazadigan ionlardan tashqari, boshqa molekulalar, masalan ATP, katta bo'shliqli teshik teshiklari orqali tarqalishi mumkin.

Kimyoviy va elektr sinapslari o'rtasida asosiy farqlar mavjud. Kimyoviy sinapslar sinaptik pufakchalardan neyrotransmitter molekulalarining ularning signaliga o'tishiga bog'liq bo'lganligi sababli, akson potentsialining presinaptik terminalga yetib borishi va neyrotransmitterning postsinaptik ion kanallarining ochilishiga olib kelishi o'rtasida taxminan bir millisekundlik kechikish mavjud. Bundan tashqari, bu signal bir tomonlama. Elektr sinapslarda signal berish, aksincha, deyarli bir zumda (bu asosiy reflekslarda ishtirok etuvchi sinapslar uchun muhim) va ba'zi elektr sinapslar ikki tomonlama. Elektr sinapslari ham ishonchliroqdir, chunki ularni blokirovka qilish ehtimoli kamroq va ular neyronlar guruhining elektr faolligini sinxronlashtirishda muhim ahamiyatga ega. Masalan, talamusdagi elektr sinapslari sekin uyquni tartibga soladi va bu sinapslarning buzilishi soqchilikni keltirib chiqarishi mumkin.

Signal yig'indisi

Ba'zida bitta EPSP postsinaptik neyronda harakat potentsialini qo'zg'atish uchun etarlicha kuchli bo'ladi, lekin ko'pincha bir vaqtning o'zida bir nechta presinaptik kirishlar EPSP -larni yaratishi kerak, bu esa postsinaptik neyron etarlicha depolarizatsiyalanishi uchun harakat potentsialini ishga soladi. Bu jarayon yig'ma deb ataladi va 7.20 -rasmda ko'rsatilgan akson tepasida sodir bo'ladi. Bundan tashqari, bitta neyronga ko'pincha presinaptik neyronlar va mdashsome qo'zg'atuvchi kirishlar kiradi, va ba'zi inhibitiv va mdashso IPSPlar EPSPlarni bekor qilishi mumkin va aksincha. Bu postsinaptik membrana kuchlanishining aniq o'zgarishi, postsinaptik hujayraning harakat potentsialini yoqish uchun zarur bo'lgan qo'zg'alish chegarasiga yetganligini aniqlaydi. Sinaptik yig'indilar va qo'zg'alish chegarasi birgalikda filtr vazifasini bajaradi, shuning uchun tizimdagi tasodifiy va rudquo muhim ma'lumotlar sifatida uzatilmaydi.

7.20 -rasm. Bitta neyron bir nechta neyronlardan qo'zg'atuvchi va inhibitiv kirishni olishi mumkin, natijada mahalliy membrana depolarizatsiyasi (EPSP usuli) va giperpolyarizatsiya (IPSP usuli) paydo bo'ladi. Ushbu kirishlarning barchasi akson tepasida qo'shiladi. Agar EPSPlar IPSPlarni yengib o'tish va qo'zg'alish chegarasiga etish uchun etarlicha kuchli bo'lsa, neyron yonadi.

Sinaptik plastika

Sinapslar statik tuzilmalar emas. Ularni kuchaytirish yoki kuchsizlantirish mumkin. Ularni sindirish va yangi sinapslar yasash mumkin. Sinaptik plastisiya asab tizimining ishlashi uchun zarur bo'lgan bu o'zgarishlarga imkon beradi. Aslida, sinaptik plastika o'rganish va xotiraning asosidir. Xususan, ikkita jarayon, uzoq muddatli potentsiyalash (LTP) va uzoq muddatli depressiya (LTD)-bu xotirani saqlash bilan shug'ullanadigan miya mintaqasi bo'lgan hipokampusdagi sinapslarda paydo bo'ladigan sinaptik plastisiyaning muhim shakllari.

Uzoq muddatli potentsial (LTP)

Uzoq muddatli potentsializatsiya (LTP)-sinaptik aloqaning doimiy mustahkamlanishi. LTP ibroniy tamoyiliga asoslanadi: bir -biriga o't ochadigan hujayralar bir -biriga sim o'tkazadi. LTP bilan ko'rilgan sinaptik kuchayishning orqasida to'liq tushunilmagan turli xil mexanizmlar mavjud. Ma'lum mexanizmlardan biri 7.21-rasmda ko'rsatilgan NMDA (N-Metil-D-aspartat) retseptorlari deb ataladigan postsinaptik glutamat retseptorlarining bir turini o'z ichiga oladi. Odatda, bu retseptorlar magniy ionlari tomonidan bloklanadi, ammo postsinaptik neyron ketma -ket bir nechta presinaptik kirishlar bilan depolarizatsiya qilinganida (bitta neyron yoki bir nechta neyronlardan), magniy ionlari Ca ionlarining postsinaptik hujayraga o'tishiga imkon beradi. Keyin hujayraga kiradigan Ca2+ionlari signal kaskadini ishga tushiradi, bu esa boshqa turdagi glutamat retseptorlarini AMPA (alfa-amin-3-gidroksi-5-metil-4-izoksazolepropion kislotasi) retseptorlari postsinaptik membranaga kiritilishiga olib keladi. , chunki faollashtirilgan AMPA retseptorlari ijobiy ionlarning hujayraga kirishiga imkon beradi. Shunday qilib, keyingi safar glutamat presinaptik membranadan ajralib chiqsa, u postsinaptik hujayraga katta qo'zg'atuvchi ta'sir ko'rsatadi (EPSP), chunki glutamatning bu AMPA retseptorlari bilan bog'lanishi hujayraga ko'proq ijobiy ionlarni kiritish imkonini beradi. Qo'shimcha AMPA retseptorlari kiritilishi sinapsni kuchaytiradi va shuni ko'rsatadiki, postsinaptik neyron presinaptik neyrotransmitterning chiqarilishiga javoban olovga ko'proq moyil bo'ladi. Ba'zi suiiste'mol qilingan dorilar LTP yo'lini tanlaydi va bu sinaptik kuchayish giyohvandlikka olib kelishi mumkin.

Uzoq muddatli depressiya (LTD)

Uzoq muddatli depressiya (LTD) asosan LTP ning teskarisi: bu sinaptik aloqaning uzoq muddatli zaiflashishi. LTDni keltirib chiqaradigan mexanizmlardan biri AMPA retseptorlarini ham o'z ichiga oladi. Bunday holatda, NMDA retseptorlari orqali kiradigan kaltsiy boshqa signalli kaskadni ishga tushiradi, natijada 7.21 -rasmda ko'rsatilgandek, postsinaptik membranadan AMPA retseptorlari olib tashlanadi. Membranada AMPA retseptorlarining kamayishi postsinaptik neyronni presinaptik neyrondan chiqarilgan glutamatga nisbatan kamroq sezgir qiladi. Garchi bu teskari tuyulishi mumkin bo'lsa-da, LTD LTP kabi o'rganish va xotira uchun muhim bo'lishi mumkin. Ishlatilmaydigan sinapslarning zaiflashishi va kesilishi ahamiyatsiz ulanishlarning yo'qolishiga imkon beradi va LTP o'tkazgan sinapslarni taqqoslaganda ancha kuchliroq qiladi.

7.21-rasm. Kaltsiyni postsinaptik NMDA retseptorlari orqali kiritish sinaptik plastisitning ikki xil shaklini boshlashi mumkin: uzoq muddatli potentsializatsiya (LTP) va uzoq muddatli depressiya (LTD). LTP bitta sinaps qayta-qayta rag'batlantirilganda paydo bo'ladi. Bu stimulyatsiya kaltsiy va CaMKII ga bog'liq bo'lgan uyali kaskadni keltirib chiqaradi, natijada postsinaptik membranaga ko'proq AMPA retseptorlari kiritiladi. Keyingi safar glutamat presinaptik hujayradan ajralib chiqsa, u NMDA va yangi kiritilgan AMPA retseptorlari bilan bog'lanib, membranani yanada samarali depolarizatsiya qiladi. LTD bir nechta glutamat molekulalari NMDA retseptorlari bilan sinapsda bog'langanda paydo bo'ladi (presinaptik neyronning past tezligi tufayli). NMDA retseptorlari orqali o'tadigan kaltsiy boshqa kalsineurin va oqsil fosfataza 1 ga bog'liq kaskadni ishga tushiradi, bu esa AMPA retseptorlarining endotsitoziga olib keladi. Bu postsinaptik neyronni presinaptik neyrondan chiqarilgan glutamatga kamroq javob beradi.

Neyron harakat potentsialini yoqishi uchun uning membranasi ________ ga yetishi kerak.
a. giperpolyarizatsiya
b. qo'zg'alish chegarasi
v. refrakter davri
d. postsinaptik inhibitiv potentsiya

Harakat potentsialidan so'ng, qo'shimcha kuchlanish bilan bog'langan ________ kanallarning ochilishi va natriy kanallarining inaktivatsiyasi membrananing dam olish membrana potentsialiga qaytishiga olib keladi.
a. natriy
b. kaliy
v. kaltsiy
d. xlorid

Elektr sinapsida ikkita neyronni bog'laydigan oqsil kanallari atamasi nima?
a. sinaptik pufakchalar
b. kuchlanishli ionli kanallar
v. bo'shliq birikmasi oqsili
d. natriy-kaliy almashinuvi nasoslari

Miyelin ta'sir potentsialining akson bo'ylab tarqalishiga qanday yordam beradi? Ranvier tugunlari bu jarayonga qanday yordam beradi?


Kimyoviy sinapslar moslashuvchan:

Aktyorlik mahorati haqida bilganingizda, harakat kuchi hamma narsaga javob beradi, deb eslashingiz mumkin. Bu shuni anglatadiki, bu sodir bo'lishi mumkin yoki bo'lmasligi mumkin. Sinaptik imzo juda o'zgaruvchan. Qabul qiluvchi hujayra o'z membranasiga yopisha oladigan retseptorlar sonini tartibga solishga qodir. Bunday o'zgarishlar aloqalarni mustahkamlash yoki sekinlashtirishga olib kelishi mumkin. Postinaptik va presinaptik hujayralar presinaptik va postsinaptik hujayralarning imzo vazifalarini keskin o'zgartirishi mumkin. Bu ichki muhitga yoki boshqa hujayralardan olinadigan signallarga bog'liq. Plastisite ko'rinishidagi transformatsion kuch sinxronizatsiyaga yordam beradi. Bu energiyani o'zgartirishda muhim omil bo'lib, o'rganish va xotirada muhim rol o'ynaydi.


Kuchli kaltsiy kanallari

Kuchli kaltsiy kanallari (VGCC)-membrana potentsialining o'zgarishiga javob beradigan heteromultimerik ion kanallarining turli guruhi. VGCC'lar farmakologik bloklarga sezuvchanligi, bitta kanalli o'tkazuvchanlik kinetikasi va kuchlanishga bog'liqligi bo'yicha L-, N-, P-, Q-, R- va T tipidagi oltita sinfga bo'linadi (Reuter, 1996). T-tipli kanallar faollashtirish uchun past kuchlanishli polga ega, L-, N-, P-, Q- va R-tipli yuqori voltli pol-faollashtirilgan kanallar. VGCClar neyronlar o'rtasida signal uzatilishida muhim rol o'ynaydi va bir nechta tadqiqotlar sinaptik plastisiyaning turli shakllarida o'ziga xos turlarni nazarda tutadi (2-rasm).

L tipli ionli kanallar moxli tolalar va CA3 piramidal neyronlari orasidagi sinapslarda LTP uchun kerak. Ushbu turdagi LTP NMDA retseptorlariga bog'liq emas va L tipidagi VGCClar (Kapur) o'tkazadigan postsinaptik kaltsiy oqimini o'z ichiga oladi. va boshqalar, 1998). Bazolateral amigdala va hipokampal tishli girus o'rtasidagi sinaptik uzatishni o'rganish LTP induksiyasida L tipidagi kaltsiy kanallari uchun xuddi shunday rolni aniqladi (Nikura). va boshqalar, 2004). Ushbu kuzatuvlarga muvofiq, L tipidagi kaltsiy kanalining antagonisti nimodipinni qabul qilish LTPni yo'q qiladi va sichqonlarda qo'rquvni yumshatadi (Shinnik-Gallagher) va boshqalar, 2003). Qizig'i shundaki, kalamushlarda qarish paytida gipokampning CA1 neyronlaridagi L tipli VGCClar orqali kaltsiy oqimlari ko'payadi, bu esa o'rganish va xotira qobiliyatining sezilarli pasayishi bilan kechadi. Surunkali nimodipin bilan davolash xotira yo'qotilishini yaxshilaydi, bu esa L tipidagi kaltsiy kanallari orqali ortiqcha kaltsiy oqimi o'rganish va xotirani yomonlashishini ko'rsatadi. va boshqalar, 2003). Qizig'i shundaki, Altsgeymer kasalligi bilan og'rigan bemorlar sog'lom odamlarga qaraganda gipokampda L tipidagi VGCC yuqori ifodasini ko'rsatadi (Coon) va boshqalar, 1999). Bu havola L tipidagi kaltsiy kanalining noto'g'ri darajalari Altsgeymerli bemorlarda xotira etishmovchiligiga yordam berishi mumkinligini ko'rsatadi.

Sinaptik plastika bilan bog'liq bo'lgan boshqa VGCClarga N-, P-, Q- va R-tipli kaltsiy kanallari kiradi (Wu va boshqalar, 1999). Bu kanallar markaziy asab tizimida neyrotransmitterlarning chiqarilishiga ta'sir qiladi. P va Q tipidagi kaltsiy kanallari neyrotransmitterlarning chiqarilishini tetiklashda N- yoki R-tipli kanallarga qaraganda samaraliroqdir, chunki ular bo'shatish joylaridan uzoqroqda joylashgan. va boshqalar, 1999). Shuning uchun, P va Q tipidagi kaltsiy kanallarining o'tkazuvchanligi modulyatsiyasi sinaptik uzatgichni bo'shatishini sozlash mexanizmini ta'minlaydi. Shunga qaramay, R-tipli kanallar presinaptik ta'sir potentsiali davomida presinaptik terminallarda umumiy kaltsiy oqimining deyarli uchdan bir qismini o'tkazadi. va boshqalar, 1998). Kaltsiyning bunday oqimi sinaptik plastisitaning ba'zi shakllarining muhim tarkibiy qismidir, masalan, moxli tolalar va CA3 gipokampal neyronlari orasidagi sinapslarda LTP indüksiyasi presinaptik kaltsiyning ko'payishini talab qiladi, lekin postsinaptik kaltsiy oqimlaridan mustaqildir. R-tipli kaltsiy kanalining faolligi ushbu sinapslarda LTP induksiyasida ishtirok etadi, ammo bitta ta'sir potentsialidan kelib chiqqan neyrotransmitterlarning tez chiqishi uchun talab qilinmaydi (Ditrich). va boshqalar, 2003 ).


Ligand va kuchlanishli ionli kanalli eshiklarning umumiy va o'ziga xos jihatlari

Ligand va kuchlanish bilan bog'langan ion kanallari sog'liq va kasalliklarda ko'plab muhim rollarni bajaradigan membrana bilan bog'langan signalizatsiya oqsillarining katta superfamilasini hosil qiladi (Hille, 2001). Voltajli ion kanallari, birinchi navbatda, qo'zg'aluvchan to'qimalarda harakat potentsiallarining paydo bo'lishi va tarqalishi uchun javobgardir (Styuart). va boshqalar. 1997 yil Katterall va boshqalar. 2005 yil Yanvar va Yanvar, 2012), holbuki ligand bilan o'ralgan ion kanallari kimyoviy sinapslarning qattiq ulanishini tashkil qiladi - garchi ular barqaror naqshli faoliyat va o'zgargan gomeostaz davrida sinaptik kuchni yaxshi sozlaydi (Turrigiano, 2008 Nicoll, 2017). Birgalikda ligand va kuchlanishli kanalli kanallarning birgalikdagi faoliyati yurak va skelet mushaklarining qisqarishidan tortib, markaziy asab tizimining bilish va xotira kabi sirli xatti-harakatlariga qadar ko'plab murakkab fiziologik jarayonlarni keltirib chiqaradi.

Ion kanallarini o'rganish so'nggi yillarda misli ko'rilmagan yutuqlarga erishdi, bu muhim tadqiqot mavzusi bo'yicha bir qancha ilmiy fanlarning yaqinlashuvi bilan. Strukturaviy biologiya ion kanallari funktsiyasini va dori ta'sirini tushunishning etakchi yondashuvi sifatida paydo bo'ldi (Gouaux & Mackinnon, 2005). Bundan tashqari, genetik manipulyatsiyalarning, ayniqsa kemiruvchilarning so'nggi yutuqlari, ion kanalli oilalarga sog'liq va kasallikda alohida rollarni tayinlashga ruxsat berdi. Fiziologiyaning bu yangi sohasini o'rganish uchun, Fiziologiya jurnali 2017-yilda Braziliyaning Rio-de-Janeyro shahrida boʻlib oʻtgan Xalqaro fiziologiya fanlari ittifoqining yigʻilishida “Ligand va kuchlanish bilan bogʻlangan ion-kanallarning oʻtish mexanizmlarining umumiy va oʻziga xos jihatlari” nomli simpoziumga homiylik qildi. Raislik qilgan Jurnal muharrirlar doktor Yoshihiro Kubo va Derek Bowie tomonidan ishlab chiqilgan bo'lib, u besh tadqiqotchini (1-rasmga qarang) birlashtirdi, ularning ishi jadal rivojlanayotgan tadqiqot sohasining boshida turadi. Bu masala Fiziologiya jurnali o'z vaqtida ko'rib chiqilgan uchta maqola va simpozium paytida paydo bo'lgan ba'zi fikrlar, munozaralar va bahslarni o'z ichiga olgan asl maqolani birlashtiradi.

Yaponiya Milliy fiziologiya fanlari institutidan doktor Yoshixiro Kubo simpoziumni o‘z laboratoriyasidan olingan so‘nggi ma’lumotlarni taqdim etib, keng spektrli parazitlarga qarshi vosita ivermektinning G oqsili bilan o‘ralgan, ichkariga rektifikatsiya qiluvchi K+ (yoki GIRK) ga kutilmagan ta’sirini ko‘rib chiqdi. kanal (Chen va boshqalar. 2017). 1970 -yillarda yapon golf maydonchasi yaqinida olingan bakteriyalarning tuproq namunalari topilganidan beri (Laing va boshqalar. 2017), ivermektin veterinariya shifokorlari va sog'liqni saqlash mutaxassislari tomonidan parazit infektsiyasiga qarshi kurashda qo'llaniladigan eng samarali dorilardan biri ekanligi isbotlangan. Garchi uning anthelmintic harakati asosan nematodli glutamat bilan qoplangan xlorid kanallarining faolligini, harakatlanishini, ovqatlanishini va reproduktiv xatti-harakatlarini kamaytirishga qaratilgan bo'lsa-da (Yates va boshqalar. 2003), ivermektin GABA kabi boshqa ion kanallari oilalariga ham ta'sir qilishi ko'rsatilgan.A, glitsin va nikotinik atsetilxolin retseptorlari (Wolstenholme & Rogers, 2005). Ivermektin farmakologiyasining ko'p qirrali tabiati Chen va Kubo tomonidan har tomonlama ligandli kanalli ion kanallarida ivermektinning umumiy va noyob modulyatsion xususiyatlarini o'rganishning asosiy mavzusidir (Chen & Kubo, 2018). Ivermektinning har bir ion kanal nishoniga ta'sirini tushunish mualliflarning har bir majburiy cho'ntakning strukturaviy determinantlarini solishtirish va solishtirish uchun rentgen kristallografik ma'lumotlardan samarali foydalanishlari bilan yaxshi tasvirlangan. Hidrofobikligini hisobga olgan holda, ivermektin Cys-loop ligandli ion kanallarining transmembran (TM) hududlarini qoplaydigan qoldiqlar, masalan, nematod glutamat bilan qoplangan xlorid kanallari va sutemizuvchilar glisin retseptorlari bilan bog'lanadi. Plazma membranasining hujayradan tashqari yuzasi yaqinida ivermektinning bog'lanishi juda muhim, chunki u kanal ochilishini osonlashtirish uchun TM mintaqalarining aylanishini keltirib chiqaradi. Ajablanarlisi shundaki, ivermektin TM mintaqasi va hujayra ichidagi domenlar (Chen) interfeysida joylashgan boshqa saytdagi GIRK kanallari bilan bog'lanadi. va boshqalar. 2017). Mualliflarning xulosasiga ko'ra, ivermektin ko'plab ion kanallari maqsadlariga bog'langan bo'lsa-da, uning klinik ahamiyati kam yon ta'sirga ega bo'lgan dori sifatida uning nematod glutamat bilan qoplangan xlorid kanallari bilan afzal ko'rilgan yuqori bog'lanishi bilan ta'minlanadi.

Doktor Sesiliya Bouzat, Janubiy Milliy Universitetidan (UNS), Bahia Blanka, Argentina, o'z laboratoriyasida a7 subunitini o'z ichiga olgan nikotinik atsetilxolin retseptorlari (nAChRs) ning funktsional va farmakologik xususiyatlari bo'yicha so'nggi ishlarini taqdim etdi. va boshqalar. 2011 yil Andersen va boshqalar. 2013, 2016 Nilsen va boshqalar. 2018). nAChR butun tanada ifodalangan bo'lsa-da, a7 retseptorlari ayniqsa sutemizuvchilarning miyasida to'plangan bo'lib, ular ionotrop va metabotrop funktsiyalarni namoyon qiladi (Wu). va boshqalar. 2016 Kabbani & Nichols, 2018). Ular, shuningdek, markaziy asab tizimining bir qator kasalliklarida ishtirok etadi (Dineley va boshqalar. 2015) va natijada selektiv dorilarni ishlab chiqish zarurati tug'ildi. Bouzat va hamkasblarining sharh maqolasi (Bouzat va boshqalar. 2018) a7 nAChR haqidagi tushunchamizdagi so‘nggi yutuqlarni ta’kidlaydi. A7 retseptorlari potentsiali Altsgeymer va Parkinson kasalliklari va yallig'lanish kasalliklarini o'z ichiga olgan bir qancha neyrodejenerativ kasalliklarni davolash uchun yangi terapevtik strategiya sifatida aniqlandi, retseptorlarning faolligini kamaytiruvchi dorilar esa saraton hujayralari proliferatsiyasini davolashda foydali bo'lishi mumkin (Bouzat va boshqalar. 2018 ).

AQShning Baltimor shahridagi Jons Xopkins universitetidan doktor Frenk Bosmans u va uning hamkasblari hayvonlarning toksinlaridan foydalanib, kuchlanish bilan bog'langan ion kanallarining, xususan, kuchlanish bilan o'ralgan Na + kanallarining (Nav) funktsional xatti-harakatlarini o'rganish uchun amalga oshirgan kashshof ish haqida gapirdi. (Bosmans & Swartz, 2010 Kalia va boshqalar. 2015). Navbatdagi kuchlanishli kanallar, birinchi navbatda, yurak va skelet mushaklarining harakat potentsialining tez ko'tarilishi uchun javobgardir, shuningdek, markaziy neyronlarning otish xususiyatlarining ajralmas qismi hisoblanadi. Nav kanallari ko'plab fiziologik jarayonlarda ishtirok etishi ajablanarli emas va ular yurak disfunktsiyasi, nevropatik og'riqlar va epilepsiya genetik shakllari, masalan Dravet sindromi (Abriel, 2010 Catterall, 2012 Waxman, 2013 Chen-Izu) va boshqalar. 2015). Bularning barchasini hisobga olgan holda, Nav kanallari hamjamiyati Nav kanallarining strukturaviy arxitekturasi ularning funktsional xatti -harakatlari bilan qanday bog'liqligi to'g'risida keng qamrovli tushuncha ishlab chiqmoqda. va boshqalar. 2016). Joriy sonida Jurnal, Gilchrist va Bosmans og'riq mexanizmlari (Xan) bilan bog'liq bo'lgan Nav kanali bo'lgan Nav1.8 (Gilchrist & Bosmans, 2018) ning sekin o'tish kinetikasini tushunish uchun hayvonlarning toksinlaridan qanday foydalanish mumkinligini batafsil tavsiflovchi original tadqiqot maqolasini taqdim etadi. va boshqalar. 2016). Buning uchun mualliflar Nav1.8 ning to'rtta kuchlanish sensori domenlarining har biriga toksin sezuvchanligini ularning ketma-ketligini Nav1.2 bilan almashish orqali kanallarni ochish va inaktivatsiya qilishdagi rolini tekshirish uchun kiritdilar. Gilchrist va Bosmans ushbu ximera yondashuvidan foydalanib, I - III kuchlanish sensori domenlari kanal ochilishida ishtirok etadi, kuchlanish sensori IV esa kanalning ochilishini, shuningdek tez inaktivatsiyaning boshlanishini tartibga soladi (Gilchrist & Bosmans, 2018).

Doktor Mark Gielen London Universiteti kollejida doktor Trevor Smart bilan postdoktorlik ishi haqida ishonchli hisobotni taqdim etdi, u erda Cys-loop GABAni har tomonlama tahlil qildi.A va glitsin retseptorlari desensitizatsiyasi (Gielen va boshqalar. 2015). Parijdagi Pasteur institutidan hamkasbi doktor Pyer-Jan Korringer bilan birgalikda yozilgan sharh maqolasi-bu tour de force Cys-loop retseptorlarining tizimli biologiyasi haqidagi risola (Gielen & Corringer, 2018). Mualliflarning ta'kidlashicha, Cys-loop retseptorlarini faollashtirish mexanizmi ikkala funktsional (Lape) da keng o'rganilgan. va boshqalar. 2008 yil Muxtasimova va boshqalar. 2009 yil Purohit va boshqalar. 2013 ) va tizimli (Corringer va boshqalar. 2010 yil Althoff va boshqalar. 2014 yil Sauguet va boshqalar. 2014) darajasida desensitizatsiyaning strukturaviy asosini tushunish endigina paydo bo'la boshladi (Miller va Aricesku, 2014). Funktsional ishlar shuni ko'rsatdiki, Cys-halqa nikotinik atsetilxolin retseptorlari desensitizatsiyasi ikkita alohida, lekin o'zaro bog'liq eshiklarni o'z ichiga oladi (Auerbach & Akk, 1998), lekin ularning kanal kanalining teshiklari ichidagi joylashuvi aniqlanmagan. Mualliflar faollashtirish va desensitizatsiya eshiklari tizimli ravishda ajralib turishini va ion kanali teshiklarining har bir uchida joylashganligini taklif qiladilar. Ushbu taklif kanal blokeri pikrotoksiniga (Gielen) tayinlangan "eshikdagi oyoq" mexanizmiga mos keladi. va boshqalar. 2015) va kanalni faollashtirish Markov modellashtirish (Gielen & Corringer, 2018). Gilen va Korringer bir nechta tizimli bog'liq bo'lmagan ion kanallarining xatti-harakati uchun umumiy tushuntirish sifatida faollashtirish va desensitizatsiyaning ikkita eshik mexanizmining muhimligini ta'kidlab, xulosa qilishadi.

Kanadaning Montréal shahridagi MakGill universitetidan doktor Derek Boui simpoziumni yopdi, u ionotropik glutamat retseptorlari (iGluR) ning aniq oilalarini belgilaydigan tizimli va funktsional mexanizmlarga bag'ishlangan taqdimot bilan yakunlandi. iGluRlar umurtqali miyada keng ifodalanadi, bu erda ular markaziy sinapslarda tez qo'zg'aluvchan translyatsiyaning ko'p qismini boshqaradi (Dingledine) va boshqalar. 1999 yil Traynelis va boshqalar. 2010). IGluRlar, shuningdek, markaziy asab tizimining ko'plab zaiflashuvlarida ishtirok etishi ajablanarli emas (Bowie, 2008). Ularning o'xshash va bir-biriga o'xshash tetramerik arxitekturasiga qaramay (Sobolevskiy, 2015), Boui turli iGluR subfamiliyalarining o'ziga xos yo'l harakati xatti-harakatlari bir-birining orqasida joylashgan ikkita kichik birlik bog'lovchi cho'ntaklar o'rtasidagi interfeysni qoplaydigan qoldiqlardagi farqlar bilan bog'liq bo'lishi mumkinligini ta'kidladi. shakllanishi (Dawe va boshqalar. 2015). Proteinning bu mintaqasi ko'pincha ligand-bog'lovchi domen (LBD) dimer interfeysi deb ataladi va dastlabki tuzilmaviy tadqiqotlar natijasida kanallar darvozasini aniqlashda muhim omil sifatida tan olingan (Horning va Mayer, 2004 Bowie, 2010). Bowie laboratoriyasida o'tkazilgan so'nggi ishlar shuni ko'rsatdiki, LBD dimer interfeysi cho'qqisi AMPA va kainat tipidagi iGluRlarning millisekundlik tez harakatlanishini aniqlashda, shuningdek ularni yordamchi oqsillar (Daniels) tomonidan boshqarilishida muhim ahamiyatga ega. va boshqalar. 2013 yil Dou va boshqalar. 2013, 2016). U o'z laboratoriyasida olib borilayotgan ishlar shuni ko'rsatdiki, NMDA tipidagi iGluR-larning kechiktirilishi ham LBD dimer interfeysidagi qoldiqlar bilan, lekin boshqa joydan aniqlangan. Birgalikda olingan bu ish LBD dimer interfeysini kodlaydigan aminokislotalar ketma-ketligidagi evolyutsiya paytida turli iGluR sinflarining paydo bo'lishiga qanday nozik, ammo muhim o'zgarishlar sabab bo'lganligini ko'rsatadi.


Sinaptik kuch

Sinapsning kuchi uning faollashishi natijasida transmembran potentsialining o'zgarishi bilan belgilanadi postsinaptik neyrotransmitter retseptorlari. Voltajning bunday o'zgarishi a deb nomlanadi postsinaptik potentsial, va ion oqimlarining bevosita natijasidir post-sinaptik retseptorlari kanallari. Sinaptik kuchning o'zgarishi qisqa muddatli bo'lishi mumkin va neyronlarning o'zida doimiy konstruktiv o'zgarishsiz, bir necha soniyadan bir necha daqiqagacha davom etishi mumkin, yoki takroriy yoki uzluksiz sinaptik faollashuv natijasida ikkinchi xabarchi paydo bo'lishi mumkin. neyron yadrosida oqsil sintezini boshlaydigan molekulalar, natijada sinapsning tuzilishi o'zgaradi. O'rganish va xotira sinaptik plastisiya deb nomlanuvchi mexanizm orqali sinaptik kuchning uzoq muddatli o'zgarishi natijasida yuzaga keladi.


183 Neyronlar qanday aloqa qilishadi

Ushbu bo'lim oxirida siz quyidagilarni amalga oshirishingiz mumkin:

  • Tinchlanadigan membrana potentsialining asosini tavsiflang
  • Harakat potentsialining bosqichlarini va harakat potentsialining qanday tarqalishini tushuntiring
  • Kimyoviy va elektr sinapslarning o'xshashligi va farqini tushuntiring
  • Uzoq muddatli potentsial va uzoq muddatli depressiyani tasvirlab bering

Asab tizimi tomonidan bajariladigan barcha funktsiyalar - oddiy vosita refleksidan tortib, xotira yoki qaror qabul qilish kabi yanada rivojlangan funktsiyalargacha - neyronlar bir -biri bilan aloqa qilishni talab qiladi. Odamlar muloqot qilish uchun so'z va tana tilidan foydalansalar, neyronlar elektr va kimyoviy signallardan foydalanadilar. Xuddi qo'mitadagi odam singari, bitta neyron, xabarni boshqa neyronlarga yuborish to'g'risida qaror qabul qilishdan oldin, boshqa neyronlarning xabarlarini oladi va sintez qiladi.

Neyron ichidagi nerv impulslarining uzatilishi

Asab tizimining ishlashi uchun neyronlar signallarni yuborishi va qabul qilishi kerak. Bu signallar mumkin, chunki har bir neyron zaryadlangan uyali membranaga ega (ichki va tashqi kuchlanish farqi) va bu membrananing zaryadi boshqa neyronlar va atrof -muhit stimullaridan chiqarilgan neyrotransmitter molekulalariga javoban o'zgarishi mumkin. Neyronlar qanday aloqa qilishini tushunish uchun avval membrananing asosiy yoki "dam oluvchi" zaryadining asosini tushunish kerak.

Neyron zaryadlangan membranalar

Neyronni o'rab turgan ikki qavatli lipidli membrana zaryadlangan molekulalar yoki ionlarni o'tkazmaydi. Neyronga kirish yoki undan chiqish uchun ionlar membranada joylashgan ion kanallari deb ataladigan maxsus oqsillardan o'tishi kerak. Ion kanallari har xil konfiguratsiyaga ega: ochiq, yopiq va faol emas (rasmda). Ionlarning hujayraga kirishi yoki tashqariga o'tishi uchun ba'zi ion kanallarini faollashtirish kerak. These ion channels are sensitive to the environment and can change their shape accordingly. Ion channels that change their structure in response to voltage changes are called voltage-gated ion channels. Voltage-gated ion channels regulate the relative concentrations of different ions inside and outside the cell. The difference in total charge between the inside and outside of the cell is called the membrane potential .


This video discusses the basis of the resting membrane potential.

Resting Membrane Potential

A neuron at rest is negatively charged: the inside of a cell is approximately 70 millivolts more negative than the outside (−70 mV, note that this number varies by neuron type and by species). This voltage is called the resting membrane potential it is caused by differences in the concentrations of ions inside and outside the cell. If the membrane were equally permeable to all ions, each type of ion would flow across the membrane and the system would reach equilibrium. Because ions cannot simply cross the membrane at will, there are different concentrations of several ions inside and outside the cell, as shown in (Figure). The difference in the number of positively charged potassium ions (K + ) inside and outside the cell dominates the resting membrane potential ((Figure)). When the membrane is at rest, K + ions accumulate inside the cell due to a net movement with the concentration gradient. The negative resting membrane potential is created and maintained by increasing the concentration of cations outside the cell (in the extracellular fluid) relative to inside the cell (in the cytoplasm). The negative charge within the cell is created by the cell membrane being more permeable to potassium ion movement than sodium ion movement. In neurons, potassium ions are maintained at high concentrations within the cell while sodium ions are maintained at high concentrations outside of the cell. The cell possesses potassium and sodium leakage channels that allow the two cations to diffuse down their concentration gradient. However, the neurons have far more potassium leakage channels than sodium leakage channels. Therefore, potassium diffuses out of the cell at a much faster rate than sodium leaks in. Because more cations are leaving the cell than are entering, this causes the interior of the cell to be negatively charged relative to the outside of the cell. The actions of the sodium potassium pump help to maintain the resting potential, once established. Recall that sodium potassium pumps brings two K + ions into the cell while removing three Na + ions per ATP consumed. As more cations are expelled from the cell than taken in, the inside of the cell remains negatively charged relative to the extracellular fluid. It should be noted that chloride ions (Cl – ) tend to accumulate outside of the cell because they are repelled by negatively-charged proteins within the cytoplasm.

The resting membrane potential is a result of different concentrations inside and outside the cell.
Ion Concentration Inside and Outside Neurons
Ion Extracellular concentration (mM) Intracellular concentration (mM) Ratio outside/inside
Na + 145 12 12
K+ 4 155 0.026
Cl − 120 4 30
Organic anions (A−) 100


Harakat potentsiali

A neuron can receive input from other neurons and, if this input is strong enough, send the signal to downstream neurons. Transmission of a signal between neurons is generally carried by a chemical called a neurotransmitter. Transmission of a signal within a neuron (from dendrite to axon terminal) is carried by a brief reversal of the resting membrane potential called an action potential . When neurotransmitter molecules bind to receptors located on a neuron’s dendrites, ion channels open. At excitatory synapses, this opening allows positive ions to enter the neuron and results in depolarization of the membrane—a decrease in the difference in voltage between the inside and outside of the neuron. A stimulus from a sensory cell or another neuron depolarizes the target neuron to its threshold potential (-55 mV). Na + channels in the axon hillock open, allowing positive ions to enter the cell ((Figure) and (Figure)). Once the sodium channels open, the neuron completely depolarizes to a membrane potential of about +40 mV. Action potentials are considered an “all-or nothing” event, in that, once the threshold potential is reached, the neuron always completely depolarizes. Once depolarization is complete, the cell must now “reset” its membrane voltage back to the resting potential. To accomplish this, the Na + channels close and cannot be opened. This begins the neuron’s refractory period , in which it cannot produce another action potential because its sodium channels will not open. At the same time, voltage-gated K + channels open, allowing K + to leave the cell. As K + ions leave the cell, the membrane potential once again becomes negative. The diffusion of K + out of the cell actually hyperpolarizes the cell, in that the membrane potential becomes more negative than the cell’s normal resting potential. At this point, the sodium channels will return to their resting state, meaning they are ready to open again if the membrane potential again exceeds the threshold potential. Eventually the extra K + ions diffuse out of the cell through the potassium leakage channels, bringing the cell from its hyperpolarized state, back to its resting membrane potential.


Potassium channel blockers, such as amiodarone and procainamide, which are used to treat abnormal electrical activity in the heart, called cardiac dysrhythmia, impede the movement of K + through voltage-gated K + channels. Which part of the action potential would you expect potassium channels to affect?


This video presents an overview of action potential.

Myelin and the Propagation of the Action Potential

For an action potential to communicate information to another neuron, it must travel along the axon and reach the axon terminals where it can initiate neurotransmitter release. The speed of conduction of an action potential along an axon is influenced by both the diameter of the axon and the axon’s resistance to current leak. Myelin acts as an insulator that prevents current from leaving the axon this increases the speed of action potential conduction. In demyelinating diseases like multiple sclerosis, action potential conduction slows because current leaks from previously insulated axon areas. The nodes of Ranvier, illustrated in (Figure) are gaps in the myelin sheath along the axon. These unmyelinated spaces are about one micrometer long and contain voltage-gated Na + and K + channels. Flow of ions through these channels, particularly the Na + channels, regenerates the action potential over and over again along the axon. This ‘jumping’ of the action potential from one node to the next is called saltatory conduction . If nodes of Ranvier were not present along an axon, the action potential would propagate very slowly since Na + and K + channels would have to continuously regenerate action potentials at every point along the axon instead of at specific points. Nodes of Ranvier also save energy for the neuron since the channels only need to be present at the nodes and not along the entire axon.


Sinaptik uzatish

The synapse or “gap” is the place where information is transmitted from one neuron to another. Synapses usually form between axon terminals and dendritic spines, but this is not universally true. There are also axon-to-axon, dendrite-to-dendrite, and axon-to-cell body synapses. The neuron transmitting the signal is called the presynaptic neuron, and the neuron receiving the signal is called the postsynaptic neuron. Note that these designations are relative to a particular synapse—most neurons are both presynaptic and postsynaptic. There are two types of synapses: chemical and electrical.

Chemical Synapse

When an action potential reaches the axon terminal it depolarizes the membrane and opens voltage-gated Na + channels. Na + ions enter the cell, further depolarizing the presynaptic membrane. This depolarization causes voltage-gated Ca 2+ channels to open. Calcium ions entering the cell initiate a signaling cascade that causes small membrane-bound vesicles, called synaptic vesicles , containing neurotransmitter molecules to fuse with the presynaptic membrane. Synaptic vesicles are shown in (Figure), which is an image from a scanning electron microscope.


Fusion of a vesicle with the presynaptic membrane causes neurotransmitter to be released into the synaptic cleft , the extracellular space between the presynaptic and postsynaptic membranes, as illustrated in (Figure). The neurotransmitter diffuses across the synaptic cleft and binds to receptor proteins on the postsynaptic membrane.


The binding of a specific neurotransmitter causes particular ion channels, in this case ligand-gated channels, on the postsynaptic membrane to open. Neurotransmitters can either have excitatory or inhibitory effects on the postsynaptic membrane, as detailed in (Figure). For example, when acetylcholine is released at the synapse between a nerve and muscle (called the neuromuscular junction) by a presynaptic neuron, it causes postsynaptic Na + channels to open. Na + enters the postsynaptic cell and causes the postsynaptic membrane to depolarize. This depolarization is called an excitatory postsynaptic potential (EPSP) and makes the postsynaptic neuron more likely to fire an action potential. Release of neurotransmitter at inhibitory synapses causes inhibitory postsynaptic potentials (IPSPs) , a hyperpolarization of the presynaptic membrane. For example, when the neurotransmitter GABA (gamma-aminobutyric acid) is released from a presynaptic neuron, it binds to and opens Cl – channels. Cl – ions enter the cell and hyperpolarizes the membrane, making the neuron less likely to fire an action potential.

Once neurotransmission has occurred, the neurotransmitter must be removed from the synaptic cleft so the postsynaptic membrane can “reset” and be ready to receive another signal. This can be accomplished in three ways: the neurotransmitter can diffuse away from the synaptic cleft, it can be degraded by enzymes in the synaptic cleft, or it can be recycled (sometimes called reuptake) by the presynaptic neuron. Several drugs act at this step of neurotransmission. For example, some drugs that are given to Alzheimer’s patients work by inhibiting acetylcholinesterase, the enzyme that degrades acetylcholine. This inhibition of the enzyme essentially increases neurotransmission at synapses that release acetylcholine. Once released, the acetylcholine stays in the cleft and can continually bind and unbind to postsynaptic receptors.

Neurotransmitter Function and Location
Neyrotransmitter Misol Manzil
Asetilkolin CNS and/or PNS
Biogenic amine Dopamine, serotonin, norepinephrine CNS and/or PNS
Aminokislota Glycine, glutamate, aspartate, gamma aminobutyric acid CNS
Neuropeptide Substance P, endorphins CNS and/or PNS

Electrical Synapse

While electrical synapses are fewer in number than chemical synapses, they are found in all nervous systems and play important and unique roles. The mode of neurotransmission in electrical synapses is quite different from that in chemical synapses. In an electrical synapse, the presynaptic and postsynaptic membranes are very close together and are actually physically connected by channel proteins forming gap junctions. Gap junctions allow current to pass directly from one cell to the next. In addition to the ions that carry this current, other molecules, such as ATP, can diffuse through the large gap junction pores.

There are key differences between chemical and electrical synapses. Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is unidirectional. Signaling in electrical synapses, in contrast, is virtually instantaneous (which is important for synapses involved in key reflexes), and some electrical synapses are bidirectional. Electrical synapses are also more reliable as they are less likely to be blocked, and they are important for synchronizing the electrical activity of a group of neurons. For example, electrical synapses in the thalamus are thought to regulate slow-wave sleep, and disruption of these synapses can cause seizures.

Signal yig'indisi

Ba'zida bitta EPSP postsinaptik neyronda harakat potentsialini qo'zg'atish uchun etarlicha kuchli bo'ladi, lekin ko'pincha bir vaqtning o'zida bir nechta presinaptik kirishlar EPSP -larni yaratishi kerak, bu esa postsinaptik neyron etarlicha depolarizatsiyalanishi uchun harakat potentsialini ishga soladi. This process is called summation and occurs at the axon hillock, as illustrated in (Figure). Additionally, one neuron often has inputs from many presynaptic neurons—some excitatory and some inhibitory—so IPSPs can cancel out EPSPs and vice versa. Bu postsinaptik membrana kuchlanishining aniq o'zgarishi, postsinaptik hujayraning harakat potentsialini yoqish uchun zarur bo'lgan qo'zg'alish chegarasiga yetganligini aniqlaydi. Sinaptik yig'ish va qo'zg'alish chegarasi birgalikda filtr vazifasini bajaradi, shuning uchun tizimdagi tasodifiy "shovqin" muhim ma'lumot sifatida uzatilmaydi.


Miya-kompyuter interfeysi
Amyotrofik lateral skleroz (ALS, Lou Gehrig kasalligi deb ham ataladi) - bu ixtiyoriy harakatlarni boshqaruvchi motorli neyronlarning degeneratsiyasi bilan tavsiflanadigan nevrologik kasallik. Kasallik mushaklarning kuchsizlanishidan va muvofiqlashtirishning etishmasligidan boshlanadi va oxir -oqibat nutqni, nafas olishni va yutishni boshqaruvchi neyronlarni yo'q qiladi, kasallik falajga olib kelishi mumkin. O'sha paytda bemorlar nafas olish va muloqot qilish uchun mashinalar yordamiga muhtoj. "Qulflangan" bemorlarga dunyoning qolgan qismi bilan muloqot qilish imkonini beradigan bir nechta maxsus texnologiyalar ishlab chiqilgan. Bitta texnologiya, masalan, bemorlarga yonoqlarini qimirlatib jumlalarni yozishga imkon beradi. Bu jumlalarni keyinchalik kompyuter ovoz chiqarib o'qishi mumkin.

A relatively new line of research for helping paralyzed patients, including those with ALS, to communicate and retain a degree of self-sufficiency is called brain-computer interface (BCI) technology and is illustrated in (Figure). This technology sounds like something out of science fiction: it allows paralyzed patients to control a computer using only their thoughts. BCI ning bir nechta shakllari mavjud. Ba'zi shakllarda bosh suyagiga yopishtirilgan elektrodlardan EEG yozuvlari qo'llaniladi. Bu yozuvlar neyronlarning katta populyatsiyasidan olingan ma'lumotlarni o'z ichiga oladi, ular kompyuter yordamida dekodlanishi mumkin. BCI ning boshqa shakllari vosita korteksining qo'l va qo'l sohasiga pochta markasidan kichikroq elektrodlar qatorini implantatsiya qilishni talab qiladi. BCI ning bu shakli, ko'proq invaziv bo'lsa-da, juda kuchli, chunki har bir elektrod bir yoki bir nechta neyronlarning haqiqiy harakat potentsiallarini yozib olishi mumkin. Keyin bu signallar kompyuterga yuboriladi, u signalni dekodlash va uni asbobga uzatishga o'rgatilgan, masalan, kompyuter ekranidagi kursor. Bu shuni anglatadiki, ALS bilan kasallangan bemor elektron pochtadan foydalanishi, Internetni o'qishi va qo'lini yoki qo'lini harakatga keltirishni o'ylab, boshqalar bilan muloqot qilishi mumkin (garchi shol bo'lgan bemor bu tana harakatini amalga oshirolmasa ham). So'nggi yutuqlar, 15 yil oldin insultga uchragan falajlangan, qulflangan bemorga robot qo'lini boshqarishga va hatto BCI texnologiyasidan foydalanib, o'zini qahva bilan boqishga imkon berdi.

BCI texnologiyasining ajoyib yutuqlariga qaramay, uning cheklovlari ham bor. Texnologiya ko'p soatlik mashg'ulotlarni va bemor uchun uzoq vaqt intensiv konsentratsiyani talab qilishi mumkin, shuningdek, asboblarni joylashtirish uchun miya jarrohligini ham talab qilishi mumkin.


Watch this video in which a paralyzed woman uses a brain-controlled robotic arm to bring a drink to her mouth, among other images of brain-computer interface technology in action.

Sinaptik plastika

Synapses are not static structures. They can be weakened or strengthened. They can be broken, and new synapses can be made. Synaptic plasticity allows for these changes, which are all needed for a functioning nervous system. In fact, synaptic plasticity is the basis of learning and memory. Two processes in particular, long-term potentiation (LTP) and long-term depression (LTD) are important forms of synaptic plasticity that occur in synapses in the hippocampus, a brain region that is involved in storing memories.

Long-term Potentiation (LTP)

Long-term potentiation (LTP) is a persistent strengthening of a synaptic connection. LTP is based on the Hebbian principle: cells that fire together wire together. There are various mechanisms, none fully understood, behind the synaptic strengthening seen with LTP. One known mechanism involves a type of postsynaptic glutamate receptor, called NMDA (N-Methyl-D-aspartate) receptors, shown in (Figure). These receptors are normally blocked by magnesium ions however, when the postsynaptic neuron is depolarized by multiple presynaptic inputs in quick succession (either from one neuron or multiple neurons), the magnesium ions are forced out allowing Ca ions to pass into the postsynaptic cell. Next, Ca 2+ ions entering the cell initiate a signaling cascade that causes a different type of glutamate receptor, called AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) receptors, to be inserted into the postsynaptic membrane, since activated AMPA receptors allow positive ions to enter the cell. So, the next time glutamate is released from the presynaptic membrane, it will have a larger excitatory effect (EPSP) on the postsynaptic cell because the binding of glutamate to these AMPA receptors will allow more positive ions into the cell. The insertion of additional AMPA receptors strengthens the synapse and means that the postsynaptic neuron is more likely to fire in response to presynaptic neurotransmitter release. Some drugs of abuse co-opt the LTP pathway, and this synaptic strengthening can lead to addiction.

Long-term Depression (LTD)

Long-term depression (LTD) is essentially the reverse of LTP: it is a long-term weakening of a synaptic connection. One mechanism known to cause LTD also involves AMPA receptors. In this situation, calcium that enters through NMDA receptors initiates a different signaling cascade, which results in the removal of AMPA receptors from the postsynaptic membrane, as illustrated in (Figure). The decrease in AMPA receptors in the membrane makes the postsynaptic neuron less responsive to glutamate released from the presynaptic neuron. While it may seem counterintuitive, LTD may be just as important for learning and memory as LTP. The weakening and pruning of unused synapses allows for unimportant connections to be lost and makes the synapses that have undergone LTP that much stronger by comparison.


Bo'lim haqida qisqacha ma'lumot

Neurons have charged membranes because there are different concentrations of ions inside and outside of the cell. Voltage-gated ion channels control the movement of ions into and out of a neuron. When a neuronal membrane is depolarized to at least the threshold of excitation, an action potential is fired. The action potential is then propagated along a myelinated axon to the axon terminals. In a chemical synapse, the action potential causes release of neurotransmitter molecules into the synaptic cleft. Through binding to postsynaptic receptors, the neurotransmitter can cause excitatory or inhibitory postsynaptic potentials by depolarizing or hyperpolarizing, respectively, the postsynaptic membrane. In electrical synapses, the action potential is directly communicated to the postsynaptic cell through gap junctions—large channel proteins that connect the pre-and postsynaptic membranes. Synapses are not static structures and can be strengthened and weakened. Two mechanisms of synaptic plasticity are long-term potentiation and long-term depression.

Vizual ulanish uchun savollar

(Figure) Potassium channel blockers, such as amiodarone and procainamide, which are used to treat abnormal electrical activity in the heart, called cardiac dysrhythmia, impede the movement of K+ through voltage-gated K+ channels. Which part of the action potential would you expect potassium channels to affect?

(Figure) Potassium channel blockers slow the repolarization phase, but have no effect on depolarization.

Takrorlash uchun savollar

For a neuron to fire an action potential, its membrane must reach ________.

  1. hyperpolarization
  2. the threshold of excitation
  3. refrakter davri
  4. inhibitory postsynaptic potential

After an action potential, the opening of additional voltage-gated ________ channels and the inactivation of sodium channels, cause the membrane to return to its resting membrane potential.

What is the term for protein channels that connect two neurons at an electrical synapse?

  1. synaptic vesicles
  2. voltage-gated ion channels
  3. gap junction protein
  4. sodium-potassium exchange pumps

Which of the following molecules is emas involved in the maintenance of the resting membrane potential?

Tanqidiy fikrlash uchun savollar

How does myelin aid propagation of an action potential along an axon? How do the nodes of Ranvier help this process?

Myelin prevents the leak of current from the axon. Nodes of Ranvier allow the action potential to be regenerated at specific points along the axon. They also save energy for the cell since voltage-gated ion channels and sodium-potassium transporters are not needed along myelinated portions of the axon.

What are the main steps in chemical neurotransmission?

An action potential travels along an axon until it depolarizes the membrane at an axon terminal. Depolarization of the membrane causes voltage-gated Ca 2+ channels to open and Ca 2+ to enter the cell. The intracellular calcium influx causes synaptic vesicles containing neurotransmitter to fuse with the presynaptic membrane. The neurotransmitter diffuses across the synaptic cleft and binds to receptors on the postsynaptic membrane. Depending on the specific neurotransmitter and postsynaptic receptor, this action can cause positive (excitatory postsynaptic potential) or negative (inhibitory postsynaptic potential) ions to enter the cell.

Describe how long-term potentiation can lead to a nicotine addiction.

Long-term potentiation describes the process whereby exposure to a stimulus increases the likelihood that a neuron will depolarize in response to that stimulus in the future. Nicotine exposure causes long-term potentiation of neurons in the amygdala, and activates reward centers of the brain. As nicotine exposure continues, long-term potentiation reinforces the activation of the reward pathways in response to nicotine consumption.

Lug'at


DMCA shikoyati

Agar siz veb-sayt orqali mavjud bo'lgan kontent (bizning xizmat ko'rsatish shartlarimizda belgilanganidek) bir yoki bir nechta mualliflik huquqlaringizni buzadi deb hisoblasangiz, quyida tavsiflangan ma'lumotlarni o'z ichiga olgan yozma bildirishnoma ("Buzilish to'g'risida bildirishnoma") orqali bizga xabar bering. agenti quyida keltirilgan. Agar Varsity Repetitorlari huquqbuzarlik to‘g‘risidagi bildirishnomaga javoban chora ko‘rsalar, u bunday kontentni taqdim etgan tomon bilan Varsity Repetitorlariga taqdim etgan eng so‘nggi elektron pochta manzili (agar mavjud bo‘lsa) orqali bog‘lanishga vijdonan harakat qiladi.

Sizning huquqbuzarlik haqidagi bildirishnomangiz kontentni taqdim etgan tomonga yoki ChillingEffects.org kabi uchinchi shaxslarga yuborilishi mumkin.

Iltimos, agar siz mahsulot yoki faoliyat mualliflik huquqlaringizni buzayotganini jiddiy ravishda noto'g'ri ko'rsatgan bo'lsangiz, siz zarar uchun (xarajatlar va advokatlarning to'lovlari bilan birga) javobgar bo'lasiz. Shunday qilib, agar siz veb-saytda joylashgan yoki u bilan bog'langan kontent sizning mualliflik huquqingizni buzayotganiga amin bo'lmasangiz, avval advokatga murojaat qilishingiz kerak.

Xabar yuborish uchun quyidagi amallarni bajaring:

Siz quyidagilarni kiritishingiz kerak:

Mualliflik huquqi egasining yoki ularning nomidan harakat qilishga vakolatli shaxsning jismoniy yoki elektron imzosi. Mualliflik huquqi buzilgan deb da'vo qilingan mualliflik huquqining identifikatsiyasi. Varsity o'qituvchilariga mazkur tarkibni topishga va ijobiy aniqlashga ruxsat beradigan tafsilotlar, masalan, biz savolga havolani talab qilamiz (faqat savolning nomi emas), unda mazmun va savolning qaysi qismi - tasvir, havola, matn va h.k. – shikoyatingiz ismingiz, manzilingiz, telefon raqamingiz va elektron pochta manzilingizga taalluqlidir hamda Sizning bayonotingiz: (a) siz mualliflik huquqini buzish deb daʼvo qilayotgan kontentdan foydalanishga vijdonan ishonasiz. qonun yoki mualliflik huquqi egasi yoki uning egasi agenti tomonidan ruxsat etilmagan (b) sizning buzilish xabarnomangizdagi barcha ma'lumotlar to'g'ri va (v) yolg'on guvohlik berish jazosi ostida. mualliflik huquqi egasi yoki ularning nomidan harakat qilishga vakolatli shaxs.

Shikoyatingizni bizning vakilimizga yuboring:

Charlz Kon Varsity Tutors MChJ
101 S. Hanley Rd, Suite 300
Sent -Luis, MO 63105


Videoni tomosha qiling: Sinapsning tuzilishi va tasnifi. Nerv tizimi. Tibbiyot (Iyul 2022).


Izohlar:

  1. Guy

    You have missed the most important thing.

  2. Meztikinos

    Menimcha, xatolar amalga oshiriladi. Buni muhokama qilishga harakat qilaylik. Menga kechqurun menga yozing, u siz bilan gaplashmoqda.

  3. Philoctetes

    Qiziq, lekin bu aniq emas

  4. Aurik

    Men sizning mavzuingizda ko'plab maqolalar mavjud bo'lgan saytga kelishni maslahat beraman.

  5. Jaylend

    To'g'ridan-to'g'ri buqaning ko'ziga



Xabar yozing