کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9425668 | 1295886 | 2005 | 15 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Brain-derived neurotrophic factor modulates GABAergic synaptic transmission by enhancing presynaptic glutamic acid decarboxylase 65 levels, promoting asynchronous release and reducing the number of activated postsynaptic receptors
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کلمات کلیدی
SSSS.Dtetramethyl rhodamine isothiocyanatevesicular inhibitory amino acid transporterRRPTRITCPPRTTXGADSSCPBSFITCEGTAHEPESROIBDNF - BDNF یا فاکتور نورونزایی مشتقشده از مغز glutamic acid decarboxylase - glutamic acid dearboxylaseN-2-hydroxyethylpiperazine-N′-2-ethanesulfonic acid - N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acidRelease probability - احتمال آزاد شدنsynaptic transmission - انتقال سیناپسیstandard deviation - انحراف معیارreadily releasable pool - به راحتی استخر آزادtetrodotoxin - تترو دوتوکسین Visual system - دستگاه بینایی، ویژوال سیستمpostnatal day - روز پس از زایمانSuperior colliculus - ستارگان برترSynapsin I - سیناپسین ICoefficient of Variation - ضریب تغییرBrain-derived neurotrophic factor - فاکتور نوروتروفی مشتق شده از مغزfluorescein isothiocyanate - فلوئورسین ایسوتیوسیاناتPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریRegions Of Interest - مناطق مورد علاقهpaired-pulse ratio - نسبت پالس زوجmap - نقشهNeurotrophins - نوروتروفین VIAAT - ویااتmicrotubule-associated protein - پروتئین مرتبط با میکروتوبولGABAAR - گابارGABAA receptor - گیرنده GABAA یا گیرنده گابا
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
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چکیده انگلیسی
Brain-derived neurotrophic factor is known to modulate the function of GABAergic synapses, but the site of brain-derived neurotrophic factor action is still a matter of controversy. This study was aimed at further dissecting the functional alterations produced by brain-derived neurotrophic factor treatment of GABAergic synaptic connections in cultures of the murine superior colliculus. The functional consequences of long-term brain-derived neurotrophic factor treatment were assessed by analysis of unitary evoked and delayed inhibitory postsynaptic currents in response to high frequency stimulation of single axons. It was found that brain-derived neurotrophic factor facilitated the asynchronous release, but had no effect on the probability of evoked release, the size of the readily releasable pool, and the paired-pulse behavior of evoked inhibitory postsynaptic currents. However, the amplitudes of evoked inhibitory postsynaptic currents, delayed inhibitory postsynaptic currents and miniature inhibitory postsynaptic currents were significantly reduced. Non-stationary fluctuation analysis revealed a decrease in the open channel number at the miniature/evoked inhibitory postsynaptic current peak, but no effect on the mean GABAA receptor single channel conductance. Quantitative immunocytochemistry uncovered a significant elevation of presynaptic levels of glutamic acid decarboxylase 65. Together, these findings indicate that brain-derived neurotrophic factor treatment induces pre- as well as postsynaptic changes. What effect predominates will depend on the presynaptic activity pattern: at low activation rates brain-derived neurotrophic factor-treated synapses display a pronounced postsynaptic depression, but at high frequencies this depression is fully compensated by an enhancement of asynchronous release.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 135, Issue 3, 2005, Pages 749-763
Journal: Neuroscience - Volume 135, Issue 3, 2005, Pages 749-763
نویسندگان
C. Henneberger, S. Kirischuk, R. Grantyn,