کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4339671 | 1295763 | 2010 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Cholinergic modulation of non-N-methyl-d-aspartic acid glutamatergic transmission in the chick ventral lateral geniculate nucleus
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کلمات کلیدی
LGNvHEPESCGPEGTAMCPGaCSFAP54-(2-hydroxyethyl)-1-piperazineethanesulfonic acid - 4- (2-hydroxyethyl) -1-piperazineethanesulfonic acidD(−)-2-amino-5-phosphonopentanoic acid - D (-) - 2-amino-5-phosphonopentanoic acidDHβE - DHBAELGNd - LGNDACh - آهethylene glycol tetraacetic acid - اتیلن گلیکول تتراستیک اسیدAcetylcholine - استیل کولینanalysis of variance - تحلیل واریانسANOVA - تحلیل واریانس Analysis of variancedihydro-β-erythroidine - دی هیدرو-β-erythroidineartificial cerebrospinal fluid - مایع مغزی نخاعی مصنوعیpresynaptic modulation - مدولاسیون پیش فرضdorsal lateral geniculate nucleus - هسته منشاء جانبی پشتی پشتیventral lateral geniculate nucleus - هسته ژنیکولت جانبی جانبی جناغیMuscarinic receptors - گیرنده های MuscarinicNicotinic receptors - گیرنده های نیکوتین
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Cholinergic modulation of non-N-methyl-d-aspartic acid glutamatergic transmission in the chick ventral lateral geniculate nucleus Cholinergic modulation of non-N-methyl-d-aspartic acid glutamatergic transmission in the chick ventral lateral geniculate nucleus](/preview/png/4339671.png)
چکیده انگلیسی
Neurotransmission between glutamatergic terminals of retinal ganglion cells and principal neurons of the ventral lateral geniculate nucleus (LGNv) was examined with patch clamp recordings in chick brain slices during electrical stimulation of the optic tract. Since muscarinic and nicotinic receptors are present in high densities in LGNv, the present study examined possible roles of both receptors in modulating retinogeniculate transmission. During whole-cell recordings from LGNv neurons, acetylcholine (ACh, 100 μM) caused an initial increase in amplitudes of optic tract-evoked non-N-methyl-d-aspartic acid (NMDA) glutamatergic postsynaptic currents (PSCs). This increase was unchanged when 1 μM atropine was present, indicating that this initial enhancement of PSCs was due entirely to activation of nicotinic receptors. However, during washout of ACh the amplitudes of evoked PSCs became significantly decreased by 40.4±5.0% for several minutes before recovering to their original amplitudes, an effect blocked by 1 μM atropine. Exogenously applied muscarine (10 μM) markedly depressed optic tract-evoked PSCs, and this decrease in amplitude was blocked by atropine. In a second set of experiments, we examined effects of releasing endogenous ACh prior to optic tract stimulation. This was accomplished by stimulation of the lateral portion of LGNv via a separate conditioning electrode. Following a brief train of low intensity conditioning stimuli, non-NMDA glutamatergic PSCs evoked by optic tract stimulation were potentiated. However, at higher conditioning stimulus intensities the PSCs were markedly decreased compared with control, and this decrease was partially blocked by atropine (1 μM). Neither ACh nor muscarine altered amplitudes of PSCs elicited by exogenously applied glutamate. Muscarine significantly reduced the frequency but not the amplitudes of miniature PSCs, consistent with a presynaptic location for muscarinic receptors mediating these effects. Thus while activation of nicotinic receptors potentiates retinogeniculate transmission, activation of muscarinic receptors mediates depression of transmission, demonstrating a complex cholinergic modulation of sensory information in LGNv.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 166, Issue 2, 17 March 2010, Pages 604-614
Journal: Neuroscience - Volume 166, Issue 2, 17 March 2010, Pages 604-614
نویسندگان
J.-Z. Guo, E.M. Sorenson, V.A. Chiappinelli,