کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6279430 | 1615072 | 2016 | 22 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Genetic knockout of the α7 nicotinic acetylcholine receptor gene alters hippocampal long-term potentiation in a background strain-dependent manner
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کلمات کلیدی
HFSpaired-pulse responseCHRNA7LFSα7 nAChRPPRfEPSPaCSFHET - ITAlpha 7 nicotinic acetylcholine receptor - آلفا 7 گیرنده استیل کولین نیکوتینlong-term depression - افسردگی طولانی مدتHippocampal slice - برش هیپوکامپlow-frequency stimulation - تحریک با فرکانس پایینhigh frequency stimulation - تحریک فرکانس بالاlong-term potentiation - تقویت درازمدتLTP - تقویت طولانی مدت یا LTP artificial cerebrospinal fluid - مایع مغزی نخاعی مصنوعیLTD - محدودMouse - موشknockout - ناکاوتwild-type - نوع وحشیheterozygous - هتروزیگوتField excitatory postsynaptic potential - پتانسیل پستنیپتیک مزمن تحریک پذیرGenetics - ژنتیکα7 nicotinic acetylcholine receptor - گیرنده استیل کولین نیکوتینیک α7
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Reduced α7 nicotinic acetylcholine receptor (nAChR) function is linked to impaired hippocampal-dependent sensory processing and learning and memory in schizophrenia. While knockout of the Chrna7 gene encoding the α7nAChR on a C57/Bl6 background results in changes in cognitive measures, prior studies found little impact on hippocampal synaptic plasticity in these mice. However, schizophrenia is a multi-genic disorder where complex interactions between specific genetic mutations and overall genetic background may play a prominent role in determining phenotypic penetrance. Thus, we compared the consequences of knocking out the α7nAChR on synaptic plasticity in C57/Bl6 and C3H mice, which differ in their basal α7nAChR expression levels. Homozygous α7 deletion in C3H mice, which normally express higher α7nAChR levels, resulted in impaired long-term potentiation (LTP) at hippocampal CA1 synapses, while C3H α7 heterozygous mice maintained robust LTP. In contrast, homozygous α7 deletion in C57 mice, which normally express lower α7nAChR levels, did not alter LTP, as had been previously reported for this strain. Thus, the threshold of Chrna7 expression required for LTP may be different in the two strains. Measurements of auditory gating, a hippocampal-dependent behavioral paradigm used to identify schizophrenia-associated sensory processing deficits, was abnormal in C3H α7 knockout mice confirming that auditory gating also requires α7nAChR expression. Our studies highlight the importance of genetic background on the regulation of synaptic plasticity and could be relevant for understanding genetic and cognitive heterogeneity in human studies of α7nAChR dysfunction in mental disorders.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience Letters - Volume 627, 3 August 2016, Pages 1-6
Journal: Neuroscience Letters - Volume 627, 3 August 2016, Pages 1-6
نویسندگان
Ronald K. Freund, Sharon Graw, Kevin S. Choo, Karen E. Stevens, Sherry Leonard, Mark L. Dell'Acqua,