کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9425644 | 1295885 | 2005 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Prefrontal cortical modulation of acetylcholine release in posterior parietal cortex
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کلمات کلیدی
BFCSPFCPPCDNQXAMPAaCSF6,7-dinitroquinoxaline-2,3-dione - 6،7-dinitroquinoxaline-2،3-dioneACh - آهAcetylcholine - استیل کولینanalysis of variance - تحلیل واریانسANOVA - تحلیل واریانس Analysis of varianceAttention - توجهCortex - قشرprefrontal cortex - قشر prefrontalposterior parietal cortex - قشر پاراوتیک خلفیartificial cerebrospinal fluid - مایع مغزی نخاعی مصنوعیmicrodialysis - میکرو دیالیزbasal forebrain - پیشانی پایهglutamate - گلوتامات
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
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چکیده انگلیسی
Attentional processing is a crucial early stage in cognition and is subject to “top-down” regulation by prefrontal cortex (PFC). Top-down regulation involves modification of input processing in cortical and subcortical areas, including the posterior parietal cortex (PPC). Cortical cholinergic inputs, originating from the basal forebrain cholinergic system, have been demonstrated to mediate important aspects of attentional processing. The present study investigated the ability of cholinergic and glutamatergic transmission within PFC to regulate acetylcholine (ACh) release in PPC. The first set of experiments demonstrated increases in ACh efflux in PPC following AMPA administration into the PFC. These increases were antagonized by co-administration of the AMPA receptor antagonist DNQX into the PFC. The second set of experiments demonstrated that administration of carbachol, but not nicotine, into the PFC also increased ACh efflux in PPC. The effects of carbachol were attenuated by co-administration (into PFC) of a muscarinic antagonist (atropine) and partially attenuated by the nicotine antagonist mecamylamine and DNQX. Perfusion of carbachol, nicotine, or AMPA into the PPC did not affect PFC ACh efflux, suggesting that these cortical interactions are not bi-directional. These studies demonstrate the capacity of the PFC to regulate ACh release in the PPC via glutamatergic and cholinergic prefrontal mechanisms. Prefrontal regulation of ACh release elsewhere in the cortex is hypothesized to contribute to the cognitive optimization of input processing.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 132, Issue 2, 2005, Pages 347-359
Journal: Neuroscience - Volume 132, Issue 2, 2005, Pages 347-359
نویسندگان
C.L. Nelson, M. Sarter, J.P. Bruno,