کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6278367 | 1295816 | 2009 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Late phase of long-term potentiation induced by co-application of N-methyl-d-aspartic acid and the antagonist of NR2B-containing N-methyl-d-aspartic acid receptors in rat hippocampus
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کلمات کلیدی
pKafEPSPAP5E-LTPNMDARNMDAN-methyl-d-aspartic acid receptorN-methyl-d-aspartic acidaCSFL-LTPPPFRo25-6981CREB2-amino-5-phosphonovaleric acid - 2-آمینو-5-فسفونوالریک اسیدBDNF - BDNF یا فاکتور نورونزایی مشتقشده از مغز DMSO - DMSOMAPK - MAPKlong-term depression - افسردگی طولانی مدتpaired-pulse facilitation - تسکین زوایای پالسیlong-term potentiation - تقویت درازمدتLTP - تقویت طولانی مدت یا LTP Dimethyl sulfoxide - دیمتیل سولفواکسیدProtein synthesis - سنتز پروتئینBrain-derived neurotrophic factor - فاکتور نوروتروفی مشتق شده از مغزartificial cerebrospinal fluid - مایع مغزی نخاعی مصنوعیLTD - محدودHippocampus - هیپوکامپ field excitatory post-synaptic potential - پتانسیل پس از سیناپسی مزمن تحریک پذیرcAMP-responsive element binding protein - پروتئین اتصال دهنده عنصر پاسخ دهنده cAMPprotein kinase A - پروتئین کیناز Amitogen-activated protein kinase - پروتئین کیناز فعال با mitogencAMP-dependent protein kinase - پروتئین کیناز وابسته به cAMP
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Late phase of long-term potentiation induced by co-application of N-methyl-d-aspartic acid and the antagonist of NR2B-containing N-methyl-d-aspartic acid receptors in rat hippocampus Late phase of long-term potentiation induced by co-application of N-methyl-d-aspartic acid and the antagonist of NR2B-containing N-methyl-d-aspartic acid receptors in rat hippocampus](/preview/png/6278367.png)
چکیده انگلیسی
Activation of N-methyl-d-aspartic acid (NMDA) glutamate receptors (NMDARs) is required for long-term potentiation (LTP) of excitatory synaptic transmission at hippocampal CA1 synapses, the proposed cellular mechanisms of learning and memory. We demonstrate here that a brief bath co-application of a low concentration of NMDA, an agonist of NMDARs, and the selective antagonist of NR2B-containing NMDARs, (α R, β S)-α-(4-hydroxyphenyl)-β-methyl-4-(phenylmethyl)-1-piperidinepropanol (Ro25-6981), to hippocampal slices from young adult rats produced a slowly developing LTP persisting at least for 6 h following a transient depression of synaptic transmission in CA1 synapses. The LTP was likely to occur at postsynaptic site and was initiated by activation of NMDARs, and its development was mediated by cAMP-dependent protein kinase (PKA) activation and protein synthesis. This chemically induced LTP and the tetanus-induced late phase of LTP (L-LTP) were mutually occluding, suggesting a common expression mechanism. Thus, we have demonstrated that a brief bath co-application of NMDA with Ro25-6981 to a slice offers an alternative to electrical stimulation as a stimulation method to induce L-LTP. The chemically induced LTP did not require the low-frequency test stimulation typically used to monitor the strength of synapses during and after drug application. Thus, the LTP may occur at a large fraction of synapses in the slice and not to be confined to a small fraction of the synapses where electrical stimulation can reach and induce LTP. Therefore, this chemically induced LTP may be useful for assessing the biochemical and morphological correlates and the molecular aspects of the expression mechanism for L-LTP that has been proven to correlate to hippocampal long-term memory.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 159, Issue 1, 3 March 2009, Pages 127-135
Journal: Neuroscience - Volume 159, Issue 1, 3 March 2009, Pages 127-135
نویسندگان
A. Oh-Nishi, M. Saji, S.-Z. Satoh, M. Ogata, N. Suzuki,