• 한국산업정보학회논문지
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• 제4권1호
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• pp.68-76
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• 1999

신경회로망을 동적 정보처리에 응용하기 위해서는 비대칭 결합 신경회로망에서 생성되는 동적 상태천이에 관한 직관적 이해가 필요하다. 본 논문에서는 각 뉴런이 최근접 뉴런에만 양자화 결합하중 +1및 -1로 연결된 환상형 신경회로망의 동적인 상태천이 특성을 해석하였다. 상태천이 해석 알고리즘을 이용한 시뮬레이션 결과, 네트워크는 고정점, 베이슨을 갖는 리미트사이클 및 베이슨이 없는 리미트사이클의 3가지 어트랙터를 가진다. 또한, 네트워크에서 생성되는 리미트사이클의 수와 주기를 이론적으로 해석하여 정식화하고, 리미트사이클을 구성하는 상태벡터의 필요조건을 나타내었다. 이론 해석의 결과는 네트워크에서 생성되는 리미트사이클의 수가 뉴런(소자)의 수 n에 대해서 지수 함수적으로 증가함을 보여준다. 따라서 순환결합형 신경회로망은 많은 동적 정보를 리미트사이클로 저장하는 메모리 시스템으로 이용할 수 있다.

• The Korean Journal of Physiology and Pharmacology
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• 제1권6호
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• pp.681-690
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• 1997

Loss of synaptic transmission and accumulation of extracellular $K^+([K^+]_O)$ are the key features in ischemic brain damage. Here, we examined the effects of several $K^+$channel modulators on the early ischemic changes in population spike (PS) and $[K^+]_o$ in the CA1 pyramidal layer of the rat hippocampal slice using electrophysiological techniques. After onset of anoxic aglycemia (AA), orthodromic field potentials decreased and disappeared in $3.3{\pm}0.22\;min$ $(mean{\pm}SEM,\;n=40)$. The hypoxic injury potential (HIP), a transient recovery of PS appeared at $6.0{\pm}0.25\;min$ (n=40) in most slices during AA and lasted for $3.3{\pm}0.43\;min$. $[K^+]_o$ increased initially at a rate of 0.43 mM/min (Phase 1) and later at a much faster rate (12.45 mM/min, Phase 2). The beginning of Phase 2 was invariably coincided with the disappearance of HIP. Among $K^+$ channel modulators tested such as 4-aminopyridine (0.03, 0.3 mM), tetraethylammonium (0.1 mM), NS1619 $(0.3{\sim}10\;{\mu}M)$, niflumic acid (0.1 mM), glibenclamide $(40\;{\mu}M)$, tolbutamide $(300\;{\mu}M)$ and pinacidil $(100\;{\mu}M)$, only 4-aminopyridine (0.3 mM) induced slight increase of $[K^+]_o$ during Phase 1. However, none of the above agents modulated the pattern of Phase 2 in $[K^+]_o$ in response to AA. Taken together, the experimental data suggest that 4-aminopyridine-sensitive $K^+$channels, large conductance $Ca^{2+}-activated$ $K^+$ channels and ATP-sensitive $K^+$ channels may not be the major contributors to the sudden increase of $[K^+]_o$ during the early stage of brain ischemia, suggesting the presence of other routes of $K^+$ efflux during brain ischemia.

• 생물정신의학
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• 제16권1호
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• pp.5-14
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• 2009

Objectives : Most of the mechanisms reported for antidepressant drugs are the enhancement of neurite outgrowth and neuronal survival in the rat hippocampus. Neural cell adhesion molecule 140(NCAM140) has been implicated as having a role in cell-cell adhesion, neurite outgrowth, and synaptic plasticity. In this report, we have performed to elucidate a correlation among chronic antidepressant treatments, NCAM140 expression, and activation of phosphorylated cyclicAMP responsive element binding protein(pCREB) which is a downstream molecule of NCAM140-mediated intracellular signaling pathway in the rat hippocampus. Methods : Fluoxetine(10mg/kg) was injected acutely(daily injection for 5days) or chronically(daily injection for 14days) in adult rats. RNA and protein were extracted from the rat hippocampus, respectively. Real-time RT-PCR was performed to analyze the expression pattern of NCAM140 gene and western blot analyses for the activation of the phosphorylation ratio of CREB. Results : Chronic fluoxetine treatments increased NCAM140 expression 1.3 times higher than control in rat hippocampus. pCREB immunoreactivity in the rat hippocampus with chronic fluoxetine treatment was increased 4.0 times higher than that of control. Conclusion : Chronic fluoxetine treatment increased NCAM140 expression and pCREB activity in the rat hippocampus. Our data suggest that NCAM140 and pCREB may play a role in the clinical efficacy of antidepressants promoting the neurite outgrowth and neuronal survival.