Stelzer A, Simon G, Kovacs G, Rai R
Department of Pharmacology, State University of New York, Brooklyn 11203.
Proc Natl Acad Sci U S A. 1994 Apr 12;91(8):3058-62. doi: 10.1073/pnas.91.8.3058.
Long-term potentiation (LTP) in the CA1 region of the hippocampus is widely believed to occur through a strengthening of efficacy of excitatory synapses between afferent fibers and pyramidal cells. An alternative mechanism of LTP, reduction of efficacy of synaptic inhibition, was examined in the present report. The present study demonstrates that the maintenance of LTP in the CA1 hippocampal subfield of guinea pigs is accompanied by impairment of type A gamma-aminobutyric acid (GABA) receptor function, particularly at apical dendritic sites of CA1 pyramidal cells. Enhanced excitability of GABAergic interneurons during LTP represents a strengthening of inhibitory efficacy. The net effect of opposite modifications of synaptic inhibition during LTP of CA1 pyramidal cells is an overall impairment of the strength of GABAergic inhibition, and disinhibition could contribute importantly to CA1 pyramidal cell LTP.
人们普遍认为，海马体CA1区的长时程增强（LTP）是通过增强传入纤维与锥体细胞之间兴奋性突触的效能而发生的。本报告研究了LTP的另一种机制，即突触抑制效能的降低。本研究表明，豚鼠海马CA1亚区LTP的维持伴随着A型γ-氨基丁酸（GABA）受体功能的损害，特别是在CA1锥体细胞的顶端树突部位。LTP期间GABA能中间神经元兴奋性的增强代表着抑制效能的增强。CA1锥体细胞LTP期间突触抑制的相反变化的净效应是GABA能抑制强度的整体损害，去抑制可能对CA1锥体细胞LTP起重要作用。
