Corticotropin-releasing factor (CRF) receptor type 1-dependent modulation of synaptic plasticity
详细信息    查看全文
文摘
CRF receptor type (CRHR) 1 exerts neuroregulatory control on associative learning processes such as fear and anxiety like behaviour. Using hippocampal slices, we investigated the neuronal excitability in mice lacking CRHR1 (Crhr1−/−). Compared to wild-type mice, long-term potentiation (LTP) elicited by 100 pulses at 100 Hz was not different. Unexpectedly, at lower frequencies (1, 5 or 10 Hz), the resulting synaptic changes in CA1 neurons of Crhr1−/− were systematically shifted towards long-term depression (LTD). Furthermore, testing paired-pulse paradigm revealed a GABA receptor-dependent decrease of paired-pulse ratio in Crhr1−/−. It might be assumed that a lack of CRHR1 induce developmental changes which resulted in altered GABAergic activity, producing attenuated synaptic potentiation after repetitive stimulation and thus favouring LTD in principal neurons. Since CRHR1 are located in GABAergic somata, axons and boutons the activity of these receptor types rather might contribute to the development of the neuronal ability for plasticity like processes on the level of NMDAR subunit composition and GABAergic activity.

© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号

地址:北京市海淀区学院路29号 邮编:100083

电话:办公室:(+86 10)66554848;文献借阅、咨询服务、科技查新:66554700