长时程增强
兴奋性突触后电位
生物
NMDA受体
突触可塑性
神经传递
抑制性突触后电位
神经科学
受体
生物化学
作者
Armen Saghatelyan,Alexander Dityatev,Sandra Schmidt,T Schuster,Udo Bartsch,Melitta Schachner
标识
DOI:10.1006/mcne.2000.0922
摘要
The role of the extracellular matrix molecule tenascin-R (TN-R) in regulation of synaptic transmission and plasticity in the CA1 region of the hippocampus was studied using mice deficient in expression of this molecule. The mutant mice showed normal NMDA-receptor-mediated currents but an impaired NMDA-receptor-dependent form of long-term potentiation (LTP) as compared to wild-type littermates. Reduced LTP in mutants was accompanied by increased basal excitatory synaptic transmission in synapses formed on CA1 pyramidal neurons. A possible mechanism for increased excitatory synaptic transmission in mutants could involve modulation of inhibition, since TN-R and its associated carbohydrate HNK-1 decorate perisomatic interneurons. Indeed, the amplitudes of unitary perisomatic inhibitory currents were smaller in mutants compared to wild-type mice. Thus, our data show that a deficit in TN-R results in reduction of perisomatic inhibition and, as a consequence, in an increase of excitatory synaptic transmission in CA1 to the levels close to saturation, impeding further expression of LTP.
科研通智能强力驱动
Strongly Powered by AbleSci AI