GABAB-receptor-mediated inhibition of the N-methyl-D-aspartate component of synaptic transmission in the rat hippocampus

摘要: GABA receptor regulation of NMDA-receptor-mediated synaptic responses was studied in area CA1 the rat hippocampus using extracellular and intracellular recording techniques. Picrotoxin (PTX) used to suppress GABAA inhibition 6,7-dinitroquinoxaline-2,3-dione (DNQX) non-NMDA receptor-mediated responses. In this manner, we were able avoid complicating factors caused by potentials induced other excitatory inhibitory amino acid receptors. Under these conditions, large EPSPs observed. When paired stimuli given at interstimulus intervals from 100 400 msec, powerful second response This reversed GABAB antagonists phaclofen 2-hydroxy-saclofen; it also depressed removal Mg2+ bath. Examination (determined presence D-2-amino-5-phosphonovalerate PTX) showed no such inhibition, thereby supporting hypothesis that NMDA is postsynaptic. difference paired-pulse leads us conclude there evidence GABAB-mediated presynaptic transmitter release. Intracellular recordings DNQX PTX revealed a phaclofen-sensitive late IPSP correlated time with period Taken together, data suggest paired-pulse-inhibition produced GABAB-receptor-mediated hyperpolarization postsynaptic membrane, causing an enhanced block channels Mg2+. Regulation NMDA-mediated receptors constitutes mechanism for control major system hippocampal pyramidal cells.