CONTRIBUTION OF VOLTAGE-GATED CA2-TERM DEPRESSION IN THE CA1 REGION IN-VITRO( CHANNELS TO HOMOSYNAPTIC LONG)

Homosynaptic long-term depression (LTD) of synaptic efficacy was induc ed in field excitatory postsynaptic potentials by administration of 90 0 pulses at either 1 or 3 Hz in 2- to 3-wk-old Sprague-Dawley rats. Th e stimulation was administered via a bipolar stimulating electrode pla ced immediately adjacent to the recording electrode in the stratum rad iatum region of the hippocampal CA1 subfield. Equivalent LTD induction occurred whether the slices were maintained at room temperature or at 32 degrees C. Lowering bath Ca2+ to 0 mM, or increasing it to 4 mM, p revented the induction of the depression. The NMDA receptor antagonist D,L-2-amino-5-phosphonovaleric acid (50 mu M) reversibly blocked the induction of homosynaptic LTD, In addition, the L-type voltage-gated c alcium channel (VGCC) antagonist nimodipine (10 mu M) and the R- and T -type VGCC antagonist NiCl2 (25 mu M) also prevented homosynaptic LTD induction. These results indicate that in addition to N-methyl-D-aspar tate receptor activity, Ca2+ influx via VGCCs can play an important ro le in the induction and expression of LTD induced by low-frequency sti mulation in the hippocampal formation.