Excitatory amino acid induced enhancement of synaptic transmission in the rat hippocampal slice
The effects of exogenous application of excitatory amino acids on synaptic transmission was investigated in the CA1 region of the rat hippocampal slice preparation using two methods of application: iontophoresis and perfusion. Iontophoretic application of N-methyl-D-aspartate (NMDA) evoked a short lasting form of potentiation, whereas application of the proposed endogenous excitatory transmitter substance L-glutamate induced a slowly-forming and long lasting potentiation of the response by both techniques. Surprisingly, brief perfusion of 50μM NMDA elicited only a long-lasting depression of the response. Application of 10μM α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) showed no long-term effects on synaptic transmission. Perfusion of (1S,3R) 1-aminocyclopentane-1,3-dicarboxylic acid (ACPD) induced only a marginal form of synaptic enhancement under normal conditions and depression of the response in conditions of low Mg2+ or in the presence of low doses (1μM) of picrotoxin. However, in the presence of the GABAA antagonist picrotoxin (1μM), perfusion of 100μM ACPD evoked a slowly-forming enhancement of the response. Application of the proposed retrograde transmitter arachidonic acid (10μM) elicited a slowly-forming depression of the response when perfused alone. Co-application of arachidonic acid (10μM) and ACPD (50μM) evoked a rapidly inducible and long-lasting form of synaptic enhancement.