SUBSTANCE-P ATTENUATES AND DAMGO POTENTIATES AMYGDALA GLUTAMATERGIC NEUROTRANSMISSION WITHIN THE VENTRAL PALLIDUM

The amygdala (AMG), nucleus accumbens (NA) and ventral pallidum (VP) i nfluence goal-oriented behaviors. However, the nature of the interacti ons among these regions has not been well characterized. Anatomical st udies indicate that excitatory amino acids are contained in VP inputs from the AMG, and the NA is a primary source of VP substance P (SP) an d opioids. The present study was designed to functionally characterize the NA and AMG projections to the VP, and to assess if opioids and SP can modulate AMG-mediated excitatory neurotransmission within the VP. To do so, extracellularly recorded electrophysiological responses of single VP neurons to electrical activation of VP afferents were monito red during microiontophoretic application of treatment ligands in chlo ral hydrate-anesthetized rats. The anatomically described glutamatergi c inputs from the AMG, and SP inputs from the NA, were pharmacological ly verified. It also was determined that even though iontophoretically applied SP increased the spontaneous activity of VP neurons, at eject ion current levels that were below those necessary to produce this eff ect (termed sub-threshold), the tachykinin attenuated AMG stimulation- evoked glutamatergic neurotransmission. SP failed to modulate the exci tations induced by iontophoretically applied glutamate suggesting that SP modulation of AMG-evoked excitations were mediated via a decrease in the pre-synaptic release of glutamate. Like SP, the effects of sub- threshold ejection currents of mu opioid agonist DAMGO on AMG-evoked r esponses were not predicted by the opioid's effects on spontaneous VP neuronal activity; DAMGO inhibited spontaneous firing but potentiated AMG-evoked glutamatergic neurotransmission. The opioid also potentiate d effects of exogenous glutamate implying an interaction at a post-syn aptic site. These results indicate that tachykinin and opioid neuropep tides contained in NA projection neurons can differentially modulate A MG glutamatergic inputs to the VP. (C) 1998 Elsevier Science B.V.