Substance P attenuates and DAMGO potentiates amygdala glutamatergic neurotransmission within the ventral pallidum.
The amygdala (AMG), nucleus accumbens (NA) and ventral pallidum (VP) influence goal-oriented behaviors. However, the nature of the interactions among these regions has not been well characterized. Anatomical studies 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) and 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 monitored during microiontophoretic application of treatment ligands in chloral hydrate-anesthetized rats. The anatomically described glutamatergic inputs from the AMG, and SP inputs from the NA, were pharmacologically verified. It also was determined that even though iontophoretically applied SP increased the spontaneous activity of VP neurons, at ejection current levels that were below those necessary to produce this effect (termed sub-threshold), the tachykinin attenuated AMG stimulation-evoked glutamatergic neurotransmission. SP failed to modulate the excitations 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 micro opioid agonist DAMGO on AMG-evoked responses 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 potentiated effects of exogenous glutamate implying an interaction at a post-synaptic site. These results indicate that tachykinin and opioid neuropeptides contained in NA projection neurons can differentially modulate AMG glutamatergic inputs to the VP.
Mitrovic
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Department of Pharmacology and Experimental Therapeutics, Loyola University Chicago, Stritch School of Medicine, Maywood, IL 60153, USA.
Napier
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TC
D000679:Amygdala / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D000701:Analgesics, Opioid / Q000494:pharmacology*; D000818:Animals; D001713:Biphenyl Compounds / Q000494:pharmacology; D004558:Electric Stimulation; D020875:Enkephalin, Ala(2)-MePhe(4)-Gly(5)-; D004745:Enkephalins / Q000494:pharmacology*; D005071:Evoked Potentials / Q000187:drug effects / Q000502:physiology; D005917:Globus Pallidus / Q000166:cytology / Q000502:physiology*; D018698:Glutamic Acid / Q000502:physiology; D006993:Hypnotics and Sedatives / Q000494:pharmacology; D008297:Male; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D018377:Neurotransmitter Agents / Q000494:pharmacology; D009714:Nucleus Accumbens / Q000166:cytology / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D011930:Reaction Time / Q000187:drug effects; D013268:Stimulation, Chemical; D013373:Substance P / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D009435:Synaptic Transmission / Q000187:drug effects*
D000701:Analgesics, Opioid; D001713:Biphenyl Compounds; D004745:Enkephalins; D006993:Hypnotics and Sedatives; D018377:Neurotransmitter Agents; D020875:Enkephalin, Ala(2)-MePhe(4)-Gly(5)-; D013373:Substance P; D018698:Glutamic Acid; C066892:CP 96345