Independent modulation of basal and feeding-evoked dopamine efflux in the nucleus accumbens and medial prefrontal cortex by the central and basolateral amygdalar nuclei in the rat.
Interactions of the central and basolateral nuclei of the amygdala with the mesocorticolimbic dopamine system are implicated in the acquisition and performance of conditioned responses for food reward. This study investigated whether dopamine transmission in the nucleus accumbens and the medial prefrontal cortex of the rat is influenced by the amygdala and if so, to assess the significance of the interaction in free feeding of a palatable food. To this end, we examined the effects of reverse-dialysis of the sodium channel blocker lidocaine into either the central or basolateral on dopamine efflux in the nucleus accumbens and the medial prefrontal cortex as determined by microdialysis and high-pressure liquid chromatography with electrochemical detection. The present results revealed for the first time that inactivation of the central decreased basal levels of dopamine efflux in the nucleus accumbens, but not in the medial prefrontal cortex. Furthermore, administration of lidocaine into the central significantly attenuated feeding-evoked increases in dopamine efflux in both terminal regions. These neurochemical effects were accompanied by feeding-related behaviours akin to the Klüver-Bucy syndrome. In contrast, inactivation of the basolateral affected neither food intake nor dopamine efflux in the nucleus accumbens, but triggered dramatic long-lasting oscillations in dopamine efflux in the medial prefrontal cortex, irrespective of whether food was presented or not. Overall, these findings indicate that the central and basolateral independently modulate dopamine transmission in both terminal regions of the mesocorticolimbic dopamine system. The central, in particular, and its influence on the dopamine system, may be involved in the regulation of food intake.
Ahn
S
S
Department of Psychiatry and the Brain Research Centre, University of British Columbia, Vancouver, BC V6T 2A1, Canada.
Phillips
A G
AG
D000679:Amygdala / Q000187:drug effects / Q000378:metabolism* / Q000502:physiology; D000818:Animals; D002851:Chromatography, High Pressure Liquid; D004298:Dopamine / Q000378:metabolism* / Q000502:physiology; D004435:Eating / Q000502:physiology; D005247:Feeding Behavior / Q000502:physiology; D008012:Lidocaine / Q000494:pharmacology; D008297:Male; D017551:Microdialysis; D009714:Nucleus Accumbens / Q000378:metabolism* / Q000502:physiology; D017397:Prefrontal Cortex / Q000378:metabolism* / Q000502:physiology; D051381:Rats; D020318:Rats, Long-Evans; D026941:Sodium Channel Blockers / Q000494:pharmacology
D026941:Sodium Channel Blockers; D008012:Lidocaine; D004298:Dopamine