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Magnitude of dopamine release in medial prefrontal cortex predicts accuracy of memory on a delayed response task.

ABSTRACT: Modulation of neural function in the prefrontal cortex (PFC) by dopamine (DA) is essential for higher cognitive processes related to attention, working memory, and planning of future behavior. The present study demonstrates that DA efflux in the PFC is increased in a phasic manner when a rat engages in search behavior for food reward on an eight arm radial maze guided by memory, independent of whether or not reward is obtained for making the correct choice. Furthermore, disruption of accurate recall of the correct pattern of arms induced by increasing the delay period from 30 min to 1 or 6 hr, is associated with attenuated DA efflux during the retrieval phase of the task. The observed increase in DA efflux in the absence of reward at a 30 min delay and the minimal increase during consumption of the same quantity of food during poor performance after an unexpected 6 hr delay, argue against a simple relationship between DA function in the PFC and reward processes. Instead, these data demonstrate a close functional relationship between the release of DA from terminals within the PFC and the retrieval of specific trial unique memories; furthermore, the magnitude of mesocortical DA efflux is predictive of the accuracy of this form of memory.

SUBMITTER: Phillips AG

PROVIDER: S-EPMC6729988 | biostudies-literature | 2004 Jan

REPOSITORIES: biostudies-literature

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Magnitude of dopamine release in medial prefrontal cortex predicts accuracy of memory on a delayed response task.

Phillips Anthony G AG Ahn Soyon S Floresco Stan B SB

The Journal of neuroscience : the official journal of the Society for Neuroscience 20040101 2

Modulation of neural function in the prefrontal cortex (PFC) by dopamine (DA) is essential for higher cognitive processes related to attention, working memory, and planning of future behavior. The present study demonstrates that DA efflux in the PFC is increased in a phasic manner when a rat engages in search behavior for food reward on an eight arm radial maze guided by memory, independent of whether or not reward is obtained for making the correct choice. Furthermore, disruption of accurate re ...[more]

PMID: 14724255

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Project description:IntroductionDisulfiram has been claimed to be useful in cocaine addiction therapy, its efficacy being attributed to dopamine-beta-hydroxylase (DBH) inhibition. Our previous results indicate that disulfiram and the selective DBH inhibitor nepicastat increase extracellular dopamine (DA) in the rat medial prefrontal cortex (mPFC), and markedly potentiated cocaine-induced increase. Concomitantly, in rats with cocaine self-administration history, cocaine-seeking behavior induced by drug priming was prevented, probably through overstimulation of D1 receptors due to the DA increase. The present research was aimed at studying the neurochemical mechanisms originating the enhanced DA release.MethodsNoradrenergic system ablation was attained by intracerebroventricular (i.c.v.) administration of the neurotoxin anti-DBH-saporin (aDBH-sap). DA, noradrenaline (NA), and DOPAC were assessed by HPLC after ex vivo tissue extraction or in vivo microdialysis. Control and denervated rats were subjected to microdialysis in the mPFC and caudate nucleus to evaluate the effect of nepicastat-cocaine combination on extracellular DA levels and their regulation by α2-adrenoceptors.ResultsFifteen days after neurotoxin or its vehicle administration, tissue and extracellular NA were reduced to less than 2% the control value, while extracellular DA was increased by approximately 100%. In control rats, nepicastat given alone and in combination with cocaine increased extracellular DA by about 250% and 1100%, respectively. In denervated rats, nepicastat slightly affected extracellular DA, while in combination with cocaine increased extracellular DA by 250%. No differences were found in the caudate nucleus. Clonidine almost totally reversed the extracellular DA elevation produced by nepicastat-cocaine combination, while it was ineffective in denervated rats.ConclusionsThis research shows that the increase of extracellular DA produced by nepicastat alone or in combination with cocaine was prevented by noradrenergic denervation. The results indicate that nepicastat enhances DA release from noradrenergic terminals supposedly by removing NA from α2-autoreceptors. In addition to the inhibition of DA uptake, the latter mechanism may explain the synergistic effect of cocaine on nepicastat-induced DA release.

Dataset Information

Magnitude of dopamine release in medial prefrontal cortex predicts accuracy of memory on a delayed response task.

Publications

Magnitude of dopamine release in medial prefrontal cortex predicts accuracy of memory on a delayed response task.

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