1991
DOI: 10.1007/bf02244322
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Voltammetric evidence that subsensitivity to reward following chronic mild stress is associated with increased release of mesolimbic dopamine

Abstract: Chronic exposure to mild unpredictable stress caused a decrease in rats' consumption of a palatable weak sucrose solution, which was reversed by chronic (5 weeks) administration of imipramine (5 mg/kg/day). Dopamine (DA) release in the nucleus accumbens (NAc) and caudate putamen (CPu) was measured in vivo using fast cyclic voltammetry, following electrical stimulation of the medial forebrain bundle. Experiments were performed under chloral hydrate anaesthesia 48 h after the termination of stress and the final … Show more

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Cited by 54 publications
(17 citation statements)
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“…The release of dopamine (DA) in the prefrontal cortex has been shown to enhance alertness, temporal discrimination and delayed alterna tion tasks [51][52][53][54][55][56][57] Mesolimbic functions include affectivity, emotionali ty, aggression, sexuality and neuroendocrine control. This dopaminergic system is closely related to the reward activity [84][85][86][87][88][89][90][91] which is enhanced by opiates and other stimulating drugs [77]. Prefrontal cortex (mesocortical) and subcortical systems have been shown to be antagonis tic.…”
Section: Behavioral C Hangessupporting
confidence: 39%
“…The release of dopamine (DA) in the prefrontal cortex has been shown to enhance alertness, temporal discrimination and delayed alterna tion tasks [51][52][53][54][55][56][57] Mesolimbic functions include affectivity, emotionali ty, aggression, sexuality and neuroendocrine control. This dopaminergic system is closely related to the reward activity [84][85][86][87][88][89][90][91] which is enhanced by opiates and other stimulating drugs [77]. Prefrontal cortex (mesocortical) and subcortical systems have been shown to be antagonis tic.…”
Section: Behavioral C Hangessupporting
confidence: 39%
“…The mesocorticolimbic system, which innervates limbic structures such as the nucleus acumbens, amygdala, ventral hippocampus, and prefrontal cortex, is involved in a variety of behavioral functions related to motivation and reward, and may thus modulate symptoms like anhedonia [55] . Moreover, chronic stress and depressive states are associated with impaired limbic dopaminergic transmission [56][57][58] , and antidepressants were shown to increase mesolimbic DA-neurotransmission [59] . Although we did not examine the exact mechanism by which intra-nasally applied DA exerts its effects on immobility in the FST, there is evidence suggesting a key role of the dopamine D 2 -receptor in mediating antidepressant-like activity [for reviews, see 60,61 ].…”
Section: Discussionmentioning
confidence: 43%
“…CMS-induced anhedonia is associated with decreases in D 2 receptor binding and D 2 receptor message in the nucleus accumbens [149][150][151] , but increases in D 2 receptor binding and D 2 receptor message were found in 'prohedonic' animals [144] . A decreased inhibition of DA turnover by quinpirole has been reported in anhedonic animals [152] , while the opposite effect was seen in 'prohedonic' animals [142] , albeit that, the former observation was made in brain slices and the latter in whole brain. Finally, CMS-induced anhedonia is associated with an increase in cortical beta-adrenergic receptor binding [153][154][155][156] , whereas a decrease in cortical beta-receptor binding has been observed in animals showing decreased immobility in the forced swim test [89] .…”
Section: Neurobiological Correlatesmentioning
confidence: 41%