ArticleAscending afferent regulation of rat midbrain dopamine neurons
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Serotonin/dopamine interaction: Electrophysiological and neurochemical evidence
2021, Progress in Brain ResearchSerotonergic modulation of the activity of mesencephalic dopaminergic systems: Therapeutic implications
2017, Progress in NeurobiologyCitation Excerpt :The inhibitory response of SNc and VTA DA neurons triggered by DRN stimulation was eliminated by 5-HT depletion with para-chlorophenylalanine (pCPA) or 5,7-dihydroxytryptamine (5,7-DHT), but the percentage of DA neurons initially excited was maintained (Fibiger and Miller, 1977; Gervais and Rouillard, 2000). Therefore, 5-HT seems to selectively inhibit a subset of DA neurons including the SNc slow firing cells and the VTA neurons projecting to the NAc (Kelland et al., 1993). This is a direct, phasic rather than tonic, inhibitory 5-HT monosynaptic input from the DRN (Dray et al., 1976; Fibiger and Miller, 1977; Gervais and Rouillard, 2000).
New therapeutic opportunities for 5-HT<inf>2C</inf> receptor ligands in neuropsychiatric disorders
2016, Pharmacology and TherapeuticsCitation Excerpt :These inhibitory effects could involve 5-HT2CRs but the demonstration is missing. Lesion of 5-HT neurons or depletion of 5-HT does not modify DA neuron firing rate (Kelland et al., 1990, 1993; Prisco et al., 1994; Prisco & Esposito, 1995; Gervais & Rouillard, 2000; Guiard et al., 2008) although it is sometimes associated with subtle changes of the discharge profile of DA neurons (Prisco et al., 1994; Guiard et al., 2008). The tonic control exerted by 5-HT2CRs on DA neuron firing rate is consequently not clear and could be related to the nature and the selectivity of the 5-HT2C antagonists/inverse agonists used to unmask the continuous regulations (see below) or the contribution of other 5-HTRs.
Mechanisms underlying sleep-wake disturbances in alcoholism: Focus on the cholinergic pedunculopontine tegmentum
2014, Behavioural Brain ResearchCitation Excerpt :Interestingly, research in drug addiction has demonstrated that the primary mechanism for relapse (i.e. reinstatement of drug-seeking behavior, an animal model of relapse) involves activation of glutamatergic cells in the medial prefrontal cortex (mPFC), which then activates dopaminergic (DAergic) projections from the ventral tegmental area (VTA) to the nucleus accumbens (NAc) [173–179]. Additionally, a number of anatomical, behavioral, physiological, and pharmacological studies have provided evidence to demonstrate that the CCC-PPT receives excitatory input from the mPFC [179–182] and sends cholinergic afferent projections to the VTA [183–186], where they synapse on DAergic neurons that then project to the NAc [180,181,187–195], resulting in the release of DA in the NAc [183,196–198]. Furthermore, administration of a partial nicotinic receptor agonist varenicline has been shown in both preclinical and clinical trials to reduce ethanol consumption [199–202].
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2010, International Review of Neurobiology