Simultaneous quantification of serotonin, dopamine and noradrenaline levels in single frontal cortex dialysates of freely-moving rats reveals a complex pattern of reciprocal auto- and heteroreceptor-mediated control of release

Gobert, Alain P.; Rivet, Jean‐Michel; Audinot, Valérie; Newman‐Tancredi, Adrian; Cistarelli, Laetitia; Millan, Mark J.

doi:10.1016/s0306-4522(97)00565-4

Cited by 190 publications

(161 citation statements)

References 100 publications

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“…Therefore, parietal and occipital areas share with prefrontal areas an a 2 -mediated control of DA transmission. Although clozapine has pronounced a 1 receptor blocking properties (Brunello et al 1995), a role of these properties in the increase of DA in cortical areas is unlikely, given the evidence that relatively selective blockade of a 1 receptors by prazosin does not increase dialysate DA in the PFCX (Gobert et al 1998). Indeed, stimulation of DA release in the cortex might eventually result from stimulation rather than blockade of a 1 receptors in the ventral tegmental area (VTA), through facilitation of burst firing of DA neurones (Grenhoff et al 1993(Grenhoff et al , 1995.…”

Section: Discussionmentioning

confidence: 99%

Noradrenaline transporter blockers raise extracellular dopamine in medial prefrontal but not parietal and occipital cortex: differences with mianserin and clozapine

Valentini

Frau

Chiara

2004

Journal of Neurochemistry

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This study compared the interaction between noradrenaline (NA) and dopamine (DA) mechanisms in the prefrontal (PFCX) and in the parietal (ParCX) and occipital (OccCX) cortex. The effect of reboxetine and desipramine, two NA transporter blockers, of mianserin, an antagonist of a 2 and 5-HT2 receptors, and of clozapine, an atypical antipsychotic, on dialysate DA in the medial PFCX, ParCX and OccCX was studied. We also assessed the influence of a prior 6-hydroxydopamine (6-OHDA) lesion of the dorsal noradrenergic bundle (DNAB) on the effect of reboxetine and clozapine on dialysate DA in the PFCX and ParCX. Systemic administration of reboxetine and desipramine dose-dependently increased dialysate DA in the PFCX but not in the ParCX and OccCX. In contrast, mianserin and clozapine raised dialysate DA in the ParCX and OccCX to an even larger extent than in the PFCX. 6-OHDA lesions of DNAB abolished the increase of dialysate DA elicited by reboxetine in the PFCX and by clozapine both in the PFCX and in the ParCX. It is concluded that, although PFCX and ParCX/OccCX share the presence of a strong control of DA transmission by NA through a 2 receptors, they differ in the extent to which DA is cleared from the extracellular compartment by uptake through the NA transporter. This process, although extensive in the PFCX, appears insignificant in the ParCX and OccCX, probably as a result of the higher ratio of NA to DA resulting in exclusion of DA from NA transporter.

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Section: Discussionmentioning

confidence: 99%

Noradrenaline transporter blockers raise extracellular dopamine in medial prefrontal but not parietal and occipital cortex: differences with mianserin and clozapine

Valentini

Frau

Chiara

2004

Journal of Neurochemistry

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“…The findings permit the proposal of the hypothesis that enhanced dopamine and serotonin levels within the medial prefrontal cortex would counteract the severity of writhing and oral movements. Furthermore, it seems that there is a positive relationship between dopamine and serotonin activity in the mPFC, as revealed by a parallel enhancement of both amines during withdrawal, and the reactive serotonergic reduction after prefrontocortical 6-OHDA lesion (Gobert et al 1998). Prefrontocortical noradrenergic system seems to escape the dopaminergic modulation during opiate withdrawal.…”

Section: Discussionmentioning

confidence: 99%

“…Prefrontal serotonin (5-HT) appears not to be involved in physical dependence to morphine (Blasig et al 1976;Bhargava 1979;Silverstone et al 1993), except for a possible role on jumping behavior during opiate withdrawal (Cervo et al 1983). However it is known that a complex interdependence between biogenic amines exists within the prefrontal cortex, suggesting that changes in dopamine and noradrenaline could also affect serotonin neurotransmission after morphine (Gobert et al 1998).…”

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confidence: 99%

Behavioral Expression of Opiate Withdrawal is Altered after Prefrontocortical Dopamine Depletion in Rats Monoaminergic Correlates

Fernández-Espejo

Serrano

Caillé

et al. 2001

Neuropsychopharmacology

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“…Occupancy of D 2 receptors may also contribute to the ability of ASE to enhance DA efflux in the NAc (Kuroki et al, 1999). There is also some evidence that the increase in DA efflux produced by the atypical antipsychotic drugs is mediated, in part, by a 2A -adrenergic-receptor blockade (Blake et al, 1998;Bymaster et al, 1996;Gobert et al, 1998;Hertel et al, 1999;Millan et al, 2000;Wadenberg et al, 2007), which may also contribute to the action of ASE in this regard, as it also an a 2A -adrenergic-receptor antagonist (Shahid et al, 2007).…”

Section: Da Effluxmentioning

confidence: 99%

Asenapine Increases Dopamine, Norepinephrine, and Acetylcholine Efflux in the Rat Medial Prefrontal Cortex and Hippocampus

Huang

Dai

et al. 2008

Neuropsychopharmacol

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Atypical antipsychotic drugs, which are more potent direct acting antagonists of brain serotonin (5-HT) 2A than dopamine (DA) D 2 receptors, preferentially enhance DA and acetylcholine (ACh) efflux in the rat medial prefrontal cortex (mPFC) and hippocampus (HIP), compared with the nucleus accumbens (NAc). These effects may contribute to their ability, albeit limited, to improve cognitive function and negative symptoms in patients with schizophrenia. Asenapine (ASE), a new multireceptor antagonist currently in development for the treatment of schizophrenia and bipolar disorder, has complex serotonergic properties based upon relatively high affinity for multiple serotonin (5-HT) receptors, particularly 5-HT 2A and 5-HT 2C receptors. In the current study, the effects of ASE on DA, norepinephrine (NE), 5-HT, ACh, glutamate, and g-aminobutyric acid (GABA) efflux in rat mPFC, HIP, and NAc were investigated with microdialysis in awake, freely moving rats. ASE at 0.05, 0.1, and 0.5 mg/kg (s.c.), but not 0.01 mg/kg, significantly increased DA efflux in the mPFC and HIP. Only the 0.5 mg/kg dose enhanced DA efflux in the NAc. ASE, at 0.1 and 0.5 mg/kg, significantly increased ACh efflux in the mPFC, but only the 0.5 mg/kg dose of ASE increased HIP ACh efflux. ASE did not increase ACh efflux in the NAc at any of the doses tested. The effect of ASE (0.1 mg/kg) on DA and ACh efflux was blocked by pretreatment with WAY100635, a 5-HT 1A antagonist/D 4 agonist, suggesting involvement of indirect 5-HT 1A agonism in both the actions. ASE, at 0.1 mg/kg, increased NE, but not 5-HT, efflux in the mPFC and HIP. ASE, at 0.1 mg/kg (s.c.), had no effect on glutamate and GABA efflux in either the mPFC or NAc. These findings indicate that ASE is similar to clozapine and other atypical antipsychotic drugs in preferentially increasing the efflux of DA, NE, and ACh in the mPFC and HIP compared with the NAC, and suggests that, like these agents, it may also improve cognitive function and negative symptoms in patients with schizophrenia.

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Simultaneous quantification of serotonin, dopamine and noradrenaline levels in single frontal cortex dialysates of freely-moving rats reveals a complex pattern of reciprocal auto- and heteroreceptor-mediated control of release

Cited by 190 publications

References 100 publications

Noradrenaline transporter blockers raise extracellular dopamine in medial prefrontal but not parietal and occipital cortex: differences with mianserin and clozapine

Noradrenaline transporter blockers raise extracellular dopamine in medial prefrontal but not parietal and occipital cortex: differences with mianserin and clozapine

Behavioral Expression of Opiate Withdrawal is Altered after Prefrontocortical Dopamine Depletion in Rats Monoaminergic Correlates

Asenapine Increases Dopamine, Norepinephrine, and Acetylcholine Efflux in the Rat Medial Prefrontal Cortex and Hippocampus

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