Characterization of the effects of serotonin on the release of [3H]dopamine from rat nucleus accumbens and striatal slices

Nurse, Barbara; Russell, Vivienne A.; Taljaard, J. J. F.

doi:10.1007/bf01268873

Cited by 28 publications

(14 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This effect has also been observed in the nucleus accumbens (Jacocks and Cox 1992;Nurse et al 1988), the olfactory tubercle (Zazpe et al 1994), the SN (Williams and Davies 1983), and the VTA (Beart and McDonald 1982). The excitatory effect of 5-HT on basal DA release occurs either on striatal slices or on synaptosomes, a model allowing the study of the presynaptic regulation of synthesis and release (De Belleroche and Bradford 1980).…”

Section: Excitatory Effectsmentioning

confidence: 79%

Presynaptic control of serotonin on striatal dopamine function

Navailles

Deurwaerdère

2010

Psychopharmacology

View full text Add to dashboard Cite

show abstract

Section: Excitatory Effectsmentioning

confidence: 79%

Presynaptic control of serotonin on striatal dopamine function

Navailles

Deurwaerdère

2010

Psychopharmacology

View full text Add to dashboard Cite

show abstract

“…Many neurochemical studies demonstrate this relationship (Nurse et al 1988;Blandina et al 1988;Yi et al 1991;Jacocks and Cox 1992;Hallbus et al 1997;Benloucif and Galloway 1991;Parsons and Justice 1993;Yadid et al 1994;Yoshimoto et al 1996). The 5-HT-DA interaction question has been approached in an elegant and novel way by Broderick and Phelix (1997).…”

Section: Discussionmentioning

confidence: 99%

“…For example, a number of in vivo microdialysis studies have clearly shown that exposure of the striatum or nucleus accumbens to serotonin results in increased release of dopamine (Benloucif and Galloway 1991;De Deurwaerdere et al 1996;Hallbus et al 1997;Parsons and Justice 1993;Yadid et al 1994;Yoshimoto et al 1996), although the mechanism underlying such an enhancement is unclear. Other methodological approaches have also shown such a relationship (Blandina et al 1988;Jacocks and Cox 1992;Nurse et al 1988;Yi et al 1991).There has also been much interest in these interactions with regard to the role of serotonin function in cocaine's psychomotor stimulating and reinforcing effects (Broderick and Phelix 1997;Cunningham et al 1996;Parsons et al 1995;Walsh and Cunningham 1997). For example, although SSRIs do not substitute for cocaine in drug discrimination tests, they do potentiate the stimulus effects of cocaine (Cunningham and Callahan 1991;Kleven and Koek 1998).…”

mentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Serotonin-Dopamine Interactions in the Control of Conditioned Reinforcement and Motor Behavior

Sasaki‐Adams

Kelley

2001

Neuropsychopharmacology

View full text Add to dashboard Cite

These studies addressed the question of serotonin (5-HT)-dopamine (DA) interactions with regard to reward-related behavior and motor activity in rats. The first experiment evaluated the effect of chronic treatment with fluoxetine (7 mg/kg/day), a serotonin-selective reuptake inhibitor, and buproprion (15 mg/kg/day), a dopamine reuptake inhibitor, on responding for conditioned reinforcement (CR). Chronic fluoxetine, but not buproprion, enhanced CR responding, and also potentiated cocaine-induced increases in CR responding. In the second experiment, animals received intra-accumbens infusions of either 1, 5, and 10 g) or DA (10, 20 g) The dopaminergic and serotonergic neurotransmitter systems are thought to play a critical role in the regulation of emotion and mood, and have been implicated in a spectrum of neuropsychiatric disorders. Psychotropic drugs affecting dopaminergic or serotonergic systems have been used to treat such disorders as depression, bipolar disorder, schizophrenia, eating disorders, obsessive compulsive disorder, and autism and have also been used to alleviate motor dysfunction associated with Tourette's syndrome, Parkinson's disease, and self-injurious behavior. Since both these transmitter systems appear to play such a critical role in mental functions, there has been a considerable amount of interest in their potential interactions. The nucleus accumbens, which has been implicated in reward and motivation, is one brain region where such an interaction may take place. There are high levels of dopamine (DA), dopamine receptors, serotonin (5-HT), and serotonin receptors in this forebrain region (Beal and Martin 1985;Bonaventure et al. 1997;Bouyer et al. 1984;Eberle-Wang et al. 1997;Joyce and Marshall 1987;Kilpatrick et al. 1987; Phelix and Broderick 1995;. The classical role of dopamine in the nucleus accumbens has been attributed to regulating motivation and reward-related behavior (Robbins and Everitt 1996;Schultz 1997;Wise and Rompré 1989). For example, drugs of abuse, such as cocaine and amphetamine, are believed to exert their euphoric effects primarily via activating the dopamine system (Di Chiara and Imperato 1988; Koob and Bloom 1988). In contrast to the substantial body of research on dopamine in the nucleus accumbens, there has been comparatively little attention given to the role of serotonin and serotonin-dopamine interactions in the nucleus accumbens.There are a number of reasons why further understanding of dopamine-serotonin interactions would be useful. Although depression undoubtedly involves a complex dysregulation of many transmitter and neuroendocrine systems, a majority of drugs used to treat depression affects the serotonin system. Serotoninselective re-uptake inhibitors (SSRIs) such as fluoxetine enhance synaptic levels of serotonin (5-HT), and are generally quite effective in ameliorating the symptoms of depression. Thus, one widely held hypothesis is that dysfunction in serotonergic neurons and their targets may underlie depressive symptomatology (van Praag et al. 1...

show abstract

“…Moreover, 5-HT increased the spontaneous release of DA from rat striatal synaptosomes or slices (Andrews et al 1978;De Belleroche and Bradford 1980;Westfall and Tittermary 1982) as well as nucleus accumbens (Nurse et al 1988) and olfactory tubercle slices (Zazpe et al 1994); the latter effect was also suggested to be mediated through activation of 5-HT 3 receptors (Blandina et al 1989) or via a mechanism involving the DA transporter (Nurse et al 1988;Yi et al 1991;Benuck and Reith 1992;Jacocks and Cox 1992). It was also proposed from in vivo experiments in rats that stimulation of DA release involves the activation of 5-HT 1 , 5-HT 3 and/or 5-HT 4 receptors in the striatum (Benloucif et al 1993).…”

Section: Introductionmentioning

confidence: 99%

5-HT1B receptors modulate release of [3H]dopamine from rat striatal synaptosomes

Sarhan¹,

Cloëz‐Tayarani²,

Massot³

et al. 1999

Naunyn-Schmiedeberg's Arch Pharmacol

View full text Add to dashboard Cite

The effect of the selective r5-HT1B agonist 3-(1,2,5,6-tetrahydro)-4-pyridil-5-pyrrolo [3,2-b] pyril-5-one (CP93,129) on the K(+)-evoked overflow of [3H]dopamine was studied in rat striatal synaptosomes loaded with [3H]dopamine. The aim of the study was to investigate the participation of 5-HT1B receptors in the serotonergic modulation of striatal dopaminergic transmission. The Ca2(+)-dependent, tetrodotoxin-resistant K(+)-evoked overflow of [3H]dopamine was inhibited by CP93,129 (0.01-100 microM) in a concentration-dependent manner (IC50=1.8 microM; maximal inhibition by 35.5% of control). [+/-]8-OH-DPAT, a 5-HT(1A) receptor agonist, [+/-]DOI, a 5-HT2 receptor agonist, and 2-methyl-5-hydroxytryptamine, a 5-HT3 receptor agonist, at concentrations ranging from 0.01 microM to 100 microM did not show any significant effect. Neither ketanserin (1 microM and 5 microM), a selective 5-HT2/5-HT1D receptor antagonist, nor ondansetron (1 microM), a 5-HT3 receptor antagonist, changed the inhibitory effect of CP93,129. SB224289, GR55562, GR127935, isamoltane and metergoline, selective and non-selective 5-HT1B receptor antagonists, in contrast, used at a concentration of 1 microM, antagonized the inhibitory effect of CP93,129 (3 microM and 10 microM). SB224289, a selective 5-HT1B receptor antagonist, inhibited the effect of CP93,129 in a concentration-dependent manner; the calculated K(i) value was 1.8 nM. Our results indicate that in rat striatal axon terminals the K(+)-evoked release of dopamine is regulated by the presynaptic 5-HT1B heteroreceptors.

show abstract

Characterization of the effects of serotonin on the release of [3H]dopamine from rat nucleus accumbens and striatal slices

Cited by 28 publications

References 32 publications

Presynaptic control of serotonin on striatal dopamine function

Presynaptic control of serotonin on striatal dopamine function

Serotonin-Dopamine Interactions in the Control of Conditioned Reinforcement and Motor Behavior

5-HT1B receptors modulate release of [3H]dopamine from rat striatal synaptosomes

Contact Info

Product

Resources

About