Effect of acute and chronic fluoxetine on extracellular dopamine levels in the caudate-putamen and nucleus accumbens of rat

Clark, Robert; Ashby, Charles R.; Dewey, Stephen L.; Ramachandran, P. Veeraraghavan; Strecker, Robert E.

doi:10.1002/(sici)1098-2396(199607)23:3<125::aid-syn1>3.0.co;2-a

Cited by 62 publications

(26 citation statements)

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“…We have not previously found effects of 10 μM fluoxetine on any aspect of DA dynamics (Budygin et al, 2002;John and Jones, 2006a;John et al, 2006), however, the results shown here only found significant effects of selective serotonergic drugs on DA release at concentrations of drug ≥100 μM. Previous studies, both in vitro and in vivo, concerning the control of DA release by 5-HT have provided conflicting results (Benloucif and Galloway, 1991;Clark et al, 1996;Dewey et al, 1995;Lucas and Spampinato, 2000;Westfall and Tittermary, 1982;Yi et al, 1991). Therefore, the precise mechanism resulting in reduced electrically-stimulated DA release by serotonergic drugs is unclear without further pharmacological characterization.…”

Section: Discussioncontrasting

confidence: 72%

Voltammetric characterization of the effect of monoamine uptake inhibitors and releasers on dopamine and serotonin uptake in mouse caudate-putamen and substantia nigra slices

2007

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SummaryFast scan cyclic voltammetry is an electrochemical technique used to measure dynamics of transporter-mediated monoamine uptake in real time and provides a tool to evaluate the detailed effects of monoamine uptake inhibitors and releasers on dopamine and serotonin transporter function. We measured the effects of cocaine, methylphenidate, 2β-propanoyl-3β-(4tolyl) tropane (PTT), fluoxetine, amphetamine, methamphetamine, 3,4-methylenedioxymethamphetamine (MDMA), phentermine and fenfluramine on dopamine and serotonin uptake following electrically stimulated release in mouse caudate-putamen and substantia nigra pars reticulata slices. We determined rank orders of uptake inhibition effects based on two variables; increases in apparent K m for dopamine and serotonin uptake and inhibition constant (K i ) values. For example, the rank order of uptake inhibition based on apparent K m values at the dopamine transporter was amphetamine ≥ PTT ≥ methylphenidate ≫ methamphetamine = phentermine = MDMA > cocaine ≫ fluoxetine = fenfluramine, and at the serotonin transporter was fluoxetine = methamphetamine = fenfluramine = MDMA > amphetamine = cocaine = PTT ≥ methylphenidate > phentermine. Additionally, changes in electrically stimulated release were documented. This is the first study using voltammetry to measure the effects of a wide range of monoamine uptake inhibitors and releasers on dopamine and serotonin uptake in mouse brain slices. These studies also highlight methodological considerations for comparison of effects between heterogeneous brain regions.

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Section: Discussioncontrasting

confidence: 72%

Voltammetric characterization of the effect of monoamine uptake inhibitors and releasers on dopamine and serotonin uptake in mouse caudate-putamen and substantia nigra slices

2007

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“…In one dialysis study of neurochemical effects in rats treated with fluoxetine (in a similar dose range to the present study), no change in baseline extracellular dopamine levels was found, whether the fluoxetine was administered chronically or acutely (Clark et al 1996). Interestingly though, these authors also found that pretreatment with fluoxetine induced a small increased in cocaine-induced dopamine release in the nucleus accumbens.…”

Section: Discussionsupporting

confidence: 68%

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

Sasaki‐Adams

Kelley

2001

Neuropsychopharmacology

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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...

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“…Increased DA release may also contribute to the cueing by fluoxetine and 5-HTP which leads to the enhanced preference for the morphine environment seen in the acute morphine treated rats (discussed above). Although a number of reports have shown that fluoxetine in the doses used in this study has no effect on DA levels in the accumbens (Clark et al 1996;Ichikawa and Meltzer 1995;Perry and Fuller 1992), one recent study found that similar doses of fluoxetine significantly increased DA levels in the frontal cortex (Gobert et al 1997). The frontal cortex is one area shown to be hypofunctional during opiate abstinence and withdrawal in human opiate addicts (Danos et al 1998;Gerra et al 1998;Krystal et al 1995) and it is possible that the treatments given in this study may be effective in changing preference by altering activity in this brain region.…”

Section: Discussionmentioning

confidence: 64%

Augmented Accumbal Serotonin Levels Decrease the Preference for a Morphine Associated Environment During Withdrawal

Harris

Aston‐Jones

2001

Neuropsychopharmacology

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Recent studies have found that acute morphine administration increases serotonin (5-HT) transmission within the nucleus accumbens and other forebrain regions. In contrast, 5-HT transmission is depressed during withdrawal from chronic morphine. We show that pharmacological agents that increase brain 5-HT levels In addition to gross neurological and somatic signs the abstinence syndrome associated with opiate dependence involves important subjective responses including anxiety, anhedonia, depression and drug craving (Jaffe 1990). The control and elimination of the subjective symptoms, which linger long after the physical symptoms of opiate withdrawal have dissipated, has been a major obstacle to the successful treatment of opiate dependence (Childress et al. 1994). Understanding the alterations in brain chemistry that occur during abstinence from opiate abuse may lead to improved treatments for these symptoms, and greater success in treating opiate addiction.Acute systemic administration of morphine enhances brain 5-HT synthesis (Garcia-Sevilla et al. 1980) and tryptophan hydroxylase activity (Boadle-Biber et al. 1987). Acute morphine also enhances the turnover and release of 5-HT and dopamine (DA) in widespread areas of the forebrain (Spampinato et al. 1985;Tao and Auerbach 1994). The effect of morphine on 5-HT release appears to be mediated by activation of dorsal raphe neurons (Spampinato et al. 1985;Tao and Auerbach 1994) and may reflect disinhibition caused by direct inhibition of GABA transmission. A similar mechanism has also been proposed for the excitatory effects of opiates on DA neurons in the ventral tegmental area (Bloom et al. 1972;Bonci and Williams 1997).Neurons in the nucleus accumbens have been shown to be critically involved in the reinforcing properties of opiates (Dworkin et al. 1988;Pettit et al. 1984;Zito et al. 1985). Although morphine administration enhances 5-HT and DA levels within the accumbens (Spampinato et al. 1985;Tao and Auerbach 1995;Wise et al. 1995) (Ettenberg et al. 1982;Gerrits and Van Ree 1996;Pettit et al. 1984) or morphine place preference in animals (Mackey and van der Kooy 1985; however, also see Bozarth and Wise 1981;Smith et al. 1985;Spyraki et al. 1983). On the other hand, chemical lesions of 5-HT terminals in the accumbens impair morphine self-administration without affecting responding for food or water (Smith et al. 1987), and also block the acquisition of morphine conditioned place preference (CPP) (Spyraki et al. 1988).Withdrawal from opiates decreases both dopamine and 5-HT transmission in the brain. A single dose of morphine induces measurable reductions in both 5-HT and DA levels at 24 hours post-injection (AntkiewiczMichaluk et al. 1995). Withdrawal from longer chronic opiate treatments produces profound decreases in both dopamine (Acquas et al. 1991;Pothos et al. 1991;Rossetti et al. 1992) and 5-HT transmission (Ahtee 1980;Tao et al. 1998). Reduced 5-HT levels have been linked to both depression (Maes and Meltzer 1995) and compulsive behavior (Dolberg et al. ...

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Effect of acute and chronic fluoxetine on extracellular dopamine levels in the caudate-putamen and nucleus accumbens of rat

Cited by 62 publications

References 14 publications

Voltammetric characterization of the effect of monoamine uptake inhibitors and releasers on dopamine and serotonin uptake in mouse caudate-putamen and substantia nigra slices

Voltammetric characterization of the effect of monoamine uptake inhibitors and releasers on dopamine and serotonin uptake in mouse caudate-putamen and substantia nigra slices

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

Augmented Accumbal Serotonin Levels Decrease the Preference for a Morphine Associated Environment During Withdrawal

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