Cocaine Increases Dopamine Release by Mobilization of a Synapsin-Dependent Reserve Pool

Venton, B. Jill; Seipel, Andrew T.; Phillips, Paul E. M.; Wetsel, William C.; Gitler, Daniel; Greengard, Paul; Augustine, George J; Wightman, R. Mark

doi:10.1523/jneurosci.4901-04.2006

Cited by 215 publications

(227 citation statements)

References 42 publications

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“…43 In addition, there is growing evidence that cocaine can also enhance DA release by mobilizing a reserve pool of DA-containing synaptic vesicles: this links its mechanism of action to that of amphetamine. 44 All these data suggest that nigrostriatal degeneration is not necessary for the development of punding; moreover, the phenomenon is triggered by the stimulation of D1 and D2 receptors, thus confirming that it should be considered as the result of a pathophysiological process different from other ICDs.…”

Section: Methods and Review Criteriamentioning

confidence: 81%

Insights into pathophysiology of punding reveal possible treatment strategies

Fasano

Petrović²

2010

Mol Psychiatry

111

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Punding is a stereotyped behavior characterized by an intense fascination with a complex, excessive, nongoal oriented, repetitive activity. Men tend to repetitively tinker with technical equipment such as radio sets, clocks, watches and car engines, the parts of which may be analyzed, arranged, sorted and cataloged but rarely put back together. Women, in contrast, incessantly sort through their handbags, tidy continuously, brush their hair or polish their nails. Punders are normally aware of the inapposite and obtuse nature of the behavior; however, despite the consequent self-injury, they do not stop such behavior. The most common causes of punding are dopaminergic replacement therapy in patients affected by Parkinson's disease (PD) and cocaine and amphetamine use in addicts. The vast majority of information about punding comes from PD cases. A critical review of these cases shows that almost all afflicted patients (90%) were on treatment with drugs acting mainly on dopamine receptors D1 and D2, whereas only three cases were reported in association with selective D2 and D3 agonists. Epidemiological considerations and available data from animal models suggest that punding, drug-induced stereotypies, addiction and dyskinesias all share a common pathophysiological process. Punding may be related to plastic changes in the ventral and dorsal striatal structures, including the nucleus accumbens, and linked to psychomotor stimulation and reward mechanisms. Possible management guidelines are proposed.

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Section: Methods and Review Criteriamentioning

confidence: 81%

Insights into pathophysiology of punding reveal possible treatment strategies

Fasano

Petrović²

2010

Mol Psychiatry

111

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“…Recent studies suggest that cocaine can control DA release by affecting synapsin phosphorylation and consequent vesicle mobilization (18). Thus, we analyzed intracellular synapsin phosphorylation in presynaptic striatal isolated terminals.…”

Section: Volume 289 • Number 1 • January 3 2014mentioning

confidence: 99%

Paradoxical Abatement of Striatal Dopaminergic Transmission by Cocaine and Methylphenidate

Federici

Latagliata

Ledonne

et al. 2014

Journal of Biological Chemistry

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Background:The dopamine transporter (DAT) regulates the outflow of dopamine from synapses. Results: We present evidence that the DAT blockers cocaine and methylphenidate increase or reduce the release of DA in the striatum. Conclusion:The reducing effects on DA release are not dependent on a typical blockade of DAT. Significance: The paradoxical blunting of dopamine (DA) release could account for differential effects of psychostimulants.

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“…It is well known that the inhibition of soma firing rate diminishes striatal release of DA due to the activation of DA autoreceptors. On the other hand, cocaine enhances DA release by way of mobilizing a synapsin-dependent reserve pool of DA-containing synaptic vesicles [27]. There are some speculations that DATindependent actions of cocaine could be involved in the behavioral activation induced by cocaine [14,15].…”

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confidence: 99%

Dopamine uptake inhibition is positively correlated with cocaine-induced stereotyped behavior

Budygin¹

2007

Neuroscience Letters

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The inhibition of dopamine (DA) uptake and the increase of extracellular DA with consequent activation of DA receptors in specific brain regions such as the nucleus accumbens (NAc) and dorsal striatum are an important, but may be not an exclusive mechanism for behavioral excitation induced by psychostimulants [2,5,14,15,24,25]. A typical spectrum of acute cocaineinduced arousal effects in animal models includes locomotor activation and stereotyped behavior consisting of continuous sniffing, rearing, licking and gnawing. At low and moderate doses, cocaine preferentially enhances locomotor activity and this effect correlates with the decrease in DA clearance in the NAc of freely moving rats [24]. At high doses, the effect of cocaine on the stereotyped activity became predominant [1]. It is unknown whether a strong relationship exists between the stereotypy and cocaine-induced DA uptake changes in the NAc.In this study we have employed fast-scan cyclic voltammetry (FSCV) on freely moving rats to determine whether a correlation exists between the increase in the stereotyped behavior and DA uptake inhibition following cocaine (20 mg/kg, i.p.) administration. The FSCV was chosen since the general characteristics of this technique allow an examination of the DA uptake kinetics without DA release or metabolism contributions [1,28,30].Male Sprague-Dawley rats (300-350 g; Charles River, Raleigh, NC) were housed on a 12:12 light/dark cycle with food and water ad libitum. Rats were group housed before surgery and singly housed after surgery. All protocols were approved by the Institutional Animal Care and Use Committee at Wake Forest University. Rats were anesthetized with ketamine (100 mg/kg) and xylazine (10 mg/kg) and placed in a stereotaxic frame. A guide cannula (Bioanalytical Systems, West Lafayette, IN) was positioned above the NAc core (AP + 1.3, L+1.3, V-2.0 mm from bregma). An Ag/AgCl reference electrode was implanted in the contralateral hemisphere. A bipolar stimulating electrode was lowered to the ventral tegmental area ipsilateral to the guide cannula at 5.2 mm posterior and 1.0 mm lateral to bregma. The stimulating electrode depth was optimized to evoke DA release in the NAc (24 rectangular pulses, 60 Hz, 120 μA, 2 ms/phase, biphasic), monitored using a carbon fiber microelectrode inserted through the guide cannula. The rats were individually housed and allowed to recover for 48 hrs, then they were placed in the test chamber and a new carbon fiber electrode was inserted into the NAc core. The reference and carbon fiber electrodes were connected to a head-mounted voltammetric amplifier (UNC Electronics Design Facility, Chapel Hill, NC) attached to a swivel at the top of the test chamber. Voltammetric recordings were made at the carbon fiber electrode every 100 ms by applying a triangular waveform (-0.4 to +1.2 V, 300 V/s). Data were Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of th...

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Cocaine Increases Dopamine Release by Mobilization of a Synapsin-Dependent Reserve Pool

Cited by 215 publications

References 42 publications

Insights into pathophysiology of punding reveal possible treatment strategies

Insights into pathophysiology of punding reveal possible treatment strategies

Paradoxical Abatement of Striatal Dopaminergic Transmission by Cocaine and Methylphenidate

Dopamine uptake inhibition is positively correlated with cocaine-induced stereotyped behavior

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