Cocaine: On-line analysis of an accumbens amine neural basis for psychomotor behavior

Broderick, Patricia A.

doi:10.1016/0091-3057(91)90112-f

Cited by 44 publications

(32 citation statements)

References 25 publications

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“…It is unclear whether the mechanism of action of CTX involves modulation of glutamate or non-glutamatergic systems, or both systems. Hyperlocomotion elicited by acute cocaine exposure is primarily dependent on enhancement of extracellular dopamine and activation of striatal dopamine D 1 receptors [5-6], but the response is also sensitive to changes in glutamate homeostasis. Initial cocaine exposure increases extracellular glutamate in the nucleus accumbens [30, 36] and produces hyperlocomotion that is attenuated to varying degrees by NMDA, AMPA and mGluR5 receptor antagonists [15, 22, 41, 45].…”

Section: Discussionmentioning

confidence: 99%

Ceftriaxone attenuates locomotor activity induced by acute and repeated cocaine exposure in mice

Tallarida

Corley

Kovalevich

et al. 2013

Neuroscience Letters

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Ceftriaxone (CTX) decreases locomotor activation produced by initial cocaine exposure and attenuates development of behavioral sensitization produced by repeated cocaine exposure. An important question that has not yet been answered is whether or not CTX reduces behavioral sensitization to cocaine in cases in which the antibiotic is administered only during the period of cocaine absence that follows repeated cocaine exposure and precedes reintroduction to cocaine. We investigated this question using C57BL/6 mice. Mice pretreated with cocaine (15 mg/kg × 14 days) and then challenged with cocaine (15 mg/kg) after 30 days of cocaine absence displayed sensitization of locomotor activity. For combination experiments, CTX injected during the 30 days of cocaine absence attenuated behavioral sensitization produced by cocaine challenge. In the case in which CTX was injected together with cocaine for 14 days, development of behavioral sensitization to cocaine challenge was also reduced. CTX attenuated the increase in locomotor activity produced by acute cocaine exposure; however, its efficacy was dependent on the dose of cocaine as inhibition was detected against 30 mg/kg, but not 15 mg/kg, of cocaine. These results from mice indicate that CTX attenuates locomotor activity produced by acute and repeated cocaine exposure and counters cocaine's locomotor activating properties in a paradigm in which the antibiotic is injected during the period of forced cocaine absence that follows repeated cocaine exposure.

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Section: Discussionmentioning

confidence: 99%

Ceftriaxone attenuates locomotor activity induced by acute and repeated cocaine exposure in mice

Tallarida

Corley

Kovalevich

et al. 2013

Neuroscience Letters

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“…Acute cocaine injections increase striatal dopamine release [33] and DA receptor 1 (D1) antagonists decrease cocaine-induced locomotion [34]. Glutamate is also involved in the acute effects of cocaine on locomotion, as both AMPA [35] and NMDA antagonists [36] exert inhibitory effects on cocaine-induced locomotion.…”

Section: Discussionmentioning

confidence: 99%

Ceftriaxone prevents the induction of cocaine sensitization and produces enduring attenuation of cue- and cocaine-primed reinstatement of cocaine-seeking

Sondheimer

Knackstedt

2011

Behavioural Brain Research

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Ceftriaxone is a beta-lactam antibiotic which has been found to increase the expression and function of the major glutamate transporter, GLT-1. It has previously been shown that GLT-1 expression is decreased in the nucleus accumbens following cocaine self-administration and extinction training; ceftriaxone given in the days immediately prior to reinstatement testing attenuates both cue- and cocaine-primed reinstatement. Here we tested the ability of ceftriaxone pre-treatment (for 5 days prior to the first cocaine exposure) to prevent the induction of cocaine sensitization and the acquisition of cocaine self-administration. We also tested whether ceftriaxone administered only during self-administration attenuates the reinstatement of extinguished cocaine-seeking. We found that ceftriaxone did not affect the acquisition of cocaine self-administration but was able to attenuate reinstatement weeks after ceftriaxone administration ceased. This attenuation in reinstatement was accompanied by a restoration of GLT-1 expression in the nucleus accumbens. Ceftriaxone also attenuated locomotor behavior following the first cocaine injection and prevented the induction of cocaine but not caffeine sensitization. While ceftriaxone-treated animals did not sensitize to caffeine, they displayed reduced caffeine-induced locomotion following repeated caffeine treatment, indicating a possible dopaminergic effect of ceftriaxone. Taken together, these results indicate that ceftriaxone produces enduring changes in glutamate homeostasis in the nucleus accumbens which counteract addiction-related behaviors.

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“…The potency of cocaine's reinforcing effects can readily lead to its self-administration and this is a phenomenon which has shown vulnerability across several species (la, 13,26,28,33). The hypothesis that a dopaminergic mesolimbic molecular component makes a significant contribution to the reinforcing properties of cocaine is generally well accepted (7,12,19,24,27,28,37). Moreover, evidence that cocaine increases mesolimbic synaptic concentrations of dopamine (DA) is abundant both from dialysis and in vivo voltammetric (electrochemical) studies (3,7,8,10,16,18,34).…”

Section: Nucleus Accumbensmentioning

confidence: 99%

“…Interestingly, data are recently emerging to include a serotonergic manipulation by cocaine (11,17). Further data show that serotonin (5-HT) may mediate, at least in part, the reinforcing properties of cocaine and other psychomotor stimulants; the role of 5-HT however may exist in an inverse relationship to that of DA in reinforcement (7,20,25,27). Thus a possible releasing mechanism for 5-HT was simultaneously studied in vivo and on-line with in vivo voltammetry using the ~/-BL model.…”

Section: Nucleus Accumbensmentioning

confidence: 99%

In vivo voltammetric studies on release mechanisms for cocaine with γ-butyrolactone

Broderick

1991

Pharmacology Biochemistry and Behavior

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The effect of cocaine (20 mg/kg SC) on presynaptic mechanisms of release for dopamine (DA) and for serotonin (5-HT) was studied in nucleus accumbens of unrestrained rats (Rattus norvegicus). The studies were done by assaying synaptic concentrations of DA and 5-HT in the presence of the neuronal impulse flow inhibitor, gamma-butyrolactone (gamma-BL). The results were compared with cocaine effects on accumbens DA and 5-HT in the freely moving rat, without gamma-BL treatment. A neurochemical time course profile showed that the cocaine-induced increase in accumbens synaptic concentrations of DA was significantly blocked (p less than 0.0001) after DA impulse flow was significantly inhibited (p less than 0.0038) by gamma-BL (35.8%). The neurochemical time course profile concurrently showed that the cocaine-induced decrease in accumbens synaptic concentrations of 5-HT was significantly blocked (p less than 0.0004) after impulse flow was significantly inhibited (p less than 0.025) by gamma-BL (50.6%). The findings show that cocaine's effects on synaptic concentrations for DA and for 5-HT in accumbens are dependent on neuronal impulse flow. The findings indicate that presynaptic releasing mechanisms, which may be different for DA vis-à-vis 5-HT, play a role in the mechanism of action of cocaine.

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Cocaine: On-line analysis of an accumbens amine neural basis for psychomotor behavior

Cited by 44 publications

References 25 publications

Ceftriaxone attenuates locomotor activity induced by acute and repeated cocaine exposure in mice

Ceftriaxone attenuates locomotor activity induced by acute and repeated cocaine exposure in mice

Ceftriaxone prevents the induction of cocaine sensitization and produces enduring attenuation of cue- and cocaine-primed reinstatement of cocaine-seeking

In vivo voltammetric studies on release mechanisms for cocaine with γ-butyrolactone

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