Endogenous GABA release is reduced in the striatum of cocaine-sensitized rats

Jung, Bruce J.; Dawson, Ralph; Sealey, Suzanne A.; Peris, Joanna

doi:10.1002/(sici)1098-2396(199911)34:2<103::aid-syn3>3.0.co;2-z

Cited by 21 publications

(7 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Repeated administration of cocaine produced a progressive enhancement of stereotyped behavior over time, in accord with previous findings (Jung et al, 1999;Canales and Graybiel, 2000;Vanderschuren and Kalivas, 2000;Haile et al, 2001), with scores reaching values of ϳ6 on the stereotypy scale by day 7 (Fig. 1 B-D).…”

Section: Coactivation Of D 1 -Class and D 2 -Class Dopamine Receptorssupporting

confidence: 91%

Concurrent Activation of Dopamine D₁and D₂Receptors Is Required to Evoke Neural and Behavioral Phenotypes of Cocaine Sensitization

et al. 2002

View full text Add to dashboard Cite

Repeated exposure to psychomotor stimulants produces a striking behavioral syndrome involving repetitive, stereotypic behaviors that occur if an additional exposure to the stimulant is experienced. The same stimulant exposure produces specific alterations in gene expression patterns in the striatum. To identify the dopamine receptor subtypes required for the parallel expression of these acquired neural and behavioral responses, we treated rats with different D1-class and D2-class dopamine receptor agonists and compared the responses of drug-naive rats with those of rats given previous intermittent treatment with cocaine. In rats exposed to repeated cocaine treatment, the effects of a subsequent challenge treatment with either a D1-class agonist (SKF 81297) or a D2-class agonist (quinpirole) were not significantly different from those observed in drug-naive animals: the drugs administered singly did not induce robust stereotyped motor behaviors nor produce significantly striosome-predominant expression of early genes in the striatum. In contrast, challenge treatment with the D1-class and D2-class agonists in combination led to marked and correlated increases in stereotypy and striosome-predominant gene expression in the striatum. Thus, immediately after repeated psychomotor stimulant exposure, only the concurrent activation of D1 and D2 receptor subclasses evoked expression of the neural and behavioral phenotypes acquired through repeated cocaine exposure. These findings suggest that D1-D2 dopamine receptor synergisms underlie the coordinate expression of both network-level changes in basal ganglia activation patterns and the repetitive and stereotypic motor response patterns characteristic of psychomotor stimulant sensitization.

show abstract

Section: Coactivation Of D 1 -Class and D 2 -Class Dopamine Receptorssupporting

confidence: 91%

Concurrent Activation of Dopamine D₁and D₂Receptors Is Required to Evoke Neural and Behavioral Phenotypes of Cocaine Sensitization

et al. 2002

View full text Add to dashboard Cite

show abstract

“…It is noteworthy that the VP GABAergic effects do not parallel that reported for other forebrain regions. For example, in striatal regions of cocaine-sensitized rats subjected to a short-term withdrawal (1-3 days), the inhibitory effects of microiontophoretically applied GABA are augmented (Henry and White, 1995) and GABA release is decreased (Jung et al, 1999). These regional differences illustrate the value of further investigations regarding GABAergic involvement in the neuronal adaptations that occur with repeated cocaine exposure.…”

Section: Morphine Cross-sensitization To Cocaine and Ventral Pallidummentioning

confidence: 99%

Cross-Sensitization to Morphine in Cocaine-Sensitized Rats: Behavioral Assessments Correlate with Enhanced Responding of Ventral Pallidal Neurons to Morphine and Glutamate, with Diminished Effects of GABA

McDaid

Dallimore

Mackie³

et al. 2005

J Pharmacol Exp Ther

View full text Add to dashboard Cite

Common neurobiological substrates contribute to the progressively increased behavioral effects (i.e., sensitization) that occur with repeated intermittent treatments of cocaine and morphine. Consequently, repeated exposure to cocaine can augment responding to morphine (termed cross-sensitization). Drug-induced sensitization in rats may model aspects of the dysfunction in motivation that are imposed by addiction. The ventral pallidum (VP) is involved in motivated behaviors and its function is altered by acute administration of cocaine and morphine, but the effects of repeated drug exposure remain unknown. Targeting this paucity, the present study evaluated electrophysiological changes in the VP of rats exposed to five once-daily cocaine treatments (15 mg/kg i.p.). This regimen also induced behavioral-sensitization that was expressed 3 days later when the rats received either an acute injection of cocaine (15 mg/kg i.p.) or morphine (10 mg/kg i.p.). VP neurons recorded in vivo 3 days after the repeated cocaine treatment regimen demonstrated increased excitatory responding to microiontophoretic applications of morphine and glutamate. The maximal effect (E max ) was increased without altering potency, suggesting a change in the functional efficacy of the respective receptor systems. This did not represent a potentiation in transmission in general, for the effects of GABA were diminished. The results provide the first evidence for cellular adaptation in the VP after a sensitizing drug treatment paradigm and reveal that crosssensitization of drug-induced behaviors temporally correlates with changes in VP neuronal responding. These findings advance an emerging theme that alterations in the VP may contribute to the increased motivation for drug seeking that occurs in drug-withdrawn addicts.

show abstract

“…Chronic cocaine treatment results in the down regulation of GABA-A receptor alpha, beta and gamma subunits (Suzuki et al, 2000) and a decrease in endogenous GABA release in the striatum (Jung et al, 1999) of rats. Cocaine abusers show significantly greater sensitivity to a challenge dose of lorazepam, a benzodiazepine which enhances the activation of GABA receptors, both in terms of enhanced sedative effects and greater reductions in cerebral metabolism (Volkow et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Valproate treatment and cocaine cue reactivity in cocaine dependent individuals

Reid

Thakkar

2009

Drug and Alcohol Dependence

View full text Add to dashboard Cite

Based on prior clinical trials indicating that γ-aminobutyric acid (GABA) based anticonvulsant medications reduce drug craving in cocaine dependent study participants, we tested the effects of valproate treatment on cue-induced cocaine craving. Crack cocaine dependent individuals (N=20) were tested in a randomized, placebo-controlled, within-subjects, crossover study design. Valproate treatment was titrated up to 1500 mg/day by Day 6 of treatment, cue testing was completed on Day 8 of treatment, and all study participants underwent a washout period of 5 days between active and placebo medication treatment periods. Testing included both cocaine and neutral cue exposure sessions, presented in a random and counterbalanced order. Main effects of cue exposure were found for subjective ratings of “desire to use cocaine now”, the cocaine craving index, cocaine-like high, and cocaine withdrawal. Treatment interaction effects were found with “desire to use cocaine now”, which underwent a greater increase following cocaine cue exposure in the valproate condition. Main effects of medication treatment were found, in which lower blood pressure and heart rate, and higher plasma cortisol levels, were associated with valproate treatment. Valproate treatment was also associated, at a trend level, with higher pre-test cocaine craving levels. The results demonstrate that cocaine cue reactivity is a robust phenomena across two assessment sessions, but fail to support the use of valproate as a means of reducing spontaneous and cue-induced cocaine craving. The use of valproate as a treatment for cocaine dependence is not supported.

show abstract

Endogenous GABA release is reduced in the striatum of cocaine-sensitized rats

Cited by 21 publications

References 49 publications

Concurrent Activation of Dopamine D₁and D₂Receptors Is Required to Evoke Neural and Behavioral Phenotypes of Cocaine Sensitization

Concurrent Activation of Dopamine D₁and D₂Receptors Is Required to Evoke Neural and Behavioral Phenotypes of Cocaine Sensitization

Cross-Sensitization to Morphine in Cocaine-Sensitized Rats: Behavioral Assessments Correlate with Enhanced Responding of Ventral Pallidal Neurons to Morphine and Glutamate, with Diminished Effects of GABA

Valproate treatment and cocaine cue reactivity in cocaine dependent individuals

Contact Info

Product

Resources

About

Endogenous GABA release is reduced in the striatum of cocaine-sensitized rats

Cited by 21 publications

References 49 publications

Concurrent Activation of Dopamine D1and D2Receptors Is Required to Evoke Neural and Behavioral Phenotypes of Cocaine Sensitization

Concurrent Activation of Dopamine D1and D2Receptors Is Required to Evoke Neural and Behavioral Phenotypes of Cocaine Sensitization

Cross-Sensitization to Morphine in Cocaine-Sensitized Rats: Behavioral Assessments Correlate with Enhanced Responding of Ventral Pallidal Neurons to Morphine and Glutamate, with Diminished Effects of GABA

Valproate treatment and cocaine cue reactivity in cocaine dependent individuals

Contact Info

Product

Resources

About

Concurrent Activation of Dopamine D₁and D₂Receptors Is Required to Evoke Neural and Behavioral Phenotypes of Cocaine Sensitization

Concurrent Activation of Dopamine D₁and D₂Receptors Is Required to Evoke Neural and Behavioral Phenotypes of Cocaine Sensitization