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Alterations in dopamine and 5-hydroxytryptamine (5-HT) function during barbiturate dependence and withdrawal in mice
P L Gray1, D Dawbarn, P V Taberner
1Department of Pharmacology, University of Bristol Medical School, University Walk, Bristol BS8 1TD, UK.
Journal of Psychopharmacology (Oxford, England)
|December 14, 2011
Summary
Barbiturate dependence in mice leads to withdrawal symptoms, including decreased serotonin (5-HT) turnover. This suggests reduced 5-HT function contributes to the withdrawal syndrome, impacting brain chemistry.
Area of Science:
- Neuroscience
- Pharmacology
- Neurochemistry
Background:
- Chronic barbital administration induces physical dependence in mice.
- Barbiturate withdrawal is associated with significant alterations in brain neurotransmitter systems.
Purpose of the Study:
- To investigate the role of serotonin (5-HT) and dopamine turnover during barbiturate withdrawal.
- To explore the relationship between 5-HT function and the severity of barbiturate withdrawal symptoms.
Main Methods:
- Induction of barbiturate dependence in mice via chronic feeding.
- Measurement of brain dopamine and 5-HT turnover.
- Assessment of withdrawal severity using mer captopropionate (MPA)-induced convulsions.
- Administration of neurotoxins and drugs affecting serotonergic pathways.
Main Results:
- Barbital withdrawal significantly increased dopamine turnover and decreased 5-HT turnover.
- Neurotoxins targeting dopamine and 5-HT systems, along with metergoline, exacerbated MPA-induced convulsions.
- Quipazine, a serotonergic agent, attenuated these convulsions.
- Enhanced behavioral responses to serotonergic drugs were observed in dependent mice, despite similar [(3)H]-5-HT binding affinities.
Conclusions:
- Diminished 5-HT function is implicated in the pathophysiology of the barbiturate withdrawal syndrome.
- Serotonergic pathways play a crucial role in modulating the severity of barbiturate withdrawal symptoms.
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