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Halothane Attenuates the Haloperidol Induced Dopamine Release and Enhanced the Clozapine Induced Dopamine Release in the Striatum of Rat Using In Vivo Microdialysis Study



Halothane Attenuates the Haloperidol Induced Dopamine Release and Enhanced the Clozapine Induced Dopamine Release in the Striatum of Rat Using In Vivo Microdialysis Study



Anesthesiology Abstracts of Scientific Papers Annual Meeting (2001): Abstract No A-719



Background: It has been shown that the volatile anesthetic isoflurane potentiates the ability of nomifensine to increase the extracellular dopamine (DA) concentration in the brain, probably by releasing DA from axon terminals. In addition, halothane has been reported to either increase or not affect the extracellular concentration of brain DA during anesthesia. The release of DA was regulated by pre-synaptic modulation, and neuroleptics (i.e. haloperidol) change the concentrations of extracellular DA by altering autoregulation. However, no attempt has been made to investigate the effect of halothane anesthesia on the extracellular concentrations of DA modulated by antipsychotic drugs. Therefore, the effect of halothane anesthesia on the changes in the extracellular concentrations of DA and its metabolites (3-methoxytyramine, 3,4-dihydroxyphenylacetic acid and homovanillic acid) induced by neuroleptics was studied using in vivo microdialysis techniques. Methods: Male SD rats were implanted microdialysis probe into the right striatum. The probe was perused with artificial CSF and 40 mcl of dialysate was directly injected to an HPLC column every 20 min. Dopamine and its metabolites were determined by an electrochemical detector. DA and its metabolites reached stable baseline concentrations in about 4.5 hours after the implantation of a microdialysis probe, thus pharmacological experiments were started. Rats were administered saline, or same volume of 200 mcg/kg haloperidol (D2 receptor antagonist), 10 mg/kg sulpiride (D3 antagonist), 10 mg/kg clozapine (D4 antagonist) or 100 mcg/kg apomorphine (D2 agonist) intraperitoneally with or without 1-hr halothane anesthesia (0.5 or 1.5%). Data were analyzed by two-way analysis of variance with drugs as a between subjects variable and time as a within subject variable. For each drug with significant (p < 0.05) drug-time interactions, analysis included a one-way analysis of variance and a subsequent Newman-Keuls post-hoc comparison. Results: Halothane anesthesia did not change the extracellular concentration of DA, but increased that of metabolites in a dose dependent manner. Increased DA concentration induced by haloperidol was significantly attenuated by halothane anesthesia, whereas the concentrations of metabolites were unaffected. Halothane showed no effect on the changes in the concentrations of DA and its metabolites induced by sulpiride or apomorphine. Clozapine induced increases of DA and metabolites were enhanced by halothane anesthesia. Conclusions: The results of the present investigation suggest that halothane modify DA release modulated by antipsychotic drugs in different manners following to the subtype of antagonized DA autoreceptor.

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