Chronic haloperidol potentiates stimulated glutamate release in caudate putamen, but not prefrontal cortex.
Rats were given haloperidol continuously for 6 months via subcutaneous implants. Extracellular concentrations of basal and high K(+)-stimulated GABA and glutamate in the lateral caudate putamen and the medial prefrontal cortex were then assessed using microdialysis. While there were no significant differences in basal extracellular concentrations in either brain region, chronic haloperidol-treated rats showed significantly greater increases in glutamate following stimulation with high K+ in the caudate putamen, but not the prefrontal cortex. This effect was accompanied by an attenuation of K(+)-stimulated GABA overflow in the caudate putamen. These results suggest regionally selective alterations in amino acid transmitter function which may be related to chronic neuroleptic-induced motor side effects.
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Department of Psychology, Washington State University, Pullman 99164-4820, USA.
Lynch
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D000818:Animals; D014150:Antipsychotic Agents / Q000494:pharmacology*; D001481:Basal Metabolism; D002421:Caudate Nucleus / Q000187:drug effects* / Q000378:metabolism; D004343:Drug Implants; D004357:Drug Synergism; D005260:Female; D018698:Glutamic Acid / Q000378:metabolism*; D006220:Haloperidol / Q000494:pharmacology*; D017551:Microdialysis; D011188:Potassium / Q000494:pharmacology; D017397:Prefrontal Cortex / Q000187:drug effects* / Q000378:metabolism; D011699:Putamen / Q000187:drug effects* / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013268:Stimulation, Chemical; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D014150:Antipsychotic Agents; D004343:Drug Implants; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; D006220:Haloperidol; D011188:Potassium