ABSTRACT
Activation of central GABA(A) systems with muscimol has been shown to facilitate stress responding and GABA is known to modulate central dopaminergic activity. To evaluate the possibility that this effect of muscimol may depend upon a dopamine mechanism we have tested the effect of intracerebroventricular coadministration of muscimol and the selective D(1) antagonist SCH 23390 on behaviors evoked by tail pinch stress. When injected by themselves muscimol (1.75 nmol) facilitated stress-evoked oral behavior while SCH 23390 (6-600 nmol) produced a dose-related suppression of oral behavior. Coadministration of muscimol and doses of SCH 23390 selected for producing no (6 and 30 nmol), or marginal (60 nmol), effects on stress responding resulted in a dose-related reversal of the increase in orality seen with muscimol alone. The results are consistent with the notion that stressful stimuli activate central GABA(A) systems which, in turn, enhance dopaminergic neurotransmission.
Subject(s)
Receptors, Dopamine/metabolism , Receptors, GABA/metabolism , Stress, Physiological/metabolism , Animals , Benzazepines/pharmacology , Dopamine Antagonists/pharmacology , Drug Interactions , Feeding Behavior/drug effects , GABA Agonists/pharmacology , Male , Muscimol/pharmacology , Psychomotor Performance/drug effects , Rats , Rats, Sprague-Dawley , Receptors, Dopamine/drug effects , Receptors, GABA/drug effectsABSTRACT
A case of male patient with hypereosinophilic syndrome is described. The diagnosis was suggested by clinical features, laboratory data, roentgenological and echosonographic findings and confirmed by cytologic and hematological findings obtained by bone, liver and heart biopsies. There was no evidence of other diseases causing hypereosinophilia. Clinically, the disease presented with cardiac decompensation due to restrictive cardiomyopathy, toxic hepatic lesion and varicosal leg ulcers. The patient improved after the institution of corticosteroids.
