Dipropylacetate-induced quasi-morphine abstinence behaviour in the rat: involvement of amygdaloid and thalamic structures.

Quasi-morphine abstinence behaviour induced by di-n-propylacetate (DPA) in rats is thought to be caused by an increased GABAergic activity in the CNS. Behavioural responses after intracerebral injections of DPA were studied to gain insight into the centre median-parafascicularis (Cm-Pf) resulted in a large number of body shakes and greater locomotor activity when compared to other brain areas. Injection of DPA into the central amygdala (Ac) resulted in an enhanced number of chewing episodes. Administration of bicuculline methiodide (BMI) into the Cm-Pf, 5 min after intraperitoneal administration of DPA, suppressed by body shakes but had only minor effects on horizontal activity, whereas injection of morphine into the same structure suppressed both behavioural symptoms. It is concluded that GABAergic and opioid mechanisms in the Cm-Pf are involved in the DPA-induced behaviour. Injection of BMI into the central amygdala shortly after i.p. injection of DPA resulted in an increase in the number of body shakes, whereas no effect was observed on activity. Morphine applied to this structure slightly potentiated the locomotor activity, but had no effect on the body shakes induced by DPA. The present results suggest a facilitatory role for a GABAergic system in the Cm-Pf on body shakes, while in the central amygdala a GABAergic system exerts an inhibitory influence on this symptom of abstinence.