Abstract
The effects of both acute and chronic T 3 administration (100 μg/kg, s.c.) on behavioural responses in the rat mediated by 5-hydroxytryptamine (5-HT) and dopamine (DA) were examined 24 hr after the last injection of hormone at a time when serum T3 levels had almost returned to control values. Concomitant changes in the biochemistry of the 5-HT and DA systems were also examined. Administration of T 3 produced complex changes in both central DA and 5-HT systems. Both acute and chronic T 3 treatment enhanced the hyperactivity response to tranylcypromine (TCP) plus L-DOPA, with chronic treatment giving a much greater enhancement. Paradoxically, the accumulation of brain DA at 20 and 30 min after L-DOPA in chronically treated rats was less than in the controls. In order to study possible T 3 effects at the DA postsynaptic receptor, behavioural responses to the DA agonist apomorphine were measured. The activity responses were slightly attenuated in chronically treated rats only. Furthermore, the cataleptogenic effect of haloperidol (0.3 mg/kg) was significantly potentiated in chronically T3-treated rats only. Because striatal [ 3H]-spiroperidol binding was unaltered in chronically treated rats, it is thought that T 3 may produce an altered sensitivity postsynaptic to striatal DA receptors, or a change in activity of a modulatory neuronal system. It was found that 24 hr after either acute or chronic T 3 injection, the hyperactivity response to TCP + L-tryptophan ( L-TP) was markedly enhanced [350% (chronic) and 220% (acute) increase above control activity]. A similar result was obtained for the 5-HT agonists (quipazine and 5-MeODMT). There was no change in whole brain 5-HT or TP accumulation measured 75 min following TP injection in the chronically-treated animals. This, together with enhanced 5-HT postsynaptic agonist responses, may be due to primary changes occurring at or beyond DA neurones, which appear to be interposed between 5-HT neurones and the site expressing the behavioural response.
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