Abstract
In fowls TRH given into the III cerebral ventricle (0.25–5 μg) produced intense behavioural stimulation, electrocortical desynchronization and a slight increase in body temperature. In particular, an intense pattern of stereotyped head-neck movements, increase in locomotor activity, repeated and preening, vocalization, erection of the tail feathers and occasionally ‘escape responses’ were observed. This picture lasted for about 30 min and was followed by slight behavioural sedation during which stereotypies continued to occur but to a lesser extent. Similar increases in locomotor activity and stereotypies were evoked by infusing TRH into the hypothalamus whereas the unilateral microinfusion into the n. basalis or the n. mesencephalicus profundus, homologous to the mammalian striatum and s. nigra respectively, produced very intense stereotyped head-neck movements, wet-dog syndrome and vocalization. TRH given into the other areas of the brain (e.g. hyperstriatum, neostriatum, olfactory ventricle, eminentia basalis and lateral part of the mesencephalon) lacked effects on behaviour and body temperature. The effects of intraventricular infusion of TRH were antagonized by prior administration of haloperidol and spiperone whereas antagonists at α and β-adrenoceptors and at 5-HT receptors were ineffective. In addition, TRH reversed sedation induced by intraventricular α-methyl-p-tyrosine. Behavioural and body temperature effects of TRH were independent of its endocrine properties since these were not observed after systemic or intracerebroventricular injection of thyrotropin, triidothyronine and thyroxine. The increase in body temperature evoked by intracerebroventricular injection of TRH was due to activation of heat production and decrease in thermodispersive mechanisms.
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