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Exposure of control quail to low ambient temperature (4 degrees) for a short duration (15 min) led to a rapid increase in plasma thyroxine (T4) levels. A peak appeared 40 min after the cold began and was followed by a progressive and slow decline. T4 levels were elevated in birds maintained for up to 3 hr at 4 degrees. Restraint stress could be accompanied by a slight and late decrease in thyroxine concentration, indicating that glucocorticoids could partly inhibit thyroid function. Both cold and restraint stresses elicited sustained adrenocortical activation. No thyroid response to cold appeared after complete or partial neural deafferentation of the hypothalamus, indicating that cold signals were conveyed to the thyrotropic centers from peripheral and/or deep thermoreceptors through neural posterior-lateral afferents to the hypothalamus. No thalamic relay appeared to be necessary since normal thyroidal stimulation was observed after thalamic-hypothalamic disconnection. Such a response persisted in hemispherectomized quail.

Muscimol was injected (0.5 mg kg-1) intravenously to either intact or thalamic-lesioned animals through a chronic catheter. Plasma samples were obtained at 7-min intervals and exhibited a moderate and transient increase in corticosterone levels in both groups, together with some symptoms of light discomfort (e.g., ptiloerection or panting). All these signs disappeared within 45 to 60 min. Intraventricular injection of bicuculline (3.5 micrograms) provoked a corticosterone profile quite similar to a stress-induced polyphasic pattern. Acute stress (electrical footshocks for 30 sec) was applied 2 hr after drug treatment. In controls, the stress-induced adrenocortical response appeared to be markedly modified after muscimol injection. The usual polyphasic rebounding profile was replaced by a monophasic one. This effect of muscimol did not occur when bicuculline had been injected in the 3rd ventricle. Bicuculline alone did not alter the stress-induced profile. GABAergic treatment had no effect on the monophasic response of thalamic-lesioned birds.