The thermoregulatory responses to dopamine (DA), noradrenaline (NA) and 5-hydroxytryptamine (5-HT), injected into the third cerebral ventricle of goats at 20 degrees C ambient temperature (Ta) or during cold exposure, were compared before and after pretreatment with the DA receptor blocker haloperidol or the 5-HT receptor blocker methysergide. At 20 degrees C Ta, intracerebroventricular (i.c.v.) injection of DA (800 microgram), NA (200 microgram) or 5-HT (800 microgram) induced a decrease in body temperature (Tb) and dilatation of the ear vessels. After DA and 5-HT, but not after NA, panting was observed. During cold exposure both DA and NA caused a suppression of shivering and a fall in Tb. Pretreatment with haloperidol (400 microgram, i.c.v.) attenuated the thermoregulatory effects of i.c.v. DA other than the dilatation of the ear vessels at 20 degrees C Ta. Haloperidol did not influence the responses after i.c.v. NA or 5-HT. Methysergide (1.0 mg, i.c.v.) blocked panting and attenuated the decrease in Tb caused by i.c.v. DA and 5-HT at 20 degrees C Ta and blocked the peripheral vasodilatation caused by 5-HT but not the dilatation caused by DA. During cold exposure methysergide antagonized the thermoregulatory effects of DA, but not those of NA. Ic.v. injection of haloperidol (400 microgram) or methysergide (1.0 mg) during heat exposure induced in panting and a rise in body temperature, which suggests that both DA and 5-HT have a physiological role in the mediation of heat loss in the goat. We conclude that in the central thermoregulatory system of the goat are excitatory DA receptors in the pathway from heat sensors to heat effectors. Activation of these receptors by i.c.v. DA or by heat exposure results in a secondaary release of 5-HT. Since the vasodilating effect of DA was not influenced by haloperidol or methysergide, this effect could be mediated by haloperidol-insensitive (possibly inhibitory) DA receptors on the pathway controlling peripheral vasomotor tone. The thermoregulatory effects of i.c.v. NA are probably mediated by inhibitory NA receptors on the pathway from cold sensors to heat production effectors.