Involvement of adrenergic receptor mechanisms within hypothalamus in the fever induced by amphetamine and thyrotropin-releasing hormone in the rat.

The mechanisms underlying the thermal effects induced by intrahypothalamic administration of either d-amphetamine or thyrotropin-releasing hormone (TRH) has been investigated in conscious rats. Direct administration of d-amphetamine (1-10 micrograms in 1 microliter) or TRH (1-4 micrograms in 1 microliter) into the preoptic anterior hypothalamus caused hyperthermia or fever at the ambient temperature (Ta: 8, 22 and 30 degrees C) studied. The fever induced by d-amphetamine or TRH was due to increased metabolic heat production at Ta 8 degrees C, while at Ta 30 degrees C the fever was due to cutaneous vasoconstriction in the rat. At Ta 22 degrees C, the fever was due to both increased metabolism and cutaneous vasoconstriction. Furthermore, the fever induced by intrahypothalamic administration of TRH was greatly reduced by pretreatment with intrahypothalamic administration of either yohimbine (a blocking agent of alpha-adrenergic receptors), phentolamine (a blocking agent of alpha-adrenergic receptors) or DL-propranolol (a blocking agent of beta-adrenergic receptors) in the rat. However, the fever induced by d-amphetamine was antagonized by pretreatment with yohimbine or phentolamine, but not with DL-propranolol in the rat. These observations indicate that the adrenergic receptor mechanisms within the hypothalamus are involved in the fever induced by both d-amphetamine and TRH.

Serotoninergic mechanisms of beta-endorphin- and clonidine-induced analgesia in rats.

Both beta-endorphin and clonidine proved to have statistically significant analgesic activity (increase in latency to hind-paw lick in hot plate test) in rats. Furthermore, the pain inhibition induced by beta-endorphin and clonidine could be antagonized by prior treatment of animals with either naloxone (a narcotic antagonist) or the depletors of central serotonin pathways such as 5,6-dihydroxytryptamine, 5,7-dihydroxytryptamine and p-chlorophenylalanine have not effect on latency to hind-paw lick. The data indicate that serotoninergic activity in the brain plays a role in the elaboration or modulation of beta-endorphin and clonidine analgesia in rats.

Effects of Shan-dou-gen (Euchresta formosana) on metabolic, respiratory and vasomotor activities as well as body temperature in rats.

The effects of the Chinese herb Shan-dou-gen, Euchresta formosana, on metabolic, respiratory and vasomotor activities as well as body temperature were assessed in conscious rats at various ambient temperatures. Systemic administration of Shan-dou-gen produced a dose-dependent hypothermia in rats at room temperature (22 degrees C) and below. The hypothermia in response to Shan-dou-gen was brought about by both cutaneous vasodilatation and decreased metabolic heat production. There were no changes in respiratory evaporative heat loss. However, in the heat (30 degrees C), administration of Shan-dou-gen produced no changes in rectal temperature or other thermoregulatory variables. Furthermore, the hypothermia induced by Shan-dou-gen was greatly antagonized by pretreatment of animals with 5,6-dihydroxytryptamine (predominantly a depletor of central serotonin nerve fiber), but not with 6-hydroxydopamine (a relative depletor of central catecholamine nerve fiber). It appears that the hypothermic effects of Shan-dou-gen may be mediated through serotonin release within the brain.