Is alcohol induced poikilothermia mediated by 5-HT and catecholamine receptors or by ionic set-point mechanism in the brain?

In adult male Sprague-Dawley rats, stainless steel guide cannulae were implanted stereotaxically in either the lateral or third cerebral ventricle. Postoperatively, each animal was maintained at an ambient temperature of 22 degrees C. Just prior to the intragastric gavage of 4.0 g/kg ethyl alcohol (20% solution) individual animals were fitted with a colonic thermistor probe. Then, control CSF, a monoaminergic receptor antagonist, or a Ca++ ion chelating agent, EGTA, was infused into either the lateral or third ventricle (ICV) in a volume of 10.0 microliter. Phentolamine (20.0 micrograms), butaclamol (10.0 micrograms), or methysergide (20.0 micrograms) injected ICV all failed to prevent the thermolytic action of alcohol. The fall of 1.5 to 2.0 degrees C in the rat's colonic temperature, ordinarily caused by alcohol, was the same as that without the antagonists and lasted 3.0 to 4.0 hrs. EGTA infused into the rat's lateral cerebral ventricle also did not interfere with alcohol's poikilothermic action. However, EGTA infused into the third cerebral ventricle completely blocked alcohol's effect in lowering the body temperature of the rat. These results suggest that: (1) alcohol's profound effects on body temperature are not mediated by 5-HT, norepinephrine or dopamine pathways which are thought to underlie the mechanisms in the hypothalamus for thermoregulation; and (2) the temperature set-point mechanism, controlled by the ratio of diencephalic Na+ to Ca++ ions, is incapacitated by alcohol. Restoration of the ratio in the diencephalon by the direct, local chelation of Ca++ ions that eliminates alcohol's deleterious effects on body temperature.