Cerebral glucose utilization after administration of apamin, a toxin active on Ca 2+ -dependent K + channels

Abstract

The quantitative 2-[ 14C]deoxyglucose autoradiographic technique 25 was used to examine the effects of acute intravenous administration of apamin, a bee venom toxin specific for one class of Ca 2+ -dependent K + channels on brain energy metabolism. With doses of 0.5 mg/kg, the effects of apamin on local cerebral glucose utilization (LCGU) were limited to the habenulo-interpeduncular tract and the interpeduncular nucleus. After a 1.0 mg/kg dose, significant increases in rates of energy metabolism were additionally seen in two other limbic structures, the medial habenula and the lacunosum moleculare of Ammon's horn as well as in the auditory cortex. Thirty minutes after the injection of 2 mg/kg apamin, LCGU was significantly decreased in the frontoparietal motor area, globus pallidus and accumbens nucleus. Ninety minutes after 2 mg/kg of the toxin, the average glucose utilization of the brain as a whole was enhanced by 35%, and rates of energy metabolism were significantly increased in 50 out of the 75 areas examined. The effects of apamin on cerebral glucose utilization are not totally related to the distribution of apamin binding sites. However, high densities of apamin binding sites are found in the habenulo-interpeducular tract and the interpeduncular nucleus, the limbic areas that are highly affected by the toxin at the LCGU level.