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PubMed1980

Regional brain glucose utilization following intrastriatal injections of kainic acid.

Regional brain glucose utilization following intrastriatal injections of kainic acid (KA) was studied by [14C]deoxyglucose autoradiography. In halothane anesthetized rats intrastriatal injections of 0.5-1.9 nmol KA produced histological lesions characterized by neuronal necrosis and glial reaction which varied in volume from approximately 3 to 25 cu. mm. These lesions were restricted to the striatal injection site. Intrastriatal injections of 3.8 nmol led to large lesions in striatum but also in ipsilateral hippocampus, pyriform cortex, entorhinal cortex, and amygdaloid nuclei. Injection doses of 0.5-3.8 nmol KA produced a large increase in striatal glucose utilization within 1 h; 7 days after injections however, glucose utilization was reduced below control levels in a dose-dependent manner. In addition to striatum there were large transient increases in glucose utilization in deep layers of frontal cortex, substantia nigra pars reticulata, ventral tier nuclei of thalamus, and lateral septum. Each of these structures bear close physical or synaptic proximity to the striatal injection site. Also, structures far distant from the striatal injection site exhibited large, transient, dose-dependent increases in glucose utilization; these regions included hippocampus, pyriform cortex, entorhinal cortex, and amygdaloid nuclei. There was a close correlation between the development of areas of neuronal necrosis and a reduction in glucose utilization. These results suggest that intrastriatal injections of KA may cause metabolic and perhaps electrical activation not only of structures near or synaptically connected to the injection site, but also of far distant, but particularly 'sensitive' brain structures probably by diffusion of small amounts of drug. The occurrence of neuronal death in limbic structures after injections of relatively high doses of KA into striatum may result from prolonged firing in those circuits which continues without the prolonged presence of KA.

Animals↗
PubMed1992

(+/-)-1-(2,5-Dimethoxy-4-iodophenyl)-2-aminopropane(DOI) and alpha-methyl-5-HT: 5-HT2 receptor agonistic action on phosphatidylinositol metabolism in the rat fronto-cingulate and entorhinal cortex.

In the present study, the effects of 5-HT and two 5-HT1c/5-HT2 receptor agonists, (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) and alpha-methyl-serotonin (alpha-Me-5-HT) on phosphoinositide hydrolysis were compared, to determine whether DOI and alpha-Me-5-HT were full agonists. Consistent with the results obtained from previous studies, both (+/-)-DOI and alpha-Me-5-HT stimulated turnover of phosphoinositide in a concentration-dependent manner. However, the response obtained with these 5-HT1c/5-HT2 receptor agonists was only 30-40% of that of 5-HT. The stimulation of hydrolysis of phosphoinositide, produced by both 5-HT2 receptor agonists, was potently antagonized by ritanserin (a 5-HT1c/5-HT2 receptor antagonist) and alpha-phenyl-1-(2-phenylethyl)-4-piperine methanol [(+)-MDL 11,939, a 5-HT2 receptor antagonist] but not by granisetron (BRL a 5-HT3 receptor antagonist), suggesting that the action of DOI and alpha-Me-5-HT was primarily mediated by 5-HT2 receptors. When the effect of increasing the concentration of 5-HT on turnover of phosphoinositide was measured in the presence of a 1 microM concentration of the 5-HT3 receptor antagonist granisetron, the response obtained was similar to the response produced by the 5-HT2 receptor agonists, DOI and alpha-Me-5-HT. These results confirm the previous finding that 5-HT stimulates hydrolysis of phosphoinositide by interacting with 5-HT1c/5-HT2 and 5-HT3 receptors. Moreover, they suggest that DOI and alpha-Me-5-HT are full agonists at the 5-HT2 receptor, coupled to hydrolysis of phosphoinositide in the cortex of the rat.

Amphetamines↗