1. Acute ethanol administration resulted in an increase in the total number of specific somatostatin receptors in rat frontoparietal cortex and hippocampus, and a decrease in the level of somatostatin-like immunoreactivity in the hippocampus but not in the frontoparietal cortex. 2. Chronic administration of ethanol caused a decrease in the number of somatostatin receptors in the frontoparietal cortex but not in the hippocampus, although the level of somatostatin-like immunoreactivity was unchanged in both brain areas. 3. A week after suppressing ethanol the value for specific binding of tracer to somatostatin receptors in the frontoparietal cortex was not significantly different from that of the control rats, although the actual number of receptors was slightly lower. 4. These results suggest a possible role for somatostatin in the nervous system during alcoholism and the post-withdrawal reaction.

Since nicotine and somatostatin have regulatory effects on locomotor activity it was of interest to determine whether the receptors for somatostatin are modulated by the cholinergic nicotine-like effects. An i.v. dose of 0.3 mg/kg nicotine induced an increase in the concentrations of somatostatin-like immunoreactivity at 4 min in the parietal cortex and at 15 min in the hippocampus. These changes were associated with a significant increase in the total number of specific somatostatin receptors in the parietal cortex at 15 min and in the hippocampus at 30 min following injection. To determine if the above mentioned changes are related to the nicotine activation of central nicotine-like acetylcholine receptors, a cholinergic nicotinic blocking agent, mecamylamine, was administered before the nicotine injection. Pretreatment with mecamylamine (5.0 mg/kg i.v.) prevented the nicotine-induced changes in somatostatin level and binding in both brain areas. Mecamylamine alone had no observable effect on the somatostatinergic system. These results suggest that the somatostatinergic system can be regulated by nicotine-like acetylcholine receptors and may be involved in some of the behavioral central effects of nicotine.

The effect of maternal ethanol ingestion on 125I-labeled [Tyr11]somatostatin (SS) binding and somatostatin-like immunoreactivity (SLI) in the rat frontoparietal cortex and hippocampus of developing offspring was explored. Female Sprague-Dawley rats were given ethanol in the drinking water before pregnancy, during gestation, and while nursing, whereas controls received a standard diet and fresh water ad libitum. In the ethanol group, food intake decreased as ethanol consumption augmented, with the ethanol calories comprising greater than 30% of the total energy intake during pregnancy. Total energy intake was similar for the ethanol group and normal controls. Maternal alcohol ingestion is associated with an enhanced SLI level in the frontoparietal cortex and hippocampus on the day of birth. This study provided evidence of a selective decrease in SS receptor binding in frontoparietal cortex but not in hippocampus in the 0- to 10-day-old offspring of the ethanol-fed rats. The SS receptor number increased from day 0 to 10 in both control and ethanol groups. However, the affinity appeared to decrease significantly in the ethanol group during this period. At day 30, no differences were found between offspring of control and ethanol-treated rats in any of the parameters. These results suggest that the development of SS receptors in the rat frontoparietal cortex can be transitorily delayed by maternal ethanol ingestion.

No abstract

No abstract