Neuroendocrine Aspects of Learning and Memory Processes

Limbic structures are involved in learning and memory processes. These structures are richly innervated by fibers containing neurotransmitters and neuropeptides. Corticosteroids and adrenomedullary hormones and peptides related to acetylcholine, corticotrophin-releasing hormone, melanophore-stimulating hormone, oxytocin, vasopressin, and several others modulate learning and memory processes and limbic system activity.

The Effects of Cardioselective and Non-Selective β-Adrenoceptor Blockade on the Hypokalaemic and Cardiovascular Responses to Adrenomedullary Hormones in Man

1. Adrenaline was infused intravenously in nine normal volunteers to plasma concentrations similar to those found after myocardial infarction. This study was undertaken on three occasions after 5 days' treatment with placebo or the β-adrenoceptor antagonists, atenolol or timolol. 2. Adrenaline increased the systolic pressure by 11 mmHg, decreased the diastolic pressure by 14 mmHg, and increased the heart rate by 7 beats/min. These changes were prevented by atenolol. However, after timolol the diastolic pressure rose (+19 mmHg) and heart rate fell (− 8 beats/min). 3. Adrenaline caused the corrected QT interval (QTc) to lengthen (0.36 ± 0.02 s to 0.41 ± 0.06 s). No significant changes were found in the QTc when subjects were pretreated with atenolol or timolol. 4. The serum potassium fell from 4.06 to 3.22 mmol/l after adrenaline. Serum potassium fell to a lesser extent to 3.67 mmol/l after atenolol and actually increased to 4.25 mmol/l after timolol. Adrenaline-mediated hypokalaemia appears to result from the stimulation of a β2-adrenoceptor linked to membrane Na+/K+-ATPase causing potassium influx.

Control of exercise-induced muscular glycogenolysis by adrenal medullary hormones in rats

We have previously shown that adrenodemedullation combined with chemical sympathectomy decreases the exercise-induced muscular glycogen breakdown in rats. Now we have elucidated to what extent the effect of combined adrenodemedullation and sympathectomy can be ascribed to the lack of either the adrenal medulla or of the peripheral sympathetic nerve endings. Rats were either adrenodemedullated or underwent sham operation and subsequent unilateral hindleg sympathectomy. Three weeks after adrenodemedullation and 1 wk after sympathectomy, the rats either rested or swam with a tail weight for 75 min or continued swimming to exhaustion. The exercise-induced muscular glycogenolysis was markedly impeded by adrenodemedullation but not by sympathectomy. During the first 75 min of exercise, hepatic glycogenolysis was decreased in adrenodemedullated rats compared with sham-operated rats, and blood glucose only increased in the latter. At exhaustion, plasma insulin and glucagon were higher and lower, respectively, in adrenodemedullated rats than in sham-operated rats, whereas blood glucose did not differ significantly between these groups. During prolonged swimming in rats, adrenomedullary hormones enhance muscular glycogenolysis, glucagon secretion, and the early hepatic glycogenolysis but inhibit insulin secretion.