Modulation of the turnover rate of acetylcholine in rat brain by intraventricular injections of thyrotropin-releasing hormone, somatostatin, neurotensin and angiotensin II.

Abstract

Abstract—The turnover rate of acetylcholine (TRACh) was measured in frontal and parietal cortex striatum, hippocampus, diencephalon and brain stem following the intraventricular injection of thyrotropin‐releasing hormone (TRH), somatostatin, neurotensin and angiotensin II. These peptides selectively change the TRACh of various brain regions suggesting specific and independent actions. This specificity of action was also tested by injecting L‐prolylglycine, poly‐L‐proline and poly‐L‐glutamate. None of these synthetic peptides affect the TRACh. TRH increases the TRACh in parietal but not in frontal cortex whereas somatostatin, neurotensin and angiotensin II failed to change the TRACh in these cortical areas. Somatostatin and neurotensin increase the TRACh in diencephalon, whereas TRH and angiotensin II do not. All four peptides decrease the acetylcholine (ACh) content of parietal cortex but not that of frontal cortex. Only somatostatin changes the TRACh in pons medulla. Larger doses of TRH, neurotensin and angiotensin II fail to elicit greater or more general changes in TRACh. In contrast, high doses of somatostatin increase the TRACh of hippocampus and induce‘barrel’rotation. Intraseptal injections of somatostatin induce a long lasting catalepsy but fail to change hippocampal TRACh or to elicit‘barrel’rotation