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MODULATION OF THE TURNOVER RATE OF ACETYLCHOLINE IN RAT BRAIN BY INTRAVENTRICULAR INJECTIONS OF THYROTROPIN‐RELEASING HORMONE, SOMATOSTATIN, NEUROTENSIN AND ANGIOTENSIN II
Author(s) -
MaltheSorenssen D.,
Wood P. L.,
Cheney D. L.,
Costa E.
Publication year - 1978
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1978.tb07841.x
Subject(s) - medicine , endocrinology , neurotensin , acetylcholine , somatostatin , thyrotropin releasing hormone , chemistry , angiotensin ii , neuropeptide , biology , hormone , receptor , blood pressure
Abstract— The turnover rate of acetylcholine (TR ACh ) 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 TR ACh 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 TR ACh . TRH increases the TR ACh in parietal but not in frontal cortex whereas somatostatin, neurotensin and angiotensin II failed to change the TR ACh in these cortical areas. Somatostatin and neurotensin increase the TR ACh 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 TR ACh in pons medulla. Larger doses of TRH, neurotensin and angiotensin II fail to elicit greater or more general changes in TR ACh . In contrast, high doses of somatostatin increase the TR ACh of hippocampus and induce‘barrel’rotation. Intraseptal injections of somatostatin induce a long lasting catalepsy but fail to change hippocampal TR ACh or to elicit‘barrel’rotation