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Interactions of γ‐aminobutyric acid and noradrenaline in the high pressure neurological syndrome
Author(s) -
Angel A.,
Halsey M.J.,
WardleySmith Bridget
Publication year - 1983
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1983.tb10010.x
Subject(s) - muscimol , neurotransmitter , agonist , medicine , endocrinology , anesthesia , central nervous system , receptor
1 The effects on the high pressure neurological syndrome (HPNS) of reducing brain noradrenaline (NA) levels were studied in adult rats. The onset of tremors and convulsions, which occur as pressure is increased, were used as endpoints for assessing the onset and severity of the HPNS. 2 Neonatal treatment with 6‐hydroxydopamine (6‐OHDA; 100 mg kg −1 i.p. alternate days from birth for 2 weeks) which depleted brain NA, produced no change in the HPNS as assessed by the appearance of tremors and convulsions. 3 A second series of NA‐depleted rats and equivalent controls were treated with a GABA agonist, muscimol, 0.1 μg intracerebroventricularly. Subsequently the rats were exposed to pressure and the onset and severity of the HPNS was assessed by observation of tremors and convulsions. A combination of NA depletion and intracerebroventricular injection of muscimol significantly raised the onset pressures for tremors and convulsions, i.e. delayed the appearance of the HPNS. 4 These results are consistent with the HPNS being associated with a disturbance in the balance of two or more neurotransmitter systems, rather than simply an increase or reduction in levels of a single transmitter.