PubMed · 9799985
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A Seebauer, A Schauer, D Schwender. 1998. [Bronchial asthma].. https://doi.org/10.1007/s001010050628
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Although a very large literature exists on the in vitro, ex vivo, and in vivo effects of nicotine on dopamine release in rodents, similar data in primates are scant. This study was initiated to compare methamphetamine to nicotine given i.v. to normal unanesthetized monkeys using positron emission tomography (PET) techniques. Release of dopamine in the striatum using [(11)C]raclopride was determined indirectly in four nicotine-naïve adult Macaca mulatta monkeys under conscious and isoflurane-anesthetized conditions using high-resolution PET. [(11)C]Raclopride was given i.v. as a bolus injection followed by continuous infusion with steady state over 30-45 min. Nicotine bitartrate was then given as a bolus plus infusion for 30 min in doses of 32 microg/kg + 0.8 microg/kg/min or 100 microg/kg + 2.53 microg/kg/min as base. The larger doses of nicotine caused significant cardiovascular effects; these doses did not displace [(11)C]raclopride binding in either dorsal or ventral striatum under the anesthetized conscious condition. In contrast, isoflurane-anesthesia induced a slight but significant dose-dependent reduction of [(11)C]raclopride binding by nicotine even at the same doses used in the anesthetized condition. Methamphetamine in bolus doses of 0.1, 0.3, and 1.0 mg/kg i.v. under conscious condition caused a significant displacement of [(11)C]raclopride and isoflurane-anesthesia facilitated the displacement induced by nicotine. These results indicate that nicotine, in high tobacco-smoking-related doses, does not release sufficient brain dopamine to displace [(11)C]raclopride in the striatum in the awake and fully conscious state, in contrast to small doses of methamphetamine.
In the conscious rabbit muscimol (1-10 nmol/side) was microinjected into the hypothalamic paraventricular nucleus to inhibit neuronal function and the acute changes in mean arterial pressure (MAP), heart rate and renal sympathetic nerve activity (RSNA) were monitored. Muscimol (1 nmol) had no effect on the cardiovascular variables, as was the case with vehicle. However, muscimol (10 nmol) elicited a significant increase in RSNA of 184+/-40% and a reduction in heart rate of 49+/-12 beats/min but no change in MAP. The effect of blocking endogenous glutamatergic inputs with the glutamate antagonist, kynurenate (25 nmol), into the PVN was also examined. Kynurenate elicited an increase in RSNA of 35+/-9% with no significant change in MAP or HR. The results suggest that muscimol inhibits a tonically active inhibitory influence on RSNA arising from the PVN in the conscious rabbit. A glutamatergic input into the PVN appears to contribute to the tonic activation of this inhibitory influence.
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