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Effect of brain acetylcholine depletion on bicuculline-induced cardiovascular and locomotor responses
1Department of Pharmacology, Marmara University, School of Medicine, Haydarpasa, Istanbul, Turkey.
Insights
Endogenous acetylcholine modulates GABAA receptor-mediated blood pressure control. Acetylcholine depletion enhanced bicuculline-induced pressor responses but not heart rate or locomotor activity in rats.
Area of Science:
- Neuroscience
- Cardiovascular Physiology
- Pharmacology
Background:
- GABAergic and cholinergic systems are crucial for central cardiovascular regulation.
- GABAA receptor antagonists are known to elevate blood pressure, heart rate, and locomotor activity.
Purpose of the Study:
- To investigate the influence of brain acetylcholine depletion on cardiovascular and locomotor responses induced by bicuculline methiodide.
- To elucidate the role of endogenous acetylcholine in GABAA receptor-mediated cardiovascular control.
Main Methods:
- Conscious Sprague-Dawley rats were used to assess cardiovascular and locomotor effects.
- Bicuculline methiodide was administered intracerebroventricularly to elicit responses.
- Brain acetylcholine was depleted using intracerebroventricular hemicholinium-3 pretreatment.
Main Results:
- Intracerebroventricular bicuculline methiodide (0.3 and 0.5 nmol) increased blood pressure, heart rate, and locomotor activity.
- Hemicholinium-3 pretreatment significantly enhanced the pressor responses to bicuculline methiodide.
- Heart rate and locomotor activity responses to bicuculline methiodide were unaffected by hemicholinium-3.
- High-dose bicuculline methiodide induced convulsions in hemicholinium-3 pretreated rats, unlike in controls.
Conclusions:
- Endogenous brain acetylcholine appears to modulate GABAA receptor-mediated blood pressure control.
- The findings suggest a modulatory role for acetylcholine in the central regulation of blood pressure via GABAA receptors.
Abstract:
Both GABAergic and cholinergic systems are involved in central cardiovascular regulation. Previous studies have shown that GABAA receptor antagonists cause increases in blood pressure, heart rate and locomotor activity. In this study, we examined the role of the depletion of brain acetylcholine on the cardiovascular responses and locomotor activity induced by bicuculline methiodide in conscious Sprague-Dawley rats. The doses of 0.3 and 0.5 nmol of intracerebroventricular bicuculline methiodide produced increases in blood pressure, heart rate and locomotor activity. The dose of 18 nmol of hemicholinium-3 to deplete brain acetylcholine was given intracerebroventricularly one hour prior to bicuculline methiodide. The pressor responses to bicuculline methiodide in animals pretreated with the hemicholinium-3 were higher than those seen in saline-pretreated groups, but locomotor activity and heart rate responses to bicuculline methiodide remained unchanged in hemicholinium-3 pretreatment group. On the other hand, high dose of bicuculline methiodide (0.5 nmol) caused convulsions in some animals pretreated with hemicholinium-3 whereas bicuculline methiodide, alone, did not cause any seizure activity. In conclusion, it seems likely that endogenous brain acetylcholine could be a modulator of GABAA receptor-mediated blood pressure control.