Kindled seizures activate both branches of the autonomic nervous system
Goodman JH, Homan RW, and Crawford IL (1999) Kindled seizures activate both branches of the autonomic nervous system. Epilepsy Res 34:2-3 169–76.
Abstract: Amygdaloid kindled seizures in the rat induce an abrupt elevation of blood pressure accompanied by a significant decrease in heart rate. The autonomic pharmacology of this response was examined in unanesthetized kindled rats. Muscarinic receptor blockade with atropine (1 mg/kg, intravenous (i.v.)) abolished the seizure-induced bradycardia. The seizure-induced hypertension was unaffected by beta-adrenergic blockade with timolol (1 mg/kg, i.v.), but was reduced by phentolamine (5 mg/kg, subcutaneous (s.c.)), an alpha-adrenergic receptor antagonist. A chemical sympathectomy was induced with 6-hydroxydopamine (100 mg/kg, i.v.), an agent that does not cross the blood-brain barrier. This eliminated the pressor response but did not completely block the seizure-induced bradycardia. The effectiveness of 6-hydroxydopamine was tested with tyramine (0.5 mg/kg, i.v.) an agent that releases endogenous catecholamines. These results indicate amygdaloid kindled seizures activate both branches of the autonomic nervous system. The bradycardia was mediated by the parasympathetic system; the pressor response was caused by an increase in peripheral resistance due to alpha-adrenergic receptor activation. More important, these findings show that kindling is a useful seizure model for future studies on the effect of seizures on cardiovascular function and possible mechanisms of seizure-related sudden unexplained death.
Keywords: Amygdala; Autonomic nervous system; Blood pressure; Bradycardia; Epilepsy; Kindling; Seizures
- Kindled amygdalar seizures cause bradycardia and hypertension (Frysinger et al., although Epstein et al. showed that amygdala-only seizures did not alter HR, and Anand and Dua showed that effects of electrical stimulation of this region varied by species). This study demonstrates that muscarinic aceteylcholine antagonist atropine blocks the bradycardic effect, consistent with paraysmpathetic involvement. Alpha-receptor block with phentolamine reduced the hypertension, consistent with sympathetic involvement.