Kainic acid stimulation of the lateral septum elicits tachycardia.
Electrical stimulation of the lateral septum results in a transient cardiodeceleration which may represent parasympathetic rebound to a brief sympathetic activation. Kainic acid (KA) is a potent neuronal excitant. Stimulation of the lateral septum by KA produced a short-latency tachycardia. Vehicle injections, as well as KA administration to adjacent structures, did not effect significant changes in heart rate. Intraventricular KA, however, did result in a significant tachycardia. Knife cuts of the fornix, interrupting the glutamatergic innervation of the septum, completely blocked the cardiovascular response to KA. Pharmacological treatments reducing sympathetic activity prevented or reversed KA-elicited tachycardia. Thus, it appears that septal administration of KA produces sympathetic activation. KA may serve as a useful tool in studies assessing central regulation of the autonomic nervous system, and the interrelationship between autonomic activity and seizure-induced neuronal loss.
D000818:Animals; D001931:Brain Mapping; D002540:Cerebral Cortex / Q000502:physiology; D004558:Electric Stimulation; D005971:Glutamates / Q000502:physiology; D018698:Glutamic Acid; D006339:Heart Rate / Q000187:drug effects*; D007608:Kainic Acid / Q000494:pharmacology*; D008297:Male; D009434:Neural Pathways / Q000502:physiology; D011759:Pyrrolidines / Q000494:pharmacology*; D051381:Rats; D012686:Septal Nuclei / Q000187:drug effects* / Q000502:physiology; D009435:Synaptic Transmission / Q000187:drug effects
D005971:Glutamates; D011759:Pyrrolidines; D018698:Glutamic Acid; D007608:Kainic Acid