Cardiovascular and respiratory responses to electrical and chemical stimulation of the hippocampus in anesthetized and awake rats

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Ruit KG and Neafsey EJ (1988) Cardiovascular and respiratory responses to electrical and chemical stimulation of the hippocampus in anesthetized and awake rats. Brain Res 457:2 310–21.

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Abstract: Electrical (30-60-s trains of 0.25-ms pulses at 25 Hz, currents 10-150 microA) and chemical (microinjections of 0.1-0.5 microliters of a 1.0 M glutamate solution) stimulation of the hippocampal formation in the anesthetized and the awake rat evokes marked decreases in heart rate, blood pressure and slower, deeper, more regular respirations. Artificial ventilation (2 ml/breath; 100 breaths/min) has no effect on the cardiovascular responses, indicating that these effects are not secondary to respiratory changes. Administration of methyl atropine (0.4 mg/kg) eliminates the bradycardia response and attenuates or obliterates the blood pressure response but does not alter the respiratory response. This suggests that the cardiovascular responses are mediated partially by the vagus nerve and partially by sympathetic influences. Ablation of the medial frontal cortex, a visceral motor region which projects directly to the nucleus of the solitary tract and which receives a heavy direct projection from the CA1 and subicular cell fields of the ventral hippocampus, markedly attenuates or eliminates the cardiovascular and respiratory responses to stimulation of the ventral but not the dorsal hippocampus. The possibility that the medial frontal cortex may be a relay by which the hippocampus influences cardiovascular responses, including those observed during stress, is discussed.

Context

  • Animal study in rat to investiate effects of stimulation of hippocampal formation on respiration rate, heart rate, and blood pressure. Electrical stimulation or microinjection of glutamate caused decreases in all 3 parameters. Atropine blocked the drop in heart rate, but did not affect the change in respiratory rate, indicating that the bradycardia is vagally mediated. Importantly the study also demonstrated that artificially ventilating subjects during the experiment did not prevent the bradycardia and hypotension, further demonstrating that the processes are independent.

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