Bradycardia and tachycardia following electrical stimulation of the amygdaloid region in monkey

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Reis DJ and Oliphant MC (1964) Bradycardia and tachycardia following electrical stimulation of the amygdaloid region in monkey. J Neurophysiol 27: 893–912.

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First Paragraph: Electrical stimulation of the forebrain in anesthetized and unanesthetized animals and humans may induce marked changes in cardiac rate and rhythm. Both cardiac acceleration and slowing have been initiated in this manner and may take place independently of alterations in systemic blood pressure, respiration, or movement. One region of the forebrain from which cardiac changes have been elicited is the amygdala and adjacent structures lying within the rostral temporal lobe including the temporal tip, periamygdalar and entorhinal cortices, and rostral hippocampal formation consisting of the uncus, hippocampal and dentate gyri and Ammon’s horn. Electrical stimulation within this morphologically heterogeneous but functionally interrelated area, which shall be referred to as the amygdaloid region, has resulted in both bradycardia and tachycardia. Although attempts have been made to correlate heart rate changes of a given type with specific anatomical structures in this region, results have been inconsistent as evidenced by the experience that stimulation of apparently identical structures in different animals or repeated stimulation at one locus in one animal on different occasions may result in variable effects on the heart rate.

Context

  • Reviews the literature on effects of experimental forebrain stimulation on heart function. The authors note that stimulating the same structure in different animals, or in the same animal at different times, may produce variable effects on heart rate. Of the hundreds of stimulation positions used in the present study no site led to the same change in heart rate each time it was stimulated. Bradycardia sometimes persisted for as long as 20 minutes after stimulation, whereas tachycardia was more short-lived. Respirations were also affected by the cortical stimulation. “After-discharges,” large-scale electrical activity that followed the cessation of the experimental stimulation, accompanied bradycardia more often than would have been expected by chance. Blood pressure changes could also be induced by stimulation. Bradycardia is blocked by atropine or vagotomy, indicating that it is vagally mediated. Tachycardia appeared not to arise from any particular nucleus, and the authors believed it to be due to activation of descending fibers from the temporal lobe.

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