Top-down brain circuits for operant bradycardia

Author:

Yoshimoto Airi1ORCID,Morikawa Shota2,Kato Eriko1ORCID,Takeuchi Haruki2ORCID,Ikegaya Yuji134ORCID

Affiliation:

1. Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo 113-0033, Japan.

2. Graduate School of Science, The University of Tokyo, Tokyo 113-0032, Japan.

3. Institute for AI and Beyond, The University of Tokyo, Tokyo 113-0033, Japan.

4. Center for Information and Neural Networks, National Institute of Information and Communications Technology, Suita City, Osaka 565-0871, Japan.

Abstract

Heart rate (HR) can be voluntarily regulated when individuals receive real-time feedback. In a rat model of HR biofeedback, the neocortex and medial forebrain bundle were stimulated as feedback and reward, respectively. The rats reduced their HR within 30 minutes, achieving a reduction of approximately 50% after 5 days of 3-hour feedback. The reduced HR persisted for at least 10 days after training while the rats exhibited anxiolytic behavior and an elevation in blood erythrocyte count. This bradycardia was prevented by inactivating anterior cingulate cortical (ACC) neurons projecting to the ventromedial thalamic nucleus (VMT). Theta-rhythm stimulation of the ACC-to-VMT pathway replicated the bradycardia. VMT neurons projected to the dorsomedial hypothalamus (DMH) and DMH neurons projected to the nucleus ambiguus, which innervates parasympathetic neurons in the heart.

Publisher

American Association for the Advancement of Science (AAAS)

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