Summary: Researchers have discovered how stress-induced cardio shifts are controlled by the brain. Research in animals show that activating the medial habenula, a stress-sensitive head area, causes changes in heart rate and blood pressure.
These changes were prevented by blocking or limiting serotonin neurotransmission, highlighting dopamine’s crucial role in regulating cardio stress responses. These findings could help us better understand how stress affects habits and biology, opening the door to treatments that keep things in balance during stressful situations.
Essential Information
- Stress Reactions: Longitudinal habenula stimulation affects heart level and blood pressure.
- Dopamine’s Role: Cardio modifications are mediated by dopaminergic neurons in the lateral tegmental area.
- Medical Potential: Insights into tension mechanisms may inform treatments for better equilibrium.
Origin: University of Tsukuba
Under pressure, animals change their behavior, such as through “fight or flight” or “freezing” answer. Together, physiological reactions necessary for stress version are triggered in the body. Cardiovascular legislation, including shifts in blood pressure and heart rate, is a crucial stress response.
Researchers have concentrated on the medial habenula, a region of the brain where neurons respond to pressure. By activating the medial habenula in investigations using animals, they investigated the neural mechanisms underlying cardiovascular actions.
Alterations in blood pressure and heart rate were caused by the stimulation of the medial habenula. But, lateral habenula activation-induced blood pressure and heart rate changes were halted by medicinally blocking dopamine serotonin.
However, these changes were likewise suppressed when the action of the lateral tegmental place, which receives input from neurons in the medial habenula, was medicinally inhibited.
These findings support the hypothesis that the serotonin system, especially serotonin neurons in the lateral tegmental region, is responsible for the cardiovascular responses brought on by longitudinal habenula activation.
Further investigation into the neural systems that control cardio actions under pressure is anticipated to provide a better understanding of the behavioral modifications brought on by stress and the systems that maintain body balance in light of the findings of this study.
Funding: The research was supported by the Japan Society for the Promotion of Science Kakenhi ( 19H03339, 22K19477, and 24K22082 ). A Japanese Science and Technology Agency scholarship SPRING ( JPMJSP2124 ) also provided financial support for YS.
About this news from neuroscience research
Author: KAMOSHITA Kimio
Source: University of Tsukuba
Contact: KAMOSHITA Kimio – University of Tsukuba
Image: The image is credited to Neuroscience News
Original Research: Open access.
” The lateral habenula-induced autonomic cardiovascular responses are mediated by the dopaminergic system.” by SATO, Yuma et al. Frontiers in Physiology
Abstract
The lateral habenula-induced autonomic cardiovascular responses are mediated by the dopaminergic system.
The lateral habenula ( LHb ) has been linked to autonomic control and stress coping. The LHb regulates the midbrain system of monoamine neurotransmitters such as dopamine, serotonin, and noradrenaline. However, it is unclear how the LHb regulates autonomic cardiovascular control in stressful circumstances.
In this study, we examined whether the midbrain dopaminergic system participated in the cardiovascular response brought on by LHb activation. We used urethane-anesthetized Wistar male rats. We monitored the LHb’s heart rate and blood pressure changes using electrical stimulation.
Bradycardia and a pressor response were caused by LHb stimulation.
Application of a nonselective dopamine receptor antagonist attenuated both the LHb’s heart rate and blood pressure changes. Additionally, we examined the effects of the dopamine receptor subtype blockade on the LHb-induced cardiovascular responses.
Application of selective dopamine D1/D5, D2/D3, or D4 , receptor antagonists attenuated the LHb-induced pressor response but did not change the HR response.
Furthermore, we examined the effect of inactivation of the ventral tegmental area (VTA ) on the cardiovascular response induced by LHb stimulation. The LHb stimulation-induced bradycardia was attenuated by the VTA’s inactivation, which attenuated the pressor response.
Our findings demonstrated that the LHb’s control of the dopaminergic system causes the autonomic cardiovascular response to emerge.
The sympathoexcitation brought on by the activation of the LHb is mediated by the dopamine D1– and D2-like receptors. One of the dopaminergic origins linked to LHb activation’s cardiovascular response is the VTA.
