Summary: Researchers have discovered how stress-induced cardiovascular changes are controlled by the brain. Experiments in rats show that activating the lateral habenula, a stress-sensitive brain region, triggers changes in heart rate and blood pressure.
Blocking dopamine neurotransmission or inhibiting activity in the ventral tegmental area suppressed these changes, highlighting dopamine’s key role in mediating cardiovascular stress responses. These findings could improve our understanding of how stress impacts behavior and physiology, paving the way for treatments to maintain balance during stress.
Key Facts
- Stress Responses: Lateral habenula activation alters heart rate and blood pressure.
- Dopamine’s Role: Cardiovascular changes are mediated by dopamine neurons in the ventral tegmental area.
- Therapeutic Potential: Insights into stress mechanisms could inform treatments for better homeostasis.
Source: University of Tsukuba
Under stress, animals change their behavior, such as through “fight or flight” or “freezing” response. Simultaneously, physiological responses essential for stress adaptation are triggered in the body. Cardiovascular regulation, including changes in blood pressure and heart rate, is a critical stress response.
Researchers have focused on the lateral habenula, a brain region where neurons are activated in response to stress. They investigated the neural mechanisms underlying cardiovascular responses by activating the lateral habenula in experiments using rats.
Activation of the lateral habenula caused changes in blood pressure and heart rate. However, pharmacologically blocking of dopamine neurotransmission suppressed the blood pressure and heart rate changes induced by lateral habenula activation.
Furthermore, these changes were also suppressed when the activity of the ventral tegmental area, which receives input from neurons in the lateral habenula, was pharmacologically inhibited.
These results suggest that the cardiovascular responses caused by lateral habenula activation are mediated by the dopaminergic system, specifically by dopamine neurons in the ventral tegmental area.
Based on the findings of this study, further research into the neural mechanisms regulating cardiovascular responses during stress is expected to provide a better understanding of the behavioral changes induced by stress and the mechanisms that maintain homeostasis in the body.
Funding: The research was supported by the Japan Society for the Promotion of Science Kakenhi (19H03339, 22K19477, and 24K22082). YS was also supported by a Japan Science and Technology Agency scholarship SPRING (JPMJSP2124).
About this neuroscience research news
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 dopaminergic system mediates the lateral habenula-induced autonomic cardiovascular responses” by SATO, Yuma et al. Frontiers in Physiology
Abstract
The dopaminergic system mediates the lateral habenula-induced autonomic cardiovascular responses
The lateral habenula (LHb) has been implicated in stress coping and autonomic control. The LHb regulates the midbrain system of monoamine neurotransmitters such as dopamine, serotonin, and noradrenaline. However, how the LHb regulates autonomic cardiovascular control in stressful situations is unclear.
In this study, we examined the participation of the midbrain dopaminergic system in the cardiovascular response elicited by activation of the LHb. We used urethane-anesthetized Wistar male rats. We performed electrical stimulation of the LHb to observe changes in heart rate and blood pressure.
Stimulation of the LHb caused bradycardia and a pressor response.
Application of a nonselective dopamine receptor antagonist attenuated both the heart rate and the blood pressure changes induced by the LHb. We also tested the effects of blockade of dopamine receptor subtypes in 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. Inactivation of the VTA turned bradycardia into tachycardia caused by the LHb stimulation and attenuated the pressor response.
Our results indicated that regulation of the dopaminergic system by the LHb mediates the generation of the autonomic cardiovascular response.
Dopamine D1-like and D2-like receptors mediate the sympathoexcitation resulting from the activation of the LHb. The VTA is one of the dopaminergic origins related to the cardiovascular response originating from LHb activation.
