When stressed, the amygdala in mouse brains releases the body’s own cannabinoid molecules, which reduces stress signals from the hippocampus, according to research from Northwestern Medicine. This study suggests a possible link between impaired cannabinoid signaling in the brain and increased risk of stress-related mental illnesses such as depression and PTSD.
Researchers have revealed how stress triggers the same receptors as THC.
In stressful situations, the brain produces its own cannabinoid substances, which can act to calm you down by stimulating the same receptors in the brain that THC from the cannabis plant does.
However, the neural networks and brain activity patterns regulated by these endogenous substances are cannabinoid It wasn’t very well known.
A new Northwestern Medicine study in mice shows that the amygdala, the brain’s main emotional center, releases endogenous (the body’s own) cannabinoid molecules under stress, and that these molecules are linked to the brain’s memory and emotional center. It was discovered that it weakens stress alerts coming from certain hippocampi. brain. These results further support the hypothesis that these endocannabinoid molecules are the body’s natural coping response to stress.
Exposure to stress increases the risk of developing or worsening mental illnesses, from generalized anxiety disorder and major depression to post-traumatic stress disorder (PTSD).
“Understanding how the brain adapts to stress at the molecular, cellular, and circuit levels may provide important insights into how stress is translated into mood disorders, and may lead to stress-related “This may reveal new therapeutic targets in the treatment of the disorder,” said corresponding study author Dr.Sachi Patel, Professor of Psychiatry and Behavioral Sciences northwestern university Psychiatrist at Feinberg School of Medicine and Northwestern Medicine.
This study may indicate that disturbances in this endocannabinoid signaling system in the brain may predispose humans to developing stress-related psychiatric disorders, including depression and PTSD. , Patel said.
The study will be published in the journal September 12th. cell report.
In this study, Northwestern scientists used a new protein sensor that can detect the presence of these cannabinoid molecules at specific brain synapses in real time, and that specific high-frequency patterns of amygdala activity produce these molecules. We have shown that there is a possibility that The sensor also showed that these molecules are released as a result of several different types of stress in mice.
When scientists removed the target of these cannabinoids, cannabinoid receptor type 1, the mice’s ability to cope with stress and lack of motivation decreased. Specifically, if the receptor targets of these endocannabinoids are removed at hippocampal-amygdala synapses, mice will adopt a more passive and immobile response to stress and will be less sensitive to sweet taste after exposure to stress. I didn’t really like drinking sucrose water. The latter finding may be related to anhedonia, or decreased pleasure, commonly experienced by patients with stress-related disorders such as depression and PTSD.
One of the major signaling systems that has been identified as a potential drug candidate for stress-related psychiatric disorders is the endocannabinoid system, Patel said.
“Determining whether increasing levels of endocannabinoids can be used as a potential treatment for stress-related disorders is the next logical step from this study and our previous work,” says Psychiatry. said Patel, who is also the Lizzie Gilman Professor of Behavioral Sciences. “Clinical trials are underway in this area and may be able to answer this question in the near future.”
Reference: “Endocannabinoid release at ventral hippocampal amygdala synapses controls stress-induced behavioral adaptations” Veronika Kondev, Mustafa Najeed, Farhana Yasmin, Amanda Morgan, Niharika Loomba, Keenan Johnson, Danielle N. Adank, Ao Dong , Eric Delpire, Yulong Li, Danny Winder, Brad A. Gruter, Sachin Patel, September 12, 2023, cell report.
DOI: 10.1016/j.celrep.2023.113027
This research was funded by: National Institutes of Health.
