Can Glutamic acid explain anxiety?
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Anxiety disorder is a neurosis characterized by anxious emotional experience. It is the most common type of neurosis, including generalized anxiety, panic attacks, and a normal emotion. But when a person often feels disproportionately anxious, it may become an obstacle. It changes the way a person handles emotions and behaviors, and it also causes physical symptoms. Mild anxiety may be vague and restless, while severe anxiety may seriously affect daily life.
Nowadays, anxiety has developed into the most common mental illness, but only a few people have received effective treatment.
Recently, a study on anxiety explored the role of l-glutamic-acid, a neurotransmitter. These findings can help scientists develop and research more effective interventions.
Almost everyone experiences some form of anxiety. Over time, evolution has trained anxiety into a survival mechanism, which is part of the "fight or flight" response. When the body is ready to take action, the heartbeat will be faster and may be accompanied by nausea.
Although anxiety is a natural reaction, it may be out of control for some people. At this time, anxiety is no longer a protective mechanism to help us cope with daily life, but a burden that affects health. In addition, it increases the risk of anxiety and depression.
In addition to mental health, anxiety can also have a serious impact on the body. The authors wrote in this new study that continued high levels of anxiety may increase the risk of cardiovascular disease.
Anxiety disorders are as common as depression, but until recently, anxiety disorders have not received enough attention and attention.
Glutamate is an amino acid and the main excitatory neurotransmitter in the brain. In recent years, many studies have shown that glutamate may be related to anxiety.
Decreased glutamate activity seems to increase anxiety behavior, and glutamate levels in the hippocampus (the brain region responsible for regulating mood and memory) seem to be particularly important.
Early research suggested that the other two areas of the brain and the hippocampus work together to regulate anxiety. These two areas are No. 25 and No. 32, respectively, which are part of the prefrontal cortex.
However, the researchers did not fully understand the role of glutamate in anxiety. There are contradictions in the conclusions of other studies. For example, a study using non-anxiety rats found that a decrease in the activity of certain glutamate receptor subtypes in the hippocampus can reduce the anxiety level of the animal.
The author of this latest study wanted to verify the role of glutamate in anxiety in more detail. To get a more definite conclusion, they conducted a series of research experiments using marmosets.
First, they tested the anxiety of each marmoset when it saw strange people (masked operators). As expected, the level of glutamate in the hippocampus of the marmoset with the highest degree of anxiety (high trait anxiety) was significantly lower.
It is known that high trait anxiety is associated with glutamate levels in the right anterior hippocampus.
Next, they artificially increased glutamate levels in the brains of highly anxious marmosets. They found that once the glutamate levels reached normal levels, the anxiety level of these animals in the psychological test was reduced.
The second part of the experiment provided researchers with evidence that showed causality: Anxious primates naturally have lower glutamate activity levels, and when their glutamate activity levels increase in the hippocampus, the degree of anxiety decreases.
To get more information about the role of brain regions 25 and 32, the team conducted further experiments.
By inhibiting the activity of these brain regions, they found that when region 25 was suppressed, the anxiolytic effect of increased glutamate disappeared, but region 32 had no effect.
The second part of the experiment provided researchers with evidence that showed causality: Anxious primates naturally have lower glutamate activity levels, and when their glutamate activity levels increase in the hippocampus, the degree of anxiety decreases.
To get more information about the role of brain regions 25 and 32, the team conducted further experiments.
By inhibiting the activity of these brain regions, they found that when region 25 was suppressed, the anxiolytic effect of increased glutamate disappeared, but region 32 had no effect.
The authors believe that the pathway between the hippocampus region 25 is likely to become a target for future drug intervention. The researchers concluded: "These findings from primate studies provide causal evidence that hypoglycemic function in the hippocampus can regulate endogenous high-specific anxiety, and that the 25 pathway in the hippocampus is a potential therapeutic target. "
Although scientists still do not fully understand the role of glutamate in anxiety, such research will bring us one step closer to fully understanding anxiety.
