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Anxiety is one of the many emotions that has helped with our survival as a species, it is part of our survival mechanism and forms part of our “fight-or-flight” response. Despite its adaptive function, levels of anxiety can spiral out of control, sometimes to a level that impairs one’s daily functioning, affecting our well-being. Being more prone to anxiety then increases the risk of developing an anxiety disorder, or another mood disorder, depression. High levels of anxiety have also been reported to affect physical health such that it could increase the risk of cardiovascular disease.
Based on statistics from the Anxiety and Depression Association of America, anxiety disorders impact almost 1 in 5 adults in the United States every year. Due to this growing prevalence, researchers are directing their attention to the neurological mechanisms involved in anxiety, particularly investigating the role of glutamate in the hippocampus. The hippocampus is evidenced to be involved in regulating emotions and memory, it also works with 2 other brain regions, area 25 and 32, to modulate anxiety. As for glutamate, there has been hints that might be involved in anxiety. It is an amino acid and the primary excitatory neurotransmitter in the brain, but its role in anxiety is still uncertain as there have been conflicting results found. The motivation for this study was then to examine the role of glutamate in anxiety in greater detail to get a better understanding of its function.
This study was conducted on marmoset’s and the procedure was as followed. They first tested each marmoset’s level of anxiety when an unfamiliar human was introduced. What was found was a negative relationship between levels of anxiety and levels of glutamate in the hippocampus. Specifically, animals with greater levels of anxiety or high-trait anxiety had significantly lower levels of glutamate in their right anterior hippocampus. The researchers then artificially increased the level of glutamate in the animals that exhibited high-trait anxiety, and found that as glutamate reached normative levels, they responded less anxiously in psychological tests. Through this study, the researchers were also able to draw a casual relationship as when anxious primates with naturally low levels of glutamate activity were artificially increased in their hippocampi, their anxiety was reduced as well.
Apart from just investigating glutamate, the researchers wanted to examine the role of the brain areas 25 and 32. This was done by blocking activity in these regions. What they found was blocking area 25 from activity led to the abolishment of the anti-anxiety effect of increasing glutamate, while blocking area 32 had no effect. This suggested the possibility of targeting hippocampal-area 25 pathway for future pharmaceutical interventions targeted at alleviating anxiety symptoms.
Though a full understanding of anxiety and its neural correlates have yet to be fully achieved especially in relation to glutamate’s role, this study does bring them a step closer to achieving that goal.
Category(s):Anxiety
Source material from Medical News Today
