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team at the University of New Mexico in the United States has identified for the first time a neural link that evolves from fear to anxiety.With the increasing pressure from social environment and work, modern people are often in a tense, even fearful mood, which is closely related to anxiety. Anxiety usually stems from a stress response caused by a sense of uncertainty, which can lead to persistent physical and psychological discomfort in the patient. Of course, fear itself does not equal anxiety, but long-term fear can turn into anxiety. In a recent study published in NeuroImage, a team from the University of New Mexico in the United States identified for the first time a neural link that evolves from fear to anxiety.Study co-author Elaine Bearer said: "So far, psychiatrists know very little about what happens in the brain after a terrible event and why some people don't recover easily, or even maintain anxiety for long periods of time later. Theto shed light on the brain's response to fear and why, in some cases, fear can lead to long-term anxiety, such as post-traumatic stress disorder. Often, life-threatening fears often lead to post-traumatic stress syndrome (PTSD) later in life.While these experiments are not suitable in humans, the researchers used rodents to create fear in mice by exposing them to a simulated predator smell and to see how animal brain activity evolved from fear to anxiety.For the study, the researchers exposed a group of normal wild mice and a group of 5-serotonin (Serotonin) transporter protein (SERT) to the smell of predators.5-Serotonin transport protein is the main target of psychoactive drugs (e.g. cocaine) and antidepressants (e.g. pyrethroids). The absence of the SERT gene (SERT-KO) leads to anxiety susceptivity, providing a unique model for studying how terrible experiences can turn into anxiety.The researchers compared the reactions of two groups of mice after smelling predators and captured their MRI images to determine the neural association of anxiety.Both groups of mice reacted defensively to predator odors. Genes knocked out mice for 23 days, while the average mouse returned to baseline exploration behavior within nine days. Therefore, nine days after the smell of predators, the differences in neural activity between wild mice and genetic knock-out mice determined the neural correlation between the mice's sustained defensive behavior.To highlight active neurons, the researchers used manganese ions, a non-toxic ion that illuminates active neurons in magnetic resonance images. The calculation of these whole-brain images resulted in a map of brain activity over a long period of time after brief exposure to the smell of terror.They identified differences in neural activity in 45 subregions of the brain. Some areas are activated by the odor of the arrested eater, while others are later activated. Anxiety susceptivity is associated with more activity in more regions.The researchers found that the function of some of these areas, including the amygdala and the lower pasum, was at least partially understood, but others, such as reward loops, were previously not known to be associated with anxiety.In the state of anxiety, coordination between regions changes, which may represent anxiety signals throughout the brain, or it may mean indesocision between brain regions, which often occurs when we feel fear or anxiety."We now know that brain activity during anxiety is different from brain activity in acute fear responses," Bearer said. Anxiety increases nerve activity in many specific areas of the brain, thus losing normal coordination between regions. In, serotonin involvement also suggests drug targets that can help reduce the likelihood of anxiety as fear develops into anxiety. Meditation, music, poetry, exercise and other stress-reducing activities can also help. In short, early intervention will bring lasting benefits. (China Biotechnology Network
): 1 . . . Evolution of brain-wide activity in the awake behaving mouse after acute fear by longitudinal manganese-enhanced MRI