Deficiency of an enzyme due to genetic mutation can be the reason behind emotional inflexibility, reveals a new research.
Scientists at the University of Southern California showed that enzyme-deficient mice were unable to properly assess threat. The mice exhibited defensive behaviors (such as biting or tail rattling) in the presence of neutral stimuli, such as plastic bottles.
Conversely, in the presence of true danger cues such as predator urine or an anesthetized rat, the mice with the enzyme mutation were less cautious and defensive than their littermates, even climbing on the unconscious rat.
Mice without the enzyme also took longer to leave an open chamber, indicating reduction in exploratory and escape tendencies, the researchers said.
"Taken together, our findings suggest that monoamine oxidase A deficiency leads to a general inability to appropriately assess contextual risk, as indicated by the inappropriateness of their defensive behaviors," said senior author Jean C. Shih, University Professor and Boyd and Elsie Welin Professor of pharmacology and pharmaceutical sciences in the USC School of Pharmacy.
Monoamine oxidase A is the main enzyme in the brain that breaks down serotonin, norepinephrine and dopamine, which have been shown to contribute to the "fight or flight" impulse by raising heart rates and increasing blood and oxygen flow.
"Mice without monoamine oxidase A exhibited a distinct inability to attune their response to the situation," said Sean Godar, a post-doctoral research associate at the USC School of Pharmacy and co-lead author of the study.
"The paradoxical responses to neutral and fear-inducing stimuli are markedly reminiscent of deficits in facial affect processing in schizophrenia and autism," he added.
The study will be published in the International Journal of Neuropharmacology.