Fear is a normal emotion in animals and humans alike, enabling us to stay safe and avoid harm. Human anxiety disorders, including conditions such as post-traumatic stress disorder and social anxiety disorder, are conceptualized as an 'over-reactivity' of normal fear responses, or inability to modulate fear once the response is no longer appropriate. In the last decade, studies have delineated fear circuitry in rodents, to build models of how normal fear responses are instantiated when threat is present, and how fear learning is 'neutralized' by new learning when threat is no longer present (a process known as extinction).
Up until now, these models had not yet been examined in brains similar to those in humans. In a new study, published in Cerebral Cortex, researchers at the University of Rochester Medical Center used very small, paired injections of neuronal tracers in the brains of nonhuman primates, and examined how the amygdala communicates with the primate analogues of the prelimbic (fear) and infralimbic (extinction) PFC. The study, co-led by Keshov Sharma, a third year MSTP graduate student, found that, as in rodent, projections from the basal nucleus of the amygdala exist in nonhuman primates. However, there is also a substantial input from a neighboring region known as accessory basal nucleus, a greatly expanded amygdala nucleus in nonhuman primates and humans.