Stress-related psychiatric disorders, including anxiety, are complex diseases that have genetic, and
environmental causes. Stressful experiences increase the release of prefrontal amygdala neurotransmitters,
a response that is relevant to cognitive, emotional, and behavioral coping. Moreover, exposure to
stress elicits anxiety-like behavior and dendritic remodeling in the amygdala. Members of the miR-34
family have been suggested to regulate synaptic plasticity and neurotransmission processes, which
mediate stress-related disorders. Using mice that harbored targeted deletions of all 3 members of the
miR-34-family (miR-34-TKO), we evaluated acute stress-induced basolateral amygdala (BLA)-GABAergic
and medial prefrontal cortex (mpFC) aminergic outflow by intracerebral in vivo microdialysis. Moreover,
we also examined fear conditioning/extinction, stress-induced anxiety, and dendritic remodeling in the
BLA of stress-exposed TKO mice.
We found that TKO mice showed resilience to stress-induced anxiety and facilitation in fear extinction.
Accordingly, no significant increase was evident in aminergic prefrontal or amygdala GABA release, and
no significant acute stress-induced amygdalar dendritic remodeling was observed in TKO mice. Differential
GRM7, 5-HT2C, and CRFR1 mRNA expressionwas noted in the mpFC and BLA between TKO andWT
mice. Our data demonstrate that the miR-34 has a critical function in regulating the behavioral and
neurochemical response to acute stress and in inducing stress-related amygdala neuroplasticity