Abstract
Post-traumatic stress disorder (PTSD) is a debilitating psychiatric condition that arises after extremely traumatic events, with clinically significant and lasting impacts on both physical and psychological health. The present study examined the role of ventral tegmental area (VTA) dopaminergic signaling in anxiety-like behaviors and the underlying mechanisms in PTSD model rats. Chemogenetic technology was employed to specifically activate VTA dopamine (DA) neurons in rats subjected to single prolonged stress (SPS), and open field and elevated plus maze tests were applied to evaluate the anxiety-like manifestations. Subsequently, in vivo extracellular electrophysiological analyses were used to examine alterations in the firing characteristics of VTA DA neurons. Chemogenetic activation enhanced the firing and burst rates of VTA DA neurons in SPS-induced PTSD model rats and concomitantly mitigated the anxiety-like behavioral phenotypes. Collectively, these findings reveal a direct association between PTSD-relevant anxiety behaviors and VTA dopaminergic activity, and further suggest that interventions designed to enhance VTA dopaminergic activity may be a potential strategy for PTSD treatment.
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