Oxytocin preserves excitatory responsiveness of VTA dopaminergic neurons in PTSD model rats

05/10/2026

AI Summary

PTSD model rats exhibit markedly suppressed baseline spontaneous firing and burst rates of VTA dopaminergic neurons.
Intracerebroventricular oxytocin increases VTA dopaminergic excitability in both cohorts, an effect nearly abolished by OXTR antagonist L-371,257.
Although absolute firing remains lower in PTSD rats, the relative fold increase to oxytocin is comparable to controls, indicating preserved responsiveness.

TL;DR (AI Generated)

Oxytocin (OXT) exerts robust stress-buffering effects, yet its direct neuromodulatory influence on VTA dopaminergic neurons under PTSD pathological conditions remains poorly defined.

Baseline spontaneous firing and burst rates were markedly suppressed in PTSD model rats; however, OXT elevated neuronal excitability in both cohorts, an effect nearly abolished by pretreatment with the selective OXTR antagonist L-371,257.

These electrophysiological findings demonstrate that PTSD-like traumatic stress depresses baseline VTA dopaminergic activity, whereas the excitatory responsiveness of VTA dopaminergic neurons to exogenous OXT is largely preserved in PTSD model animals.

Basic summary

IBRO Neurosci Rep. 2026 Sep 20;21:868-873. doi: 10.1016/j.ibneur.2026.09.011. eCollection 2026 Dec.

ABSTRACT

Dysfunction of the ventral tegmental area (VTA) dopaminergic circuits is strongly implicated in the pathological progression of post-traumatic stress disorder (PTSD). Oxytocin (OXT) exerts robust stress-buffering effects, yet its direct neuromodulatory influence on VTA dopaminergic neurons under PTSD pathological conditions remains poorly defined. Here, we performed in vivo extracellular recordings to quantify spontaneous firing and burst activity in normal control and single prolonged stress (SPS)-induced PTSD model rats. Graded intracerebroventricular OXT infusions and OXTR antagonist pretreatment were used to characterize OXT-mediated neuronal modulation. Baseline spontaneous firing and burst rates were markedly suppressed in PTSD model rats; however, OXT elevated neuronal excitability in both cohorts, an effect nearly abolished by pretreatment with the selective OXTR antagonist L-371,257. Although absolute firing values remained persistently lower in PTSD model rats at baseline and following OXT administration, the relative fold increase in response to OXT was comparable to that observed in normal controls. These electrophysiological findings demonstrate that PTSD-like traumatic stress depresses baseline VTA dopaminergic activity, whereas the excitatory responsiveness of VTA dopaminergic neurons to exogenous OXT is largely preserved in PTSD model animals.

PMID:42830945 | PMC:PMC13634406 | DOI:10.1016/j.ibneur.2026.09.011

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