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

In vivo electrophysiological study in rats

“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.”

Male Sprague-Dawley rats

“Healthy male Sprague-Dawley rats (2 months old, 230–260 g; total n = 62) were purchased from the Guangdong Medical Laboratory Animal Center (Foshan, China).”

62 rats total (30 normal controls, 29 SPS-induced PTSD models, 3 for immunofluorescence)

“Healthy male Sprague-Dawley rats (2 months old, 230–260 g; total n = 62) were purchased from the Guangdong Medical Laboratory Animal Center (Foshan, China).”

Acute recording sessions with 7-day post-stress recovery period

“After a 15-min recovery interval, rats were exposed to ether vapor until loss of consciousness, then returned to home cages and left undisturbed for 7 days to develop PTSD-like phenotypes.”

Baseline spontaneous firing and burst rates were significantly lower in PTSD model rats compared to normal controls.

“VTA dopaminergic neurons in PTSD model rats exhibited significantly lower baseline firing and burst rates than those in normal control animals (both p < 0.01, Table 1).”

The relative fold increase in neuronal response to oxytocin was comparable between normal and PTSD model rats, indicating preserved responsiveness.

“Two-way ANOVA revealed no significant main effect of animal group on either firing fold change (F1,196 = 2.127, p = 0.146) or burst fold change (F1,196 = 1.396, p = 0.239).”

Lack of behavioral validation, potential indirect effects due to intracerebroventricular delivery, and use of only male subjects.

“First, despite the well-validated SPS paradigm for generating PTSD-like phenotypes (Huang et al., 2024, Zhou et al., 2025), independent behavioral and endocrine validation (e.g., fear-conditioning paradigms, plasma corticosterone measurements) is absent in this study.”