Thalamic Htr3a Gene Expression in Hemi-Parkinsonian Rats Subjected to Persistent Pain

Background: Pain is a frequent and debilitating non-motor symptom of Parkinson's disease; however, its central neurochemical mechanisms remain incompletely understood. Serotonin modulates nociceptive processing, and the 5-HT3A receptor has been implicated in excitatory signaling and central sensitization. However, thalamic Htr3a transcript regulation during persistent pain associated with dopaminergic injury remains unclear. Objective: To evaluate thalamic Htr3a mRNA expression in 6-OHDA hemi-Parkinsonian rats subjected to formalin-induced persistent pain. Methods: Male Wistar rats were assigned to six groups (n = 6/group): Saline, Formalin, SHAM + Saline, SHAM + Formalin, 6-OHDA + Saline, and 6-OHDA + Formalin. 6-OHDA lesions were validated via apomorphine-induced rotations (>7 turns/min). Nociceptive behavior (flinches) was recorded over 60 min post-formalin injection. Bilateral thalamic Htr3a mRNA expression was quantified by RT-qPCR using Rpl27 as a validated reference gene. Results: 6-OHDA + Formalin rats exhibited a significant increase in persistent-phase nociceptive behavior compared to controls (p < 0.05). Htr3a mRNA expression showed a significant bilateral reduction in 6-OHDA-lesioned rats compared to controls (p < 0.05), with the decrease being significantly more severe in the ipsilateral thalamus (p < 0.001). Conclusions: Unilateral 6-OHDA lesion is associated with a region-dependent reduction in thalamic Htr3a mRNA expression during persistent pain. These results demonstrate transcriptional adaptations of the thalamic serotonergic system in experimental parkinsonian persistent pain.