Thalamic Htr3a Gene Expression in Hemiparkinsonian Rats Subjected to Persistent Pain
Thalamic Htr3a Gene Expression in Hemiparkinsonian Rats Subjected to Persistent Pain
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Original abstract
Background: Pain is one of the most common and disabling non-motor symptoms of Parkinson’s disease; however, the neurochemical mechanisms that modulate it remain incompletely understood. Serotonin plays an active role in central nociceptive processing, and the 5-HT3A receptor has been linked to excitatory pain transmission and central sensitization. However, its role in the thalamus during persistent pain associated with dopaminergic neurodegeneration remains unclear. Objective: This study aimed to evaluate the Htr3a gene expression in the thalamus of hemi-Parkinsonian rats subjected to a model of persistent formalin-induced pain. Methods: Male Wistar rats were divided into six experimental groups: saline solution, formalin, SHAM + saline solution, SHAM + formalin, 6-hydroxydopamine (6-OHDA) lesion + saline solution, and 6-OHDA + formalin. We assessed nociceptive behavior by counting withdrawals during the 60 minutes following formalin administration. We then performed bilateral thalamic dissection and quantified Htr3a gene expression by real-time PCR using Rpl27 as an endogenous reference gene. Results: Rats in the 6-OHDA + formalin group showed a significant increase in nociceptive behavior during the persistent phase of the formalin test compared with the control and SHAM groups (p < 0.05). Similarly, rats with 6-OHDA lesions showed a significant decrease of approximately 78% in relative Htr3a gene expression in the thalamus compared with the control group (p < 0.05). Conclusions: These findings suggest that dopaminergic neurodegeneration is associated with altered Htr3a gene expression in the thalamus and support the possible involvement of serotonergic mechanisms in processing persistent pain in Parkinson’s disease.