Background: Spinal cord injury (SCI) is a severe pathological condition resulting in persistent motor and sensory impairments. The trace amine-associated receptor 5 (TAAR5) is a potential modulator of central nervous system functions; however, its role in CNS repair remains poorly understood. Methods: We comprehensively evaluated the effect of TAAR5 gene knockout on functional recovery following lateral spinal cord hemisection in TAAR5-KO and wild-type (WT) male mice. Sensorimotor recovery after SCI was assessed using the horizontal ladder, grasp, and hindlimb mobility tests. Exploratory and anxiety-like behaviors were evaluated using the open field and elevated plus maze tests before and 5 weeks after SCI. Results: TAAR5-KO mice exhibited accelerated recovery of sensorimotor functions, as assessed by joint mobility and grasping tests, compared to WT animals. In contrast, no significant intergroup differences were found in the Horizontal Regular Ladder test, likely due to the task complexity and an insufficient recovery period. Nevertheless, SCI induced elevated anxiety-like behavior regardless of genotype. Conclusions: These findings indicate that TAAR5 deficiency exerts a positive modulatory effect on the restoration of specific components of sensorimotor function after SCI. This effect may be mediated through the modulation of dopaminergic neurotransmission and inflammatory processes. The observed beneficial effect of TAAR5 knockout identifies this receptor as a promising target for developing novel therapeutic strategies aimed at improving functional outcomes following spinal cord injury.
Buglinina et al. (Tue,) studied this question.