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Excessive synaptic glutamate release, mitochondrial Ca\u00b2\u207a overload, and progressive neurodegeneration critically shape these outcomes, with preclinical and clinical data revealing neuronal loss and proteinopathy resembling motor neuron disorders. Here, we investigated whether pregabalin blockade of the presynaptic \u03b1\n                    <jats:sub>2<\/jats:sub>\n                    \u03b4\n                    <jats:sub>1-2<\/jats:sub>\n                    subunit of voltage-gated Ca\u00b2\u207a channels could mitigate excitotoxicity and promote sensorimotor recovery after TBI. Mice subjected to controlled cortical impact (CCI) received daily pregabalin (i.p., 60 mg.kg\n                    <jats:sup>-1<\/jats:sup>\n                    ) or saline for 10 days, and neurobehavioral performance was assessed at 24\u00a0h, 11-, and 12-days post-injury. In addition to robust and persistent deficits detected by the modified neurological severity score (mNSS), complementary tests including open field, grip strength, cylinder, wire-hanging, and inverted screen, captured sensitive impairments in corticospinal integrity and global motor function. Pregabalin treatment downregulated \u03b1\n                    <jats:sub>2<\/jats:sub>\n                    \u03b4\n                    <jats:sub>2<\/jats:sub>\n                    subunit expression, reduced cerebrospinal fluid glutamate levels, and restored mitochondrial Ca\u00b2\u207a handling by improving influx\u2013efflux dynamics through Na\u207a\/Ca\u00b2\u207a exchange. At the molecular level, pregabalin decreased hallmarks of neurodegeneration, including Cyclin dependent kinase 5, Tau\n                    <jats:sup>Ser396<\/jats:sup>\n                    hyperphosphorylation, caspase-12, and caspase-3 within synaptic terminals. These neuroprotective effects translated into significant improvements in both mNSS and multidimensional sensorimotor outcomes following TBI. Together, our findings confirm the neurodegenerative trajectory underlying TBI-induced neuromotor deficits and highlight the presynaptic \u03b1\n                    <jats:sub>2<\/jats:sub>\n                    \u03b4\n                    <jats:sub>1\u20132<\/jats:sub>\n                    subunit antagonism as a promising therapeutic target to mitigate long-term neurological sequelae.\n                  <\/jats:p>","DOI":"10.1007\/s11064-026-04729-3","type":"journal-article","created":{"date-parts":[[2026,3,25]],"date-time":"2026-03-25T09:35:50Z","timestamp":1774431350000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Blockade of Presynaptic \u03b12\u03b41\u22122 Subunits of Voltage-Gated Ca\u00b2\u207a Channels Attenuates Neurobiochemical and Sensorimotor Deficits After Traumatic Brain Injury in Mice"],"prefix":"10.1007","volume":"51","author":[{"given":"Jijo S.","family":"Justus","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marcelo S.","family":"Rodolphi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Afonso","family":"Kopczynski","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nathan R.","family":"Strogulski","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gabriela C. 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