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Abstract <p>Spinal cord injury (SCI) triggers a complex cascade of secondaryprocesses, including chronic neuroinflammation and neuroplasticremodeling both at the lesion site and in remote regions, such as thecerebral cortex. This study explores the role of trace amine-associatedreceptor 1 (TAAR1) in modulating neuroinflammatory responses inthe somatosensory cortex following lateral spinal cord hemisectionin wild-type and TAAR1-knockout (TAAR1-KO) mice. While sensorimotorrecovery was comparable between genotypes, suggesting a limitedimpact of TAAR1 on functional recovery, TAAR1 deficiency significantlyaltered glial reactivity. Specifically, TAAR1-KO mice exhibiteda marked increase in GFAP+ astrocyte density within the granularand pyramidal cortical layers, indicating enhanced astrogliosis.At the same time, the number of pro-inflammatory S100β+ astrocytesremained unchanged, which emphasizes the selective effect of TAAR1on distinct astrocyte subpopulations. Additionally, TAAR1-KO miceshowed a reduction in the density of Iba-1+ microglial cells. Furthermore,a decline in pyramidal neuron counts was noted, potentially indicativeof impaired survival. Crucially, these differences emerged onlypost-injury, as genotypes were indistinguishable under baselineconditions. The obtained data demonstrate the key role of TAAR1in modulating the glial response and expand our understanding ofthe molecular mechanisms of neuroinflammation in SCI, opening newavenues for the development of TAAR1-targeted neuroprotective strategies.</p>

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TAAR1 Modulates Neuronal and Glial Density in the Neocortex Following Spinal Cord Injury

  • 期刊论文

  • 发表日期：

    2025年10月1日

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  • D. S. Kalinina,
  • A. A. Chesnokov,
  • E. A. Romanyuk,
  • А. D. Buglinina,
  • D. V. Khuzin,
  • S. I. Milov,
  • S. P. Konovalova,
  • P. Yu. Shkorbatova,
  • N. V. Pavlova,
  • A. D. Belskaya,
  • R. R. Gainetdinov,
  • P. E. Musienko

摘要

Abstract

Spinal cord injury (SCI) triggers a complex cascade of secondaryprocesses, including chronic neuroinflammation and neuroplasticremodeling both at the lesion site and in remote regions, such as thecerebral cortex. This study explores the role of trace amine-associatedreceptor 1 (TAAR1) in modulating neuroinflammatory responses inthe somatosensory cortex following lateral spinal cord hemisectionin wild-type and TAAR1-knockout (TAAR1-KO) mice. While sensorimotorrecovery was comparable between genotypes, suggesting a limitedimpact of TAAR1 on functional recovery, TAAR1 deficiency significantlyaltered glial reactivity. Specifically, TAAR1-KO mice exhibiteda marked increase in GFAP+ astrocyte density within the granularand pyramidal cortical layers, indicating enhanced astrogliosis.At the same time, the number of pro-inflammatory S100β+ astrocytesremained unchanged, which emphasizes the selective effect of TAAR1on distinct astrocyte subpopulations. Additionally, TAAR1-KO miceshowed a reduction in the density of Iba-1+ microglial cells. Furthermore,a decline in pyramidal neuron counts was noted, potentially indicativeof impaired survival. Crucially, these differences emerged onlypost-injury, as genotypes were indistinguishable under baselineconditions. The obtained data demonstrate the key role of TAAR1in modulating the glial response and expand our understanding ofthe molecular mechanisms of neuroinflammation in SCI, opening newavenues for the development of TAAR1-targeted neuroprotective strategies.