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Related Concept Videos

Spinal Cord Injury ll: Pathophysiology01:14

Spinal Cord Injury ll: Pathophysiology

25
Spinal cord injury progresses through two interconnected phases: primary injury and secondary injury.Primary InjuryPrimary injury happens at the moment of trauma and involves immediate mechanical damage to the spinal cord.Compression happens when broken vertebrae, herniated discs, or accumulating blood (such as a hematoma) press directly against the spinal cord, distorting its normal shape and function. In cases of contusion, the cord is bruised by a blunt force (like penetrating injuries or...
25
Secondary Spinal Cord Injury llI: Pathophysiology01:25

Secondary Spinal Cord Injury llI: Pathophysiology

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Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...
52

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TAAR5 Modulates Sensorimotor Recovery After Spinal Cord Injury.

Anastasiia D Buglinina1, Ekaterina A Romanyuk1, Alexander A Chesnokov1

  • 1Neurobiology Department, Sirius University of Science and Technology, Sochi 354340, Russia.

Biomedicines
|May 4, 2026
PubMed
Summary
This summary is machine-generated.

Trace amine-associated receptor 5 (TAAR5) knockout accelerated sensorimotor recovery after spinal cord injury (SCI) in mice. TAAR5 deficiency shows potential for novel therapeutic strategies targeting SCI functional outcomes.

Keywords:
TAAR5dopaminesensorimotor functionsspinal cord injurytrace amines

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Area of Science:

  • Neuroscience
  • Regenerative Medicine
  • Pharmacology

Background:

  • Spinal cord injury (SCI) causes significant motor and sensory deficits.
  • The role of trace amine-associated receptor 5 (TAAR5) in central nervous system (CNS) repair is largely unknown.
  • TAAR5 may influence CNS functions, making it a potential therapeutic target.

Purpose of the Study:

  • To investigate the impact of TAAR5 gene knockout on functional recovery following spinal cord hemisection.
  • To assess sensorimotor and behavioral changes in TAAR5-knockout (KO) versus wild-type (WT) mice post-SCI.
  • To explore TAAR5's role in CNS repair mechanisms.

Main Methods:

  • Utilized a lateral spinal cord hemisection model in TAAR5-KO and WT male mice.
  • Assessed sensorimotor recovery using horizontal ladder, grasp, and hindlimb mobility tests.
  • Evaluated anxiety-like behaviors via open field and elevated plus maze tests pre- and post-SCI.

Main Results:

  • TAAR5-KO mice demonstrated enhanced sensorimotor function recovery, particularly in joint mobility and grasping.
  • No significant differences were observed in the Horizontal Regular Ladder test between groups.
  • Spinal cord injury induced increased anxiety-like behavior in both TAAR5-KO and WT mice.

Conclusions:

  • TAAR5 deficiency positively modulates specific sensorimotor functions post-SCI.
  • Potential mechanisms involve modulation of dopaminergic neurotransmission and inflammatory pathways.
  • TAAR5 knockout presents a promising therapeutic target for improving functional outcomes after spinal cord injury.