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Acute and Chronic Tactile Sensory Testing after Spinal Cord Injury in Rats
Published on: April 4, 2012
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Complete spinal cord injury (SCI) transforms how brain derived neurotrophic factor (BDNF) affects nociceptive
Yung-Jen Huang1, Kuan H Lee2, James W Grau1
1Behavioral and Cellular Neuroscience, Department of Psychology, Texas A&M University, College Station, TX 77843, USA.
Experimental Neurology
|November 8, 2016
Summary
Fixed spaced stimulation prevents pain hypersensitivity after spinal cord injury by up-regulating brain-derived neurotrophic factor (BDNF), which alters GABAergic inhibition. This suggests BDNF
Area of Science:
- Neuroscience
- Spinal Cord Injury Research
- Pain Mechanisms
Background:
- Noxious stimulation causes central sensitization, increasing neural excitability and leading to maladaptive plasticity and pain.
- Brain-derived neurotrophic factor (BDNF) influences neural plasticity and central sensitization, particularly through alterations in GABA-dependent inhibition.
- Previous studies in spinalized rats showed fixed spaced stimulation counters maladaptive plasticity via BDNF up-regulation.
Purpose of the Study:
- To investigate the role of BDNF and GABAergic function in capsaicin-induced pain hypersensitivity after spinal cord injury (SCI).
- To determine if fixed spaced stimulation can prevent SCI-induced pain hypersensitivity and if this effect is mediated by BDNF.
- To explore how SCI alters the effect of BDNF on GABAergic inhibition.
Main Methods:
- Induction of enhanced mechanical reactivity (EMR) using capsaicin in rats with SCI.
- Administration of fixed spaced shock or BDNF sequestering antibody (TrkB-IgG) as pretreatment.
- Intrathecal (i.t.) administration of BDNF in both uninjured and SCI rats.
- Assessment of EMR, cellular markers (ERK, pERK), and GABAergic function (KCC2 expression, muscimol effects).
Main Results:
- Fixed spaced shock prevented capsaicin-induced EMR after SCI, an effect abolished by TrkB-IgG.
- Intrathecal BDNF prevented, but did not reverse, capsaicin-induced EMR and attenuated central sensitization markers in SCI rats.
- In uninjured rats, BDNF enhanced EMR and sensitization markers, reducing KCC2 and GABAergic inhibition.
- After SCI, BDNF increased KCC2 expression, potentially restoring GABAergic inhibition.
Conclusions:
- SCI transforms the effect of BDNF on GABAergic function, shifting from inhibitory to potentially restorative.
- Fixed spaced stimulation may offer a therapeutic strategy for SCI-induced pain by modulating BDNF and GABAergic pathways.
- The clinical efficacy of BDNF for SCI pain management may depend on the degree of residual spinal cord fiber sparing.
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