Background
Neuropathic pain has been shown to increase excitability of neurons. This indicates
altered inhibitory mechanism of the nervous system.
Objective
This work was aimed to assess GABAA receptors plasticity in the brain and spinal
cord.
Materials and methods
Fifteen adult female rats were used. Ten animals have their sciatic nerve ligated
with no treatment (LIG), and with diazepam treatment for 14 days (LIG+GABA) and
the other five were used as the sham group. Pain was assessed using a hot plate
and formalin test, while the spatial memory was assessed using Y-maze. At the end
of the treatment, the animals were euthanized and fixed using the transcardial
perfusion fixation method. The spinal cord, cingulate cortex, and the hippocampus
were serially sectioned and stained for GABAA receptor immunohistochemically.
Quantification was done using ImageJ software. Data were analyzed using oneway
analysis of variance and Newman Tukey post-hoc test significant level was set
at P less than 0.05.
Results
A low level of pain was observed in LIG and LIG+GABA animals on both formalin
and hot plate test compared with the control. Memory impairment was found only in
the LIG+GABA group. Stereology counting showed that GABAA receptors reduced
in the dentate gyrus of the hippocampus of LIG-treated animals which was reversed
in LIG+GABA, but in the cingulate cortex, GABAA receptors were increased in LIG
animals and LIG+GABA more than the control while the spinal cord shows no
significant difference.
Conclusion
GABAA agonist treatment did not alleviate the symptoms of neuropathic pain due to
GABA signaling changing to excitatory in nature