Central pain syndrome (CPS) is a debilitating
state and one of the consequences of spinal cord injury in
patients. Many pathophysiological aspects of CPS are not
well documented. Spinal glia activation has been identified
as a key factor in the sensory component of chronic pain. In
this study, the role of glial subtypes in the process of CPS
induced by unilateral electrolytic lesion of spinothalamic
tract (STT) is investigated. Male rats received a laminectomy
at T8–T9 and then unilateral electrolytic lesion centered
on the STT. Thermal and mechanical thresholds as
well as locomotor function were measured on days 0, 3, 7,
14, 21, and 28 post-injuries by tail flick, von Frey filament,
and open field tests, respectively. To investigate the spinal
glial activation following denervation in STT-lesioned
groups, Iba1 and GFAP were detected by immunohistochemistry
and Western blotting at the same time points.
Data showed that STT lesion significantly decreased thermal
pain at day 3 in comparison with sham groups. Significant
bilateral allodynia appeared in hind paws at day 14
after spinal cord injury and continued to day 28 (P<0.05).
Additionally, electrolytic spinal lesion attenuated locomotor
function of injured animals after 7 days (P<0.05). In both
histological assessments and Western blotting, Iba1 increased
at days 3 and 7 while increased GFAP occurred
from day 14 to 28 after lesion. It appears that microglial
activation is important in the early stages of pain development
and astrocytic activation occurs later. These events
may lead to behavioral outcomes especially central neuropathic
pain
