Role of microglia and astrocyte in central pain syndrome following electrolytic lesion at the spinothalamic tract in rats.
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.
Department of Pharmacology, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Chamran Exp. way, Evin, Tehran, Iran. naseri5674@yahoo.com
Kobra
K
Naseri
Elham
E
Saghaei
Fatemeh
F
Abbaszadeh
Mina
M
Afhami
Ali
A
Haeri
Farzaneh
F
Rahimi
Masoumeh
M
Jorjani
D000818:Animals; D001253:Astrocytes / Q000502:physiology*; D002058:Burns, Electric; D002135:Calcium-Binding Proteins / Q000096:biosynthesis / Q000235:genetics; D005106:Exploratory Behavior; D005904:Glial Fibrillary Acidic Protein / Q000096:biosynthesis / Q000235:genetics; D005911:Gliosis / Q000209:etiology / Q000503:physiopathology; D006358:Hot Temperature / Q000009:adverse effects; D006930:Hyperalgesia / Q000209:etiology / Q000503:physiopathology*; D008297:Male; D008840:Microfilament Proteins / Q000096:biosynthesis / Q000235:genetics; D017628:Microglia / Q000502:physiology*; D009419:Nerve Tissue Proteins / Q000096:biosynthesis / Q000235:genetics; D009437:Neuralgia / Q000209:etiology / Q000503:physiopathology*; D059226:Nociceptive Pain / Q000209:etiology / Q000503:physiopathology; D058748:Pain Perception / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D045442:Rotarod Performance Test; D013119:Spinal Cord Injuries / Q000209:etiology / Q000503:physiopathology*; D013133:Spinothalamic Tracts / Q000293:injuries* / Q000473:pathology; D013314:Stress, Mechanical
C100745:Aif1 protein, rat; D002135:Calcium-Binding Proteins; D005904:Glial Fibrillary Acidic Protein; D008840:Microfilament Proteins; D009419:Nerve Tissue Proteins