Temporospatial expression and cellular localization of glutamine synthetase following traumatic spinal cord injury in adult rats.
نویسندگان
چکیده
Glutamine synthetase (GS) is an enzyme involved in an endogenous mechanism of protection against glutamate neurotoxicity and is important in the regulation of astrocyte migration. To date, limited information is available concerning the expression of GS in normal spinal cords and following injury. In the present study, GS expression was identified in astrocytes, oligodendrocytes and microglia in normal rat spinal cords. Following traumatic spinal cord injury (SCI), the glutamate concentration increased rapidly at 1 h and returned to baseline rapidly. However, the GS activity and protein levels were found to decrease at 4 h and then increase gradually from day 3 following SCI. The quantification of astrocytes, oligodendrocytes and activated microglia/macrophages, as well as immunohistochemistry staining of day 7 post‑injured spinal cords, indicated that the astrocytes and microglia/macrophages contributed to the increase in GS. Collectively, the results provided evidence for the temporospatial expression and location of GS following SCI and suggested that the changes in GS levels may contribute to glutamate neurotoxicity and glial cell response following SCI.
منابع مشابه
Cellular and Molecular Mechanisms Involved in Neuroinflammation after Acute Traumatic Spinal Cord Injury
Introduction: Spinal cord injury (SCI) following traumatic events is associated with the limited therapeutic options and sever complications, which can be partly due to inflammatory response. Therefore, this study aims to explore the role of inflammation in spinal cord injury. The findings showed that the pathological conditions of nervous system lead to activation of microglia, astrocyte, neut...
متن کاملMinocycline Enhance Restorative Ability of Olfactory Ensheathing Cells by Upregulation of BDNF and GDNF Expression After Spinal Cord Injury
Purpose: Spinal cord injury is a global public health issue that results in extensive neuronal degeneration, axonal and myelin loss and severe functional deficits. Neurotrophic factors are potential treatment for reducing secondary damage, promoting axon growth, and are responsible for inducing myelination after injury. Olfactory ensheathing cells (OECs) and minocycline have been shown to promo...
متن کاملThe Expression implication of GDNF in ventral horn and associated remote cortex in rhesus monkeys with hemisected spinal cord injury
Objective(s): Glial cell line-derived neurotrophic factor (GDNF) can effectively promote axonal regeneration,limit axonal retraction,and produce a statistically significant improvement in motor recovery after spinal cord injury (SCI). However, the role in primate animals with SCI is not fully cognized. Materials and Methods:18 healthy juvenile rhesuses were divided randomly into six groups, obs...
متن کاملNeuroprotective effects of atomoxetine against traumatic spinal cord injury in rats
Objective(s):Spinal cord injury (SCI) often causes serious and irreversible neurological deficit leading to disability or impairment of normal physical activity. Atomoxetine, a selective norepinephrine transporter (NET) inhibitor has gained much attention in the field of the neurodevelopmental disorder, but its effect on SCI has not been evaluated. The present study has been undertaken to inves...
متن کاملEffect of chondroitinase ABC on inflammatory and oxidative response following spinal cord injury
Objective(s): Chondroitinase ABC (cABC) treatment improves functional recovery following spinal cord injury (SCI) through degrading inhibitory molecules to axon growth. However, cABC involvement in other pathological processes contributing to SCI remains to be investigated. Here, we studied the effect of cABC I on oxidative stress and inflammation developed in a rat model of SCI.Materials and M...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- Molecular medicine reports
دوره 7 5 شماره
صفحات -
تاریخ انتشار 2013