Spinal cord ischemic injury usually results in
paraplegia, which is a major cause of morbidity after thoracic aorta operations. Ample evidence indicates that massive release of
excitatory amino acids (EAAs;
glutamate) plays an important role in the development of neuronal ischemic
injuries. However, there is a lack of direct evidence to indicate the involvement of EAAs in the
glutamate metabolizing system (including the
glutamate transporter isoforms, i.e. the
Glu-Asp transporter (GLAST), Glu transporter-1 (GLT-1), and
excitatory amino acid carrier one (EAAC1);
glutamine synthetase (GS); and
glutamate dehydrogenase (GDH)) in
spinal cord ischemia. In the present results, we found that
methylprednisolone (MP; intrathecal (i.t.) injection, 200 mug twice daily administered for 3 days before
ischemia), a synthetic
glucocorticoid, is the therapeutic agent for the treatment of
spinal injuries in humans, can significantly reduce the
ischemia-induced motor function defect and down-regulate the
glutamate metabolizing system (including GLAST, GLT-1, GS, and GDH) in male Wistar rats. The
spinal cord ischemia-induced down-regulation of EAAC1
protein expression in the ventral portion of the lumbar spinal cord was partly inhibited by pretreatment with i.t. MP. However, MP did not affect the down-regulation of EAAC1 in the dorsal portion of the lumbar spinal cord after
spinal cord ischemia. The i.t. injection of MP alone did not change the neurological functions and the expression of
proteins of the
glutamate metabolizing system in the spinal cord. Our results indicate that
spinal cord ischemia-induced neurological deficits accompany the decrease in the expression of
proteins of the
glutamate metabolizing system in the lumbar portion of the spinal cord. The i.t. MP pretreatment significantly prevented these symptoms. These results support the observation that MP delivery through an i.t. injection, is beneficial for the treatment of spinal cord ischemic
injuries.