Post-traumatic alterations in glutamine synthetase activity in peripheral and central nerves.
Glutamine synthetase (GS) was assessed distal to the site of axonal injury in traumatized rat central (optic) or peripheral (tibial) nerve prior to and during periods of reactive PNS and CNS glial cell hypertrophy. GS activity in crushed optic nerve remained equivalent to that in unoperated control tissue at 2 days postoperatively, but rose by 30% at 7 and 12 days after surgery. In contrast, GS activity in traumatized peripheral nerve was significantly lower than in unoperated controls at 7 and 12 days postoperatively. Administration of mitotic inhibitor (AraC, cytosine arabinofuranoside) prevented significant trauma-induced alterations in GS activity in optic nerves at 7, and in peripheral nerves at 7 and 12 days postoperatively. Results suggest significant alterations in glial/Schwann GS activity after nerve fiber injury and that these alterations can be delayed/prevented by administration of mitotic inhibitors.
Politis
M J
MJ
Miller
J E
JE
D000818:Animals; D003561:Cytarabine / Q000494:pharmacology; D005260:Female; D005974:Glutamate-Ammonia Ligase / Q000378:metabolism*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D009457:Neuroglia / Q000378:metabolism; D009900:Optic Nerve / Q000201:enzymology; D020221:Optic Nerve Injuries; D051381:Rats; D011919:Rats, Inbred Strains; D012583:Schwann Cells / Q000378:metabolism; D013127:Spinal Nerves / Q000201:enzymology / Q000293:injuries*
D003561:Cytarabine; D007770:L-Lactate Dehydrogenase; D005974:Glutamate-Ammonia Ligase