Effects of spinal transection on presynaptic markers for glutamatergic neurons in the rat |
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Authors: | Harvey S. Singer Joseph T. Coyle James Frangia Donald L. Price |
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Affiliation: | (1) Departments of Neurology, Pediatrics, Neuroscience, Pharmacology and Experimental Therapeutics, and Psychiatry, Johns Hopkins Hospital, 21205 Baltimore, Maryland;(2) Behavioral Sciences, Johns Hopkins Hospital, 21205 Baltimore, Maryland |
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Abstract: | To evaluate the hypothesis that glutamic acid may be the neurotransmitter of descending, excitatory supraspinal pathways, the uptake and release ofl-[3H] glutamate and the levels of endogenous glutamate were measured in preparations from rat lumbar spinal cord following complete mid-thoracic transection. Following transection, the activity of the synaptosomal high-affinty glutamate uptake process was increased in both dorsal and ventral halves of lumbar cord between 1 and 14 days after transection and returned to control levels by 21 days posttransection. At 7 days, the increased activity of the uptake process forl-[3H] glutamate resulted in elevation ofVmax with no significant alteration inKt as compared to age-matched controls. Depolarization-induced release ofl-[3H]glutamate from prelabeled slices did not differ significantly from control in the lesioned rat except at 21 days after lesion when the amount of tritium release was significantly greater in the transected preparations than in control. Amino acid analysis of the lumbar cord from control and transected rats indicated only a 10% decrease in the level of endogenous glutamate and no alterations in the concentration of GABA and glycine 7 days after lesion. These findings do not support the hypothesis that glutamate serves as a major excitatory neurotransmitter in supraspinal pathways innervating the lumbar cord of the rat. |
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