Decreased Uptake and Release of D‐Aspartate in the Guinea Pig Spinal Cord After Partial Cordotomy

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Abstract
Whether L-glutamate and/or L-aspartate are transmitters of neural tracts descending from the brain to the spinal cord was studied. The uptake and electrically evoked release of D-[3H] asparate, a putative marker for L-glutamate and L-aspartate, were measured in the cervical enlargement of the guinea pig spinal cord. These activities were compared using unlesioned animals and others with a lesion on the right side of the spinal cord. Partial cordotomy (segment C[cervical]5) produced a heavy loss of descending fibers, a small loss of primary sensory fibers and a depression of the uptake and the Ca2+-dependent, electrically evoked release of D-aspartate ipsilateral and caudal to the lesion. Contralaterally, there was a moderate loss of corticospinal fibers, some loss of other descending axons and a depression of D-aspartate release. Dorsal rhizotomy (segments C4-T[thoracic]1) produced a heavy loss of primary sensory fibers ipsilateral to the lesion. Ipsilaterally, but not contralaterally, the uptake and release of D-aspartate were depressed. Degeneration after partial cordotomy in combination with dorsal rhizotomy was assumed to be the sum of that produced by each lesion separately. This combined lesion depressed D-aspartate release on both sides of the cervical enlargement. None of the lesions altered the uptake and the evoked release of [3H]GABA. Evidently, the synaptic endings of 1 or more neural tracts descending from the brain to the spinal cord mediate the uptake and release of D-aspartate and, therefore, may use L-glutamate or L-aspartate as a transmitter.