Glutamate antagonists applied to midbody spinal cord segments reduce the excitability of the fictive rostral scratch reflex in the turtle.

Glutamate antagonists applied to the cutaneous-processing region of the rostral scratch circuit in turtles reduced the excitability of the rostral scratch reflex. Segments D3-D6 (D3 = 3rd postcervical) of the midbody spinal cord receive cutaneous afferents from the rostral scratch receptive field and perform the initial integration of this cutaneous sensory input. These cutaneous-processing segments are located anterior to the rostral scratch motor pattern generator that resides mainly in segments D7-D10 located in and near the hindlimb enlargement. We prepared 1 or 2 of the midbody segments for bath application of glutamate antagonists in preparations with a complete transection of the spinal cord anterior to segment D3. Each preparation was immobilized by neuromuscular blockade and fictive scratch motor output was recorded from hindlimb muscle nerves. Application of the NMDA N-methyl-D-aspartate) antagonist APV (D-2-amino-5-phosphonovaleric acid, 50 microM) to a midbody segment significantly reduced the motor burst frequency of rostral scratch responses evoked by 3-Hz electrical stimulation of a site in that segment's dermatome. These data suggest that NMDA receptors contribute to cutaneous processing in the rostral scratch circuit. Application of APV to a midbody segment also reduced the magnitude of temporal summation in the scratch circuit in response to electrical stimuli delivered to the shell at 4- to 5-s intervals. Temporal summation was monitored at the level of hindlimb motor output as well as at the level of unit activity from 'long-afterdischarge' neurons in the midbody segments. Our observations are consistent with the hypothesis that NMDA receptors contribute to the prolonged activation of 'long-afterdischarge' neurons and the multisecond storage of excitation in the scratch reflex pathway.