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. 2002 Nov 11;159(3):489–498. doi: 10.1083/jcb.200207058

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Copyright © 2002, The Rockefeller University Press

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Figure 5. — Impairment of the VRP of the spinal cord in the absence of cGKI. (a) In vitro–hemisected spinal cord preparation to measure monosynaptic and polysynaptic reflexes evoked by primary afferents. A scheme of a cross section of the spinal cord is shown and stimulating and recording electrodes are indicated. Dorsal is up. (b) VRPs of wild-type and cGKI-deficient neonatal mice. Electrical stimulation of dorsal root fibers generates a potential that can be recorded at the ventral root. The VRP is composed of a fast component evoked by A-fibers and a slower one activated by C-fibers (Heppenstall and Lewin, 2001). (c and d) Quantification of the VRP in wild-type and cGKI-deficient mice. The integrated area of the C-fiber area is significantly reduced in cGKI-deficient mice (P < 0.05; n = 6 per group). The integrated area of the A-fiber response was reduced but did not reach significance (P = 0.06). (e) Wind-up in wild-type and cGKI-deficient neonatal mice. Repetitive electrical stimulation of dorsal root fibers (20 times, 1 Hz) evokes an increase in the potential recorded from the ventral root. (f) Quantification of wind-up in wild-type and cGKI-deficient mice. Wind-up, measured as the percentage increase in the potential, is not different between wild-type and cGKI-deficient mice (P = 0.7; n = 6 per group).