The blockade of spinal
glycine receptors with intrathecal
strychnine produces a reversible
allodynia-like state in the rat. Thus, hair deflection, in the presence of intrathecal
strychnine, induces cardiovascular and motor withdrawal responses comparable with those evoked by noxious thermal, mechanical, or chemical stimulation in the absence of
strychnine. In the present study, we mapped the cutaneous sites of abnormal sensitivity to hair deflection throughout the
strychnine time course to investigate the segmental distribution of
strychnine-induced
allodynia. The ability of intrathecal
glycine and the
glycine derivative
betaine to reverse
strychnine-induced
allodynia was also determined using dose-response analysis. Following intrathecal
strychnine (40 micrograms), stroking the legs, flanks, lower back, and tail with a cotton-tipped applicator evoked a pronounced increase in mean arterial pressure,
tachycardia, and an abrupt motor withdrawal response in
urethane-anesthetized rats. These abnormal responses were only evoked by hair deflection at discrete sites, corresponding to the cutaneous dermatomes innervated by spinal segments near the site of
strychnine injection. In rats with intrathecal
catheters lying laterally in the subarachnoid space, allodynic sites were observed unilaterally on the ipsilateral side of intrathecal
strychnine injection. Recovery from
strychnine was complete by 30 min in all affected dermatomes. The cardiovascular and motor withdrawal responses to hair deflection were dose dependently inhibited by intrathecal
glycine and intrathecal
betaine. The ED50 (95% confidence interval) for intrathecal
glycine was 609 (429-865) micrograms for the heart rate response, 694 (548-878) micrograms for the pressor response, and 549 (458-658) micrograms for the motor withdrawal response. The corresponding values for intrathecal
betaine were 981 (509-1889), 1045 (740-1476), and 1083 (843-1391) micrograms, respectively. There was no difference in the effect of
betaine on sensory-evoked cardiovascular and motor responses. Cortical electroencephalographic activity was not affected by intrathecal
glycine or
betaine, consistent with a spinal locus of action in reversing
strychnine-induced
allodynia. These results support the hypothesis that removal of spinal glycinergic modulation from low threshold afferent input with intrathecal
strychnine results in segmentally localized, tactile-evoked
allodynia.