After the administration of intrathecal
strychnine,
allodynia is manifested as activation of supraspinal sites involved in
pain processing and enhancement of cardiovascular responses evoked by normally innocuous stimuli. The objective of this study was to investigate the effect of
strychnine-induced
allodynia on
adrenergic neuronal activity in the C1 area of the rostral ventrolateral medulla (RVLM), a major site involved in cardiovascular regulation. The effect of intrathecal
strychnine (40 microg) or saline followed by repeated hair deflection to caudal lumbar dermatomes in the
urethane-anesthetized rat was assessed by measuring voltammetric changes in the RVLM
catechol oxidation current (CA x OC), mean arterial pressure (MAP), and heart rate (HR). After the administration of intrathecal
strychnine, hair deflection evoked a significant and sustained increase in the RVLM CA x OC and MAP (peak 146.4%+/-5.6% and 159%+/-18.4% of baseline, respectively; P < 0.05). There was a nonsignificant increase in HR (peak 128%+/-8.2%). In the absence of hair deflection, there was no demonstrable change. Intrathecal saline-treated rats failed to demonstrate changes in RVLM CA x OC, MAP, or HR. In the present study, we demonstrated that, after the administration of intrathecal
strychnine, innocuous hair deflection evokes temporally related neuronal activation in the rat RVLM and an increase in MAP. This suggests that the RVLM mediates, at least in part, the cardiovascular responses during
strychnine allodynia.
IMPLICATIONS: Neural injury-associated
pain, as manifested by
allodynia, is resistant to conventional treatment. In a rat model of
allodynia, we demonstrated activation of the brain region involved in sympathetic control.
Innovative therapies that target this region may be successful in managing this debilitating condition.