h-89 and Radiculopathy

With a model of chronically compressed dorsal root ganglion (CCD), the present study was undertaken to test how the plasticity of sympathetic-sensory coupling is and whether the coupling is mediated by intracellular messenger PKA by analysing extracellularly recorded spontaneous activity of single A-fibers originating from the CCD neurons in vitro. Eighty-five out of 95 neurons from injured DRGs during application of norepinephrine (NE) were adrenosensitive. Among the 85 neurons, 44 exhibited excitation, 21 showing excitation followed by suppression, 6 displaying alternated excitation and suppression, and 14 suppression. In addition, adrenosensitivity was observed in 15 silent injured DRGs. The excitatory effect of NE was blocked by alpha 1 and alpha 2 adrenoceptor antagonists yohimbine (10 mumol/L) or prazosin (5 mumol/L). Rp-cAMPS (50-250 mumol/L, n = 6), a specific inhibitor of PKA, and H-89 (10 mumol/L, n = 6), an inhibitor of PKA catalytic subunit, obviously suppressed the NE-evoked excitation. Furthermore, the excitatory effect of NE was attenuated by SQ 22, 536 (1 mmol/L), an adenylate cyclase inhibitor (n = 6). The above results demonstrate that injury to DRG neuron body triggered the adrenosensitivity, which was mediated by alpha 1, alpha 2 adrenoceptors and PKA.

Topics: Adrenergic Fibers; Afferent Pathways; Animals; Cyclic AMP; Cyclic AMP-Dependent Protein Kinases; Electrophysiology; Female; Ganglia, Spinal; In Vitro Techniques; Isoquinolines; Male; Neurons; Radiculopathy; Rats; Rats, Sprague-Dawley; Sulfonamides; Thionucleotides