TY - JOUR
T1 - Adrenoreceptor subtype mediating sympathetic-sensory coupling in injured sensory neurons
AU - Chen, Yong
AU - Michaelis, Martin
AU - Janig, Wilfrid
AU - Devor, Marshall
PY - 1996/12
Y1 - 1996/12
N2 - 1. Teased axon recordings were made from 167 spontaneously active Aβ- and Aδ-afferents that ended in sciatic nerve end neuromas of 6-12 days standing. When challenged with a standard bolus of systemically applied adrenaline, 100 (60%) responded, either with an increase in baseline firing frequency (excitation, 96/100) or with a decrease (suppression, 4/100). 2. Experiments using receptor type-selective antagonists indicated that the adreno-sensitivity was mediated by α2 adrenoreceptors in 65% of the afferents sampled, by α1 adrenoreceptors in 13%, and about equally by α1 and α2 adrenoreceptors in ~10%. In the remaining 13%, neither type of antagonist blocked adrenaline-evoked excitation, at least not at the doses used. Both excitatory and suppressive responses were primarily sensitive to α2 antagonists. 3. Experiments using receptor type-selective agonists substantiated the conclusion that sympathetic-sensory coupling at sites of nerve injury is mediated primarily by α2 adrenoreceptors. 4. Recordings were also made from 14 afferent neurons with spontaneous ectopic discharge originating in dorsal root ganglia (DRGs) L4 and L5. The rats had undergone transection of the ipsilateral sciatic nerve 8-93 days previously. All neurons responded to systemic adrenaline and/or trains of activity evoked in postganglionic sympathetic efferents with either excitation or suppression. As in the neuroma endings, responses in the large majority of cases were blocked by α2-selective, but not by α1-selective adrenoreceptor antagonists. 5. The results indicate that sympathetic sensory coupling, both at nerve injury sites and in axotomized DRG neurons, is mediated primarily by α2 adrenoreceptors. In a minority of afferent neurons, however, it appears to be mediated by α1 adreno-receptors or by both α1 and α2 adrenoreceptors. These functional results are consistent with receptor-type expression profiles from studies based on in situ hybridization and immunocytochemistry.
AB - 1. Teased axon recordings were made from 167 spontaneously active Aβ- and Aδ-afferents that ended in sciatic nerve end neuromas of 6-12 days standing. When challenged with a standard bolus of systemically applied adrenaline, 100 (60%) responded, either with an increase in baseline firing frequency (excitation, 96/100) or with a decrease (suppression, 4/100). 2. Experiments using receptor type-selective antagonists indicated that the adreno-sensitivity was mediated by α2 adrenoreceptors in 65% of the afferents sampled, by α1 adrenoreceptors in 13%, and about equally by α1 and α2 adrenoreceptors in ~10%. In the remaining 13%, neither type of antagonist blocked adrenaline-evoked excitation, at least not at the doses used. Both excitatory and suppressive responses were primarily sensitive to α2 antagonists. 3. Experiments using receptor type-selective agonists substantiated the conclusion that sympathetic-sensory coupling at sites of nerve injury is mediated primarily by α2 adrenoreceptors. 4. Recordings were also made from 14 afferent neurons with spontaneous ectopic discharge originating in dorsal root ganglia (DRGs) L4 and L5. The rats had undergone transection of the ipsilateral sciatic nerve 8-93 days previously. All neurons responded to systemic adrenaline and/or trains of activity evoked in postganglionic sympathetic efferents with either excitation or suppression. As in the neuroma endings, responses in the large majority of cases were blocked by α2-selective, but not by α1-selective adrenoreceptor antagonists. 5. The results indicate that sympathetic sensory coupling, both at nerve injury sites and in axotomized DRG neurons, is mediated primarily by α2 adrenoreceptors. In a minority of afferent neurons, however, it appears to be mediated by α1 adreno-receptors or by both α1 and α2 adrenoreceptors. These functional results are consistent with receptor-type expression profiles from studies based on in situ hybridization and immunocytochemistry.
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U2 - 10.1152/jn.1996.76.6.3721
DO - 10.1152/jn.1996.76.6.3721
M3 - Article
C2 - 8985870
AN - SCOPUS:0030451129
SN - 0022-3077
VL - 76
SP - 3721
EP - 3730
JO - Journal of neurophysiology
JF - Journal of neurophysiology
IS - 6
ER -