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Normal distribution of alpha‐1‐adrenoceptors in the rat spinal cord and its modification after noradrenergic denervation: A quantitative autoradiographic study
Author(s) -
Roudet C.,
Savasta M.,
Feuerstein C.
Publication year - 1993
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.490340106
Subject(s) - spinal cord , denervation , prazosin , lesion , lumbar , receptor , distribution (mathematics) , central nervous system , anatomy , adrenergic receptor , cord , chemistry , medicine , neuroscience , antagonist , biology , pathology , surgery , mathematical analysis , mathematics
The distribution of alpha 1 (α1)‐adrenoceptors along the different segments of the spinal cord (cervical, thoracic, lumbar, and sacral) of normal rats has been studied by quantitative autoradiography using the specific α‐antagonist [ 3 H]Prazosin as a ligand. In addition, the influence of noradrenergic (NA) denervation [obtained either by complete transection of the spinal cord at vertebrae level T8‐T9 or by selective lesion of NA spinal cord system carried out by intracisternal injection of 6‐hydroxydopamine (6‐OHDA)] on eventual variations of α1‐adrenoceptor density at spinal cord target cells was studied in parallel. In control rats, the quantitative analysis of α1‐adrenoceptor densities revealed a widespread distribution of these receptors along all segments of the spinal cord with a similar pattern in the various subregions of gray matter studied. This distribution of α1‐adrenoceptors was quite well correlated with the distribution of NA terminals, when referring to previous descriptions by immunohistochemistry. After 6‐OHDA lesion, as well as caudally to the transection, a significant increase of α1‐adrenoceptor densities was observed in all spinal subregions thus evidencing supersensitivity. These results suggest that NA may act in the spinal cord, at least partly, via α‐adrenoceptors and that the expression of these receptors could be influenced by NA dysfunction, as demonstrated here through the effects observed in lesioned animals. © 1993 Wiley‐Liss, Inc.