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The deafferentation syndrome in the rat: Effects of intraventricular apomorphine

Authors
Journal
Experimental Neurology
0014-4886
Publisher
Elsevier
Publication Date
Volume
100
Issue
1
Identifiers
DOI: 10.1016/0014-4886(88)90211-7

Abstract

Abstract A deafferentation syndrome, produced in rats by dorsal root ganglionectomies, is expressed as scratching of partially deafferented limb areas and/or biting of anesthetic limb areas. This self-mutilation may be objective evidence of dysesthesias, thus serving as an experimental model to study chronic dysesthesias and/or pain from deafferentation in man. This study included behavioral observations of the syndrome and the effects of intraventricular apomorphine, a dopamine agonist, on its expression. Thirty-eight female Sprague-Dawley rats underwent unilateral C5-T2 dorsal root ganglionectiomies followed immediately by stereotactically guided cannulation of the right lateral ventricle in 20 of the rats. For 2 weeks continuously via an osmotic minipump, 10 rats received apomorphine (5 μg/h) and 10 others received l-ascorbate (the vehicle). Rats with ganglionectomies only, as well as those receiving l-ascorbate, demonstrated early onset, more severe and later onset, less severe biting groups ( P < 0.05 Mann-Whitney U). Animals receiving apomorphine exhibited low autotomy scores irrespective of time of bite onset. Among the control groups, but not the experimental animals, the earlier the onset of biting, the more severe was the autotomy. The rats receiving vehicle via the minipump had earlier bite onsets than the rats in the ganglionectomy only group. This may indicate that the presence of the minipump is a stress which can accelerate the onset of biting. Intraventricular apomorphine can affect the deafferentation syndrome in the rat; it seems to decrease the level of autotomy and disrupt the relationship of bite onset with degree of biting.

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