TY - JOUR
T1 - Abnormalities of sympathetic sudomotor function in experimental acrylamide neuropathy
AU - Navarro, Xavier
AU - Verdú, Enrique
AU - Guerrero, Javier
AU - Butí, Miquel
AU - Goñalons, Eduard
PY - 1993/1/1
Y1 - 1993/1/1
N2 - The possible involvement of sympathetic sudomotor function by acrylamide intoxication was investigated in the mouse, and compared with nerve conduction studies and global motor tests. Acrylamide (40 mg/kg, 3 days per week, 8 weeks) was given per os to a group of mice (A1). Their motor ability to stand on the rotarod was impaired from day 11, reaching a minimum between 46 and 60 days. The number of pilocarpine reactive sweat glands (SG), evaluated by the silicone mold technique, was similar to controls at 40 days and slightly decreased at 54 days. Another group of mice (A2), given acrylamide at a higher dose (50 mg/kg, 5 days per week, 5 weeks), showed abnormalities on the rotarod by 11 days, a progressive decrease of muscle action potential (CMAP) amplitude, and significantly decreased number of reactive SG from 15 days, with respect to controls. Comparatively, sudomotor dysfunction was milder and appeared later in time than alphamotor involvement, being noticeable only after severe poisoning. The decrease in SG response is attributable to damage by acrylamide intoxication of postganglionic sudomotor nerve fibers, which are unmyelinated sympathetic efferents. © 1993.
AB - The possible involvement of sympathetic sudomotor function by acrylamide intoxication was investigated in the mouse, and compared with nerve conduction studies and global motor tests. Acrylamide (40 mg/kg, 3 days per week, 8 weeks) was given per os to a group of mice (A1). Their motor ability to stand on the rotarod was impaired from day 11, reaching a minimum between 46 and 60 days. The number of pilocarpine reactive sweat glands (SG), evaluated by the silicone mold technique, was similar to controls at 40 days and slightly decreased at 54 days. Another group of mice (A2), given acrylamide at a higher dose (50 mg/kg, 5 days per week, 5 weeks), showed abnormalities on the rotarod by 11 days, a progressive decrease of muscle action potential (CMAP) amplitude, and significantly decreased number of reactive SG from 15 days, with respect to controls. Comparatively, sudomotor dysfunction was milder and appeared later in time than alphamotor involvement, being noticeable only after severe poisoning. The decrease in SG response is attributable to damage by acrylamide intoxication of postganglionic sudomotor nerve fibers, which are unmyelinated sympathetic efferents. © 1993.
KW - Acrylamide
KW - Motor function
KW - Neuropathy
KW - Neurotoxicity
KW - Sweat gland
KW - Sympathetic nerve
U2 - 10.1016/0022-510X(93)90049-5
DO - 10.1016/0022-510X(93)90049-5
M3 - Article
VL - 114
SP - 56
EP - 61
JO - Journal of the Neurological Sciences
JF - Journal of the Neurological Sciences
SN - 0022-510X
IS - 1
ER -