Abstract
mdx mice are considered as a genetic homologous of human Duchenne muscular dystrophy. Recent evidence demonstrates that in mouse sympathetic ganglion dystrophin is involved in the stabilization of nicotinic acetylcholine receptor clusters. The purpose of this study was to verify possible effects of dystrophin alterations at the central level. This was assessed by evaluating the response to nicotine administration in mdx and wild-type mice. Thus the effects of post-training nicotine administrations (0.1, 0.25 and 0.5 mg/kg) were tested in mice subjected to a passive avoidance memory task, that measures the ability of mice to remember on test day a shock received 24 h before. Nicotine enhanced memory in wild-type as well as in mdx mice. However, the doses needed to increase memory in mdx were higher than in wild-type. These results are discussed in terms of possible functional changes in central nicotinic acetylcholine receptor in mdx mice.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Acetylcholine / metabolism*
-
Animals
-
Avoidance Learning / drug effects
-
Avoidance Learning / physiology
-
Brain / drug effects*
-
Brain / metabolism
-
Brain / physiopathology
-
Dose-Response Relationship, Drug
-
Dystrophin / deficiency*
-
Dystrophin / genetics
-
Female
-
Male
-
Memory Disorders / genetics
-
Memory Disorders / metabolism
-
Memory Disorders / physiopathology
-
Mice
-
Mice, Inbred mdx
-
Motor Activity / drug effects
-
Motor Activity / physiology
-
Muscular Dystrophies / genetics
-
Muscular Dystrophies / metabolism*
-
Muscular Dystrophies / physiopathology
-
Neurons / drug effects*
-
Neurons / metabolism
-
Nicotine / pharmacology*
-
Reaction Time / drug effects
-
Reaction Time / physiology
-
Receptors, Nicotinic / drug effects*
-
Receptors, Nicotinic / genetics
-
Receptors, Nicotinic / metabolism
-
Sex Characteristics
-
Synaptic Transmission / genetics
Substances
-
Dystrophin
-
Receptors, Nicotinic
-
Nicotine
-
Acetylcholine