Nicotine does not improve recovery from learned nonuse nor enhance constraint-induced therapy after motor cortex stroke in the rat.

Nicotine, a cholinergic agonist, rapidly crosses the blood-brain barrier, promotes neuronal plasticity and has been suggested to enhance behavior in a variety of neurological conditions. Nicotine has also been suggested to benefit functional recovery in rodent models of stroke. At present there has been no systematic investigation of the potential benefits of nicotine therapy in both the acute and chronic post-stroke period. This was the objective of the present study and to that end, the effects of nicotine administration prior to and following motor cortex stroke were examined in a skilled reaching task. The task provides a thorough assessment of learned nonuse and constraint-induced recovery of behavior as determined by both end-point and movement element analysis. Nicotine (0.3 mg/kg p.o.) was administered twice daily during reach training and following motor cortex stroke. Rats were divided into four groups based on their pre-/post-stroke treatment: nicotine/nicotine, nicotine/vehicle, vehicle/nicotine, vehicle/vehicle. After stroke, nicotine did not counteract learned nonuse, facilitate constraint-induced therapy, or improve long-term recovery as measured by end-point analysis and movement element analysis. The results are discussed in relation to the problem of identifying pharmacotherapeutic agents that augment rehabilitation following stroke.