Tuesday, June 28, 2011

Nicotinergic impact on focal and non-focal neuroplasticity induced by non-invasive brain stimulation in non-smoking humans

I think this says nicotine in patch form helps with neuroplasticity. 32 pages in all.
http://repository.peerproject.eu:8080/jspui/bitstream/123456789/15484/1/PEER_stage2_10.1038%252Fnpp.2010.227.pdf
Abstract
Nicotine improves cognitive performance and modulates neuroplasticity in brain networks. The
neurophysiological mechanisms underlying nicotine-induced behavioral changes have been
sparsely studied, especially in humans. Global cholinergic activation focuses plasticity in
humans. However, the specific contribution of nicotinic receptors to these effects is unclear.
Henceforth, we explored the impact of nicotine on non-focal neuroplasticity induced by
transcranial direct current stimulation (tDCS) and focal, synapse-specific plasticity induced by
paired associative stimulation (PAS) in healthy non-smoking individuals. Forty eight subjects
participated in the study. Each subject received placebo and nicotine patches combined with one
of the stimulation protocols to the primary motor cortex in different sessions. Transcranial
magnetic stimulation (TMS) - elicited motor evoked potential (MEP) amplitudes were recorded
as a measure of corticospinal excitability until the evening of the second day following the
stimulation. Nicotine abolished or reduced both PAS- and tDCS-induced inhibitory
neuroplasticity. Non-focal facilitatory plasticity was also abolished, whereas focal facilitatory
plasticity was slightly prolonged by nicotine. Thus, nicotinergic influence on facilitatory, but not
inhibitory plasticity mimics that of global cholinergic enhancement. Therefore, activating
nicotinic receptors has clearly discernable effects from global cholinergic activation. These
nicotine-generated plasticity alterations might be important for the effects of the drug on
cognitive function.

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