Acute and chronic nicotine exposure differentially facilitate the induction of LTP.
We report here that acute and chronic nicotine exposure facilitated the induction of long-term potentiation (LTP), a leading candidate for a cellular mechanism underlying learning and memory, in the hippocampus. Furthermore, acute application of nicotine in chronic nicotine-treated hippocampus further facilitated the induction of LTP, suggesting that acute and chronic nicotine effects on LTP induction are mediated by different mechanisms. These findings not only provide evidence for chronic nicotine-induced synaptic changes in the hippocampus, but also an explanation of the cellular basis of nicotine-induced cognitive enhancement.
Fujii
S
S
Department of Neurobiology and Behavior, University of California, Irvine, CA 92697-4550, USA.
Ji
Z
Z
Morita
N
N
Sumikawa
K
K
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D003071:Cognition / Q000187:drug effects; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects; D006624:Hippocampus / Q000737:chemistry* / Q000187:drug effects / Q000502:physiology; D017774:Long-Term Potentiation / Q000187:drug effects*; D008464:Mecamylamine / Q000494:pharmacology; D009538:Nicotine / Q000494:pharmacology*; D018722:Nicotinic Agonists / Q000494:pharmacology*; D018733:Nicotinic Antagonists / Q000494:pharmacology; D009924:Organ Culture Techniques; D051381:Rats; D011978:Receptors, Nicotinic / Q000502:physiology*
D018722:Nicotinic Agonists; D018733:Nicotinic Antagonists; D011978:Receptors, Nicotinic; D008464:Mecamylamine; D009538:Nicotine