Hippocampal synaptic transmission enhanced by low concentrations of nicotine

Nicotine obtained from tobacco can improve learning and memory on various tasks and has been linked to arousal, attention, rapid information processing, working memory, and long-term memories that can cause craving years after someone has stopped smoking. One likely target for these effects is the h...

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Published in:	Nature (London) Vol. 383; no. 6602; pp. 713 - 716
Main Authors:	Gray, Richard, Rajan, Arun S, Radcliffe, Kristofer A, Yakehiro, Masuhide, Dani, John A
Format:	Journal Article
Language:	English
Published:	London Nature Publishing 24-10-1996 Nature Publishing Group
Subjects:	Action Potentials - drug effects Alzheimer's disease Animals Biological and medical sciences Calcium - metabolism Central nervous system Central neurotransmission. Neuromudulation. Pathways and receptors Cognition & reasoning Culture Techniques Dementia disorders Fundamental and applied biological sciences. Psychology Glutamic Acid - metabolism Hippocampus - drug effects Hippocampus - metabolism Medical research Nicotine Nicotine - pharmacology Rats Rats, Sprague-Dawley Receptors, Nicotinic - metabolism Synaptic Membranes - drug effects Synaptic Membranes - metabolism Synaptic Transmission - drug effects Tobacco Vertebrates: nervous system and sense organs Rat Rodentia Central nervous system Tobacco smoking Electrophysiology Ionic current In vitro Cholinergic receptor Vertebrata Mammalia Synaptic transmission Nicotinic receptor Hippocampus Brain (vertebrata) Nicotine
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Abstract	Nicotine obtained from tobacco can improve learning and memory on various tasks and has been linked to arousal, attention, rapid information processing, working memory, and long-term memories that can cause craving years after someone has stopped smoking. One likely target for these effects is the hippocampus, a centre for learning and memory that has rich cholinergic innervation and dense nicotinic acetylcholine receptor (nAChR) expression. During Alzheimer's dementia there are fewer nAChRs and the cholinergic inputs to the hippocampus degenerate. However, there is no evidence for fast synaptic transmission mediated by nAChRs in the hippocampus, and their role is not understood. Nicotine is known to act on presynaptic nAChRs within the habenula of chick to enhance glutamatergic transmission; here we report that a similar mechanism operates in the hippocampus. Measurements of intracellular Ca2+ in single mossy-fibre presynaptic terminals indicate that nAChRs containing the alpha7 subunit can mediate a Ca2+ influx that is sufficient to induce vesicular neurotransmitter release. We propose that nicotine from tobacco influences cognition by enhancing synaptic transmission. Conversely, a decreased efficacy of transmission may account for the deficits associated with the loss of cholinergic innervation during Alzheimer's disease.
AbstractList	Nicotine obtained from tobacco can improve learning and memory on various tasks and has been linked to arousal, attention, rapid information processing, working memory, and long-term memories that can cause craving years after someone has stopped smoking. One likely target for these effects is the hippocampus, a centre for learning and memory that has rich cholinergic innervation and dense nicotinic acetylcholine receptor (nAChR) expression. During Alzheimer's dementia there are fewer nAChRs and the cholinergic inputs to the hippocampus degenerate. However, there is no evidence for fast synaptic transmission mediated by nAChRs in the hippocampus, and their role is not understood. Nicotine is known to act on presynaptic nAChRs within the habenula of chick to enhance glutamatergic transmission; here we report that a similar mechanism operates in the hippocampus. Measurements of intracellular Ca2+ in single mossy-fibre presynaptic terminals indicate that nAChRs containing the alpha7 subunit can mediate a Ca2+ influx that is sufficient to induce vesicular neurotransmitter release. We propose that nicotine from tobacco influences cognition by enhancing synaptic transmission. Conversely, a decreased efficacy of transmission may account for the deficits associated with the loss of cholinergic innervation during Alzheimer's disease. Nicotine obtained from tobacco can improve learning and memory on various tasks and has been linked to arousal, attention, rapid information processing, working memory, and long-term memories that can cause craving years after someone has stopped smoking. One likely target for these effects is the hippocampus, a centre for learning and memory that has rich cholinergic innervation and dense nicotinic acetylcholine receptor (nAChR) expression. During Alzheimer's dementia there are fewer nAChRs and the cholinergic inputs to the hippocampus degenerate. However, there is no evidence for fast synaptic transmission mediated by nAChRs in the hippocampus, and their role is not understood. Nicotine is known to act on presynaptic nAChRs within the habenula of chick to enhance glutamatergic transmission; here we report that a similar mechanism operates in the hippocampus. Measurements of intracellular Ca super(2+) in single mossy-fibre presynaptic terminals indicate that nAChRs containing the alpha 7 subunit can mediate a Ca super(2+) influx that is sufficient to induce vesicular neurotransmitter release. We propose that nicotine from tobacco influences cognition by enhancing synaptic transmission. Conversely, a decreased efficacy of transmission may account for the deficits associated with the loss of cholinergic innervation during Alzheimer's disease. Gray et al present evidence that nicotine from tobacco influences cognition by enhancing synaptic transmission. A decreased efficacy of transmission may account for the deficits associated with the loss of cholinergic innervation during Alzheimer's disease.
Author	Radcliffe, Kristofer A Rajan, Arun S Yakehiro, Masuhide Gray, Richard Dani, John A
Author_xml	– sequence: 1 givenname: Richard surname: Gray fullname: Gray, Richard – sequence: 2 givenname: Arun S surname: Rajan fullname: Rajan, Arun S – sequence: 3 givenname: Kristofer A surname: Radcliffe fullname: Radcliffe, Kristofer A – sequence: 4 givenname: Masuhide surname: Yakehiro fullname: Yakehiro, Masuhide – sequence: 5 givenname: John A surname: Dani fullname: Dani, John A
BackLink	http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3249306$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/8878480$$D View this record in MEDLINE/PubMed
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Keywords	Rat Rodentia Central nervous system Tobacco smoking Electrophysiology Ionic current In vitro Cholinergic receptor Vertebrata Mammalia Synaptic transmission Nicotinic receptor Hippocampus Brain (vertebrata) Nicotine
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Snippet	Nicotine obtained from tobacco can improve learning and memory on various tasks and has been linked to arousal, attention, rapid information processing,... Gray et al present evidence that nicotine from tobacco influences cognition by enhancing synaptic transmission. A decreased efficacy of transmission may...
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SubjectTerms	Action Potentials - drug effects Alzheimer's disease Animals Biological and medical sciences Calcium - metabolism Central nervous system Central neurotransmission. Neuromudulation. Pathways and receptors Cognition & reasoning Culture Techniques Dementia disorders Fundamental and applied biological sciences. Psychology Glutamic Acid - metabolism Hippocampus - drug effects Hippocampus - metabolism Medical research Nicotine Nicotine - pharmacology Rats Rats, Sprague-Dawley Receptors, Nicotinic - metabolism Synaptic Membranes - drug effects Synaptic Membranes - metabolism Synaptic Transmission - drug effects Tobacco Vertebrates: nervous system and sense organs
Title	Hippocampal synaptic transmission enhanced by low concentrations of nicotine
URI	http://dx.doi.org/10.1038/383713a0 https://www.ncbi.nlm.nih.gov/pubmed/8878480 https://www.proquest.com/docview/204458550 https://search.proquest.com/docview/15667638 https://search.proquest.com/docview/743080542 https://search.proquest.com/docview/78456706
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