Journal Article10.1038/383713A0
Hippocampal synaptic transmission enhanced by low concentrations of nicotine
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TL;DR: It is proposed that nicotine from tobacco influences cognition by enhancing synaptic transmission, and a decreased efficacy of transmission may account for the deficits associated with the loss of cholinergic innervation during Alzheimer's disease.
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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.
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Citations
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Novel Regulation of Cortical Acetylcholine Release and Cognitive Behavior
Kristen Gardner
- 01 Jun 2008
TL;DR: In this article, the authors express their gratitude to the College of Biological Sciences, Department of Microbiology for its financial contribution to my undergraduate education through the Anne H. Baumhofer Scholarship and the college for specifically funding my undergraduate research through the Dean's Undergraduate Research Fund.
•Dissertation
Nicotinic modulation of excitatory amino acid release in the rat frontal cortex
Stephen John Rousseau
- 01 Jan 2004
TL;DR: This document breaches copyright and will remove access to the work immediately, and the author will investigate the claim.
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Molecular cloning, functional properties, and distribution of rat brain alpha 7: a nicotinic cation channel highly permeable to calcium
TL;DR: The results imply that alpha 7-containing receptors may play a role in activating calcium-dependent mechanisms in specific neuronal populations of the adult rat limbic system.
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Distribution of alpha2, alpha3, alpha4, and beta2 neuronal nicotinic receptor subunit mRNAs in the central nervous system: A hybridization histochemical study in the rat
Etsuko Wada,Keiji Wada,Jim Boulter,Evan S. Deneris,Steve Heinemann,Jim Patrick,Larry W. Swanson +6 more
TL;DR: Nine different [35S]‐complementary ribonucleic acid (cRNA) probes were used in the present study to map the distribution of these nAChR subunit mRNAs throughout the central nervous system (CNS) of the rat.
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Nicotine enhancement of fast excitatory synaptic transmission in CNS by presynaptic receptors
TL;DR: Findings reveal that CNS nAChRs enhance fast excitatory transmission, providing a likely mechanism for the complex behavioral effects of nicotine.
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Physiological Diversity of Nicotinic Acetylcholine Receptors Expressed by Vertebrate Neurons
Daniel S. McGehee,Lorna W. Role +1 more
TL;DR: The work s ummarized in this review has helped answer a long-standing question: How can wellknown behavioral, cognit ive, and addict ive eff ects of ni cotine be reconci led with the paucity of evidence for CNS s ynapses where t he t rans mission is mediat ed by nicot inic recept ors?
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