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
Live Imaging of Nicotine Induced Calcium Signaling and Neurotransmitter Release Along Ventral Hippocampal Axons.
TL;DR: A gene-chimeric preparation of ventral hippocampal (vHipp)-accumbens (nAcc) circuit in vitro is introduced that allows direct live imaging to analyze both the pre and post-synaptic components of transmission while selectively varying the genetic profile of the pre- vs post- synaptic neurons.
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Exaggeration of epileptic-like patterns by nicotine receptor activation during the GABA withdrawal syndrome.
TL;DR: It is suggested that both dihydro-beta-erythroidine and alpha-bungarotoxin-sensitive sites control paroxysmic activities in GWS and could be involved in some human and animal epilepsies presenting mutations of nicotinic cholinergic receptors.
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Choline induces opposite changes in pyramidal neuron excitability and synaptic transmission through a nicotinic receptor-independent process in hippocampal slices
E. Albiñana,J.G. Luengo,Andrés M. Baraibar,M.D. Muñoz,Luis Gandía,J. M. Solis,Jesús M. Hernández-Guijo +6 more
TL;DR: Choline caused a reversible depression of evoked field excitatory postsynaptic potentials (fEPSPs) and population spike observed in rat slices were completely reproduced in slices obtained from α7 nAChR knockout mice, reinforcing the conclusion that choline modulates synaptic transmission and neuronal excitability by a mechanism independent of nicotinic receptor activation.
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Electrically evoked release of glutamate in rat hippocampal slices: effects of various drugs and fimbria-fornix lesions.
Sehmisch S,Blauth E,Thorn D,Jean-Christophe Cassel,Kelche C,Thomas J. Feuerstein,Rolf Jackisch +6 more
TL;DR: It is concluded that the present model was able to detect lesion-induced differences in electrically evoked release of [3H]glutamate, but the relationship of these differences to changes of noradrenergic, cholinergic or serotonergic hippocampal innervations remains to be established.
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Neuronal Ca2+ Channels and Nicotinic ACh Receptors as Functional Targets of the Nootropic Nefiracetam
Mitsunobu Yoshii,Shigeo Watabe,Yoshiya L. Murashima,Toshihide Nukada,Tadashi Shiotani,Tomoyuki Nishizaki +5 more
TL;DR: Nfiracetam is distinguished from other nootropic agents for its preferential actions on both presynaptic Ca2+ channels and nicotinic ACh receptors, and could therefore be of great therapeutic importance to the neurotransmission failure that contributes to the symptoms of Alzheimer's disease and associated disorders.
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References
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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