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
Subtype-selective nicotinic receptor antagonists: potential as tobacco use cessation agents.
Linda P. Dwoskin,Sangeetha P. Sumithran,Jun Zhu,A. Gabriela Deaciuc,Joshua T. Ayers,Peter A. Crooks +5 more
TL;DR: The most potent and subtype-selective analogue, N,N'-dodecyl-bis-picolinium bromide (bPiDDB), inhibited nAChRs mediating nicotine-evoked [(3)H]dopamine release (IC(50)=5 nM; I(max) of 60%), and did not interact with alpha4beta2* or alpha7* nA ChRs.
Allosteric Modulation of Related Ligand-Gated Ion Channels Synergistically Induces Long-Term Potentiation in the Hippocampus and Enhances Cognition
Timothy B C Johnstone,Zhenglin Gu,Ryan F. Yoshimura,Anne-Sophie Villégier,Derk J. Hogenkamp,Edward R. Whittemore,Jin-Cheng Huang,Minhtam B. Tran,James D. Belluzzi,Jerrel L. Yakel,Kelvin W. Gee +10 more
TL;DR: Combined transient application of two allosteric modulators that individually inhibit α5 GABAARs and enhance α7 nAChRs causes long-term potentiation of mossy fiber stimulation-induced excitatory postsynaptic currents (EPSC) from CA1 pyramidal neurons of rat hippocampal slices.
Choline and acetylcholine have similar kinetic properties of activation and desensitization on the α7 nicotinic receptors in rat hippocampal neurons
TL;DR: The results established that the main difference between choline and ACh is of affinity, and support the concept that the switching of endogenous agonist may change the desensitized-resensitization dynamics of alpha7 nAChRs.
α7 nicotinic acetylcholine receptors as therapeutic targets in schizophrenia: Update on animal and clinical studies and strategies for the future.
TL;DR: In this review, several topics are discussed that may impact the success of α7-nAChR ligands as pro-cognitive agents for schizophrenia including the translational value of the animal models used, clinical trial design limitations, confounding effects of polypharmacy, dose-effect relationships, and chronic versus intermittent dosing considerations.
Analysis of Relations between NMDA Receptors and GABA Release at Olfactory Bulb Reciprocal Synapses
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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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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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