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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Kiyohiro Fujino,Donata Oertel +1 more
TL;DR: Cholinergic efferent innervation enhances excitation by sounds of T stellate cells, opposing the inhibitory action of cholinergic innervation in the cochlea that is conveyed indirectly through the glutamatergic afferents.
The impact of sleep deprivation on neuronal and glial signaling pathways important for memory and synaptic plasticity
TL;DR: The different methods used to sleep deprive animals and the effects of different durations of sleep deprivation on learning and memory are discussed and those thought to play a critical role in the memory and synaptic plasticity deficits observed after sleep deprivation are reviewed.
Use of knock-out mice to determine the molecular basis for the actions of nicotine.
TL;DR: Experiments using mice lacking the beta2 subunit of the nAChR have shown that binding of nicotine to receptors containing this subunit is the first step in a pathway leading to increased dopamine levels in the mesolimbic dopamine system, and ultimately to the behavioral effects of nicotine in a test of nicotine reinforcement.
Nicotinic cholinergic signaling in hippocampal astrocytes involves calcium-induced calcium release from intracellular stores
TL;DR: A mechanism by which αBgt-AChRs on astrocytes can efficiently modulate calcium signaling in the central nervous system in a manner distinct from that observed with these receptors on neurons is revealed.
Nicotinic regulation of CREB activation in hippocampal neurons by glutamatergic and nonglutamatergic pathways.
TL;DR: It is shown here that nicotine can alter gene expression in rat hippocampal neurons, as reflected by activation of the transcription factor CREB and appearance of the immediate early gene product c-Fos.
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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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