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Cholinergic NeuronsNeuronsCholinergic FibersCholine O-AcetyltransferaseProsencephalonSeptum PellucidumParasympathetic Nervous SystemSubstantia InnominataSeptum of BrainNeurons, AfferentVesicular Acetylcholine Transport ProteinsMotor NeuronsBasal Nucleus of MeynertDiagonal Band of BrocaAcetylcholineRibosome Inactivating Proteins, Type 1Cholinergic AgentsAcetylcholinesteraseTegmentum MesencephaliNerve Growth FactorsReceptor, Nerve Growth FactorSeptal NucleiHippocampusAction PotentialsPedunculopontine Tegmental NucleusReceptors, Nerve Growth Factorgamma-Aminobutyric AcidHemicholinium 3Synaptic TransmissionImmunohistochemistryReceptor, trkANerve Tissue ProteinsGABAergic NeuronsElectrophysiologyPonsElectric StimulationPatch-Clamp TechniquesCerebral CortexBrainCholineAxonsCells, CulturedSynapsesDopaminergic NeuronsNerve DegenerationRats, Sprague-DawleyCell CountTetrodotoxinDendritesInterneuronsRats, WistarSpinal CordCorpus StriatumMembrane PotentialsNeural InhibitionNerve Growth FactorBrain StemAnimals, NewbornMesencephalonGlutamic AcidTyrosine 3-MonooxygenaseGanglia, ParasympatheticEnteric Nervous SystemDopamineBehavior, AnimalNeuropeptidesGanglia, SpinalMice, TransgenicMuscarinic AgonistsReceptors, CholinergicAziridinesSensory Receptor CellsImmunotoxinsTime FactorsCalbindin 2Glutamate DecarboxylaseOlfactory Receptor NeuronsAutonomic PathwaysMyenteric PlexusGangliaExcitatory Postsynaptic PotentialsCatsStilbamidinesReceptors, MuscarinicSerotoninMaze LearningMice, Inbred C57BLAtropineS100 Calcium Binding Protein GVesicular Glutamate Transport Protein 2Neurotransmitter AgentsCalbindinsInjections, IntraventricularGrowth Differentiation Factor 2Neuroanatomical Tract-Tracing TechniquesPresynaptic TerminalsAnalysis of VarianceAfferent PathwaysGreen Fluorescent ProteinsDose-Response Relationship, Drug

Neurogenic abnormalities in Alzheimer's disease differ between stages of neurogenesis and are partly related to cholinergic pathology. (65/184)

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Continuous estrone treatment impairs spatial memory and does not impact number of basal forebrain cholinergic neurons in the surgically menopausal middle-aged rat. (66/184)

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Symptoms of rapid eye movement sleep behavior disorder are associated with cholinergic denervation in Parkinson disease. (67/184)

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Diverse populations of intrinsic cholinergic interneurons in the mouse olfactory bulb. (68/184)

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Pentobarbital decreased nitric oxide release in the rat striatum but ketamine increased the release independent of cholinergic regulation. (69/184)

Pentobarbital (PB) and ketamine (Ket) influence the concentration of neurotransmitters in the brain. PB has been reported to decrease the extracellular nitric oxide (NO) concentration through a decrease in acetylcholine (ACh) release, while Ket has been shown to increase the NO concentration via an increase in ACh release. Here, we investigated effects of PB and Ket on NO release and the relationship between NO and ACh in the rat striatum by in vivo microdialysis experiments. Male Sprague-Dawley rats were used. A microdialysis probe was inserted into the right striatum and perfused with modified Ringer's solution. Samples were collected every 15 min and injected into an HPLC system. The rats were freely moving, and PB and Ket were administered intraperitoneally. Neostigmine (1 and 10 microM) and mecamylamine (100 microM) were added to the perfusate. Calcium and magnesium concentrations were modified for each anesthetic to influence ACh release. PB decreased NO products (NOx) while Ket increased them. While perfusion with neostigmine showed no effect on baseline NOx concentrations, it diminished the PB-induced NOx reduction at low concentrations and abolished it at high concentrations. Magnesium-free perfusion had no effect on baseline NOx concentrations, whereas perfusion at a low magnesium concentration antagonized the PB-induced NOx reduction. Mecamylamine and calcium-free perfusion had no effect on baseline NOx concentrations and Ket-induced NOx increases. PB may decrease NO release through reduction in ACh release, whereas Ket may increase NO release independent of ACh regulation.  (+info)

Associations between a neurophysiological marker of central cholinergic activity and cognitive functions in young and older adults. (70/184)

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Prior pathology in the basal forebrain cholinergic system predisposes to inflammation-induced working memory deficits: reconciling inflammatory and cholinergic hypotheses of delirium. (71/184)

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Selenium induces cholinergic motor neuron degeneration in Caenorhabditis elegans. (72/184)

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