Search results for "Long-Term Synaptic Depression"

showing 5 items of 5 documents

Perceptual correlates of nociceptive long-term potentiation and long-term depression in humans.

2004

Long-term potentiation (LTP) and long-term depression (LTD) of synaptic strength are ubiquitous mechanisms of synaptic plasticity, but their functional relevance in humans remains obscure. Here we report that a long-term increase in perceived pain to electrical test stimuli was induced by high-frequency electrical stimulation (HFS) (5 × 1 sec at 100 Hz) of peptidergic cutaneous afferents (27% above baseline, undiminished for >3 hr). In contrast, a long-term decrease in perceived pain (27% below baseline, undiminished for 1 hr) was induced by low-frequency stimulation (LFS) (17 min at 1 Hz). Pain testing with punctate mechanical probes (200 μm diameter) in skin adjacent to the HFS–LFS con…

AdultMalePain ThresholdLong-Term PotentiationPainStimulationNeocortexBehavioral/Systems/CognitiveHippocampusSensitivity and SpecificitySynaptic TransmissionConditioning PsychologicalmedicineHumansLong-term depressionPain MeasurementSkinAnalysis of VarianceHypoalgesiaNeuronal Plasticityintegumentary systemGeneral NeuroscienceLong-Term Synaptic DepressionNociceptorsLong-term potentiationMiddle AgedElectric StimulationForearmAllodyniaNociceptionSpinal CordSynaptic plasticityHyperalgesiaFemalemedicine.symptomPsychologyNeuroscienceThe Journal of neuroscience : the official journal of the Society for Neuroscience
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Dopamine restores limbic memory loss, dendritic spine structure, and NMDAR-dependent LTD in the nucleus accumbens of alcohol-withdrawn rats

2018

Alcohol abuse leads to aberrant forms of emotionally salient memory, i.e., limbic memory, that promote escalated alcohol consumption and relapse. Accordingly, activity-dependent structural abnormalities are likely to contribute to synaptic dysfunctions that occur from suddenly ceasing chronic alcohol consumption. Here we show that alcohol-dependent male rats fail to perform an emotional-learning task during abstinence but recover their functioning byl-3,4-dihydroxyphenylalanin (l-DOPA) administration during early withdrawal.l-DOPA also reverses the selective loss of dendritic “long thin” spines observed in medium spiny neurons of the nucleus accumbens (NAc) shell of alcohol-dependent rats d…

Male0301 basic medicineDendritic spineDendritic SpinesAlcohol abuseDopamineDopamine AgentsAMPA receptorMotor ActivityNucleus accumbensMedium spiny neuronReceptors N-Methyl-D-AspartateNucleus AccumbensLevodopaRats Sprague-Dawley03 medical and health sciences0302 clinical medicineDopamineMemoryLimbic SystemmedicineAnimalsReceptors AMPAResearch ArticlesMemory DisordersAlcohol Abstinencebusiness.industryLong-Term Synaptic DepressionGeneral NeuroscienceDopaminergicRatsConfocal microscopyAlcoholism030104 developmental biologySynaptic plasticityLTDSettore BIO/14 - FarmacologiaNMDA receptorGlutamatebusinessNeuroscience030217 neurology & neurosurgerymedicine.drug
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Hampered long-term depression and thin spine loss in the nucleus accumbens of ethanol-dependent rats.

2014

Alcoholism involves long-term cognitive deficits, including memory impairment, resulting in substantial cost to society. Neuronal refinement and stabilization are hypothesized to confer resilience to poor decision making and addictive-like behaviors, such as excessive ethanol drinking and dependence. Accordingly, structural abnormalities are likely to contribute to synaptic dysfunctions that occur from suddenly ceasing the use of alcohol after chronic ingestion. Here we show that ethanol-dependent rats display a loss of dendritic spines in medium spiny neurons of the nucleus accumbens (Nacc) shell, accompanied by a reduction of tyrosine hydroxylase immunostaining and postsynaptic density 95…

MaleDendritic spineDendritic SpinesGlutamic AcidNucleus accumbensNeurotransmissionMedium spiny neuronSynaptic TransmissionNucleus AccumbensOrgan Culture TechniquesAnimalsRats WistarLong-term depressionLong-Term Synaptic Depressiondopamine synaptic plasticity Golgi glutamateMultidisciplinaryNeuronal PlasticityEthanolDopaminergic NeuronsLong-Term Synaptic DepressionCentral Nervous System DepressantsRatsAlcoholismPNAS PlusSynaptic plasticitySettore BIO/14 - FarmacologiaPsychologyNeurosciencePostsynaptic densityProceedings of the National Academy of Sciences of the United States of America
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Alterations in the Hippocampal Endocannabinoid System in Diet-Induced Obese Mice

2010

The endocannabinoid (eCB) system plays central roles in the regulation of food intake and energy expenditure. Its alteration in activity contributes to the development and maintenance of obesity. Stimulation of the cannabinoid receptor type 1 (CB1receptor) increases feeding, enhances reward aspects of eating, and promotes lipogenesis, whereas its blockade decreases appetite, sustains weight loss, increases insulin sensitivity, and alleviates dysregulation of lipid metabolism. The hypothesis has been put forward that the eCB system is overactive in obesity. Hippocampal circuits are not directly involved in the neuronal control of food intake and appetite, but they play important roles in hed…

Malemedicine.medical_specialtyPolyunsaturated Alkamidesmedicine.medical_treatmentmedia_common.quotation_subjectArachidonic AcidsBiologyHippocampusArticlegamma-Aminobutyric acidGlyceridesMice03 medical and health sciences0302 clinical medicineReceptor Cannabinoid CB1Internal medicineCannabinoid Receptor ModulatorsCannabinoid receptor type 1medicineAnimalsObesityReceptorgamma-Aminobutyric Acid030304 developmental biologymedia_commonMice KnockoutNeurons0303 health sciencesLong-Term Synaptic DepressionGeneral NeuroscienceAppetiteDietary FatsEndocannabinoid systemMice Inbred C57BLDisease Models AnimalLipoprotein LipaseEndocrinologynervous systemSynapsesSynaptic plasticitylipids (amino acids peptides and proteins)CannabinoidDiet-induced obese030217 neurology & neurosurgeryEndocannabinoidsmedicine.drugThe Journal of Neuroscience
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Presynaptic CB1 Receptors Regulate Synaptic Plasticity at Cerebellar Parallel Fiber Synapses

2011

Endocannabinoids are potent regulators of synaptic strength. They are generally thought to modify neurotransmitter release through retrograde activation of presynaptic type 1 cannabinoid receptors (CB1Rs). In the cerebellar cortex, CB1Rs regulate several forms of synaptic plasticity at synapses onto Purkinje cells, including presynaptically expressed short-term plasticity and, somewhat paradoxically, a postsynaptic form of long-term depression (LTD). Here we have generated mice in which CB1Rs were selectively eliminated from cerebellar granule cells, whose axons form parallel fibers. We find that in these mice, endocannabinoid-dependent short-term plasticity is eliminated at parallel fiber…

PhysiologyPresynaptic TerminalsNeural facilitationNonsynaptic plasticityParallel fiberSynaptic TransmissionMice03 medical and health sciences0302 clinical medicineReceptor Cannabinoid CB1CerebellumMetaplasticitymedicineAnimalsLong-term depression030304 developmental biologyMice Knockout0303 health sciencesNeuronal PlasticitySynaptic scalingHomosynaptic plasticityChemistryLong-Term Synaptic DepressionGeneral NeuroscienceArticlesMice Inbred C57BLmedicine.anatomical_structurenervous systemSynaptic plasticityNeuroscience030217 neurology & neurosurgeryJournal of Neurophysiology
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