2017
L-theanine prevent quinolinic acid induced motor deficit and striatal neurotoxicity: Reduction in oxido-nitrosative stress and restoration of striatal neurotransmitters level
Jamwal S, Singh S, Gill JS, Kumar P. L-theanine prevent quinolinic acid induced motor deficit and striatal neurotoxicity: Reduction in oxido-nitrosative stress and restoration of striatal neurotransmitters level. European Journal Of Pharmacology 2017, 811: 171-179. PMID: 28624333, DOI: 10.1016/j.ejphar.2017.06.016.Peer-Reviewed Original ResearchConceptsStriatal neurotransmitter levelsOxido-nitrosative stressNeurotransmitter levelsProtective effectL-NAMEMotor deficitsQuinolinic acidL-arginineL-theanineNitric oxide synthase inhibitorPro-inflammatory cytokinesNitric oxide pathwayOxide synthase inhibitorOpen field testL-theanine treatmentRota-rodBeam walkingNeuro-inflammationNeurotransmitter alterationsNeuroprotective potentialStriatal neurotoxicityOxide pathwayQA injectionGrip strengthMotor coordination
2016
Sertraline and venlafaxine improves motor performance and neurobehavioral deficit in quinolinic acid induced Huntington’s like symptoms in rats: Possible neurotransmitters modulation
Gill JS, Jamwal S, Kumar P, Deshmukh R. Sertraline and venlafaxine improves motor performance and neurobehavioral deficit in quinolinic acid induced Huntington’s like symptoms in rats: Possible neurotransmitters modulation. Pharmacological Reports 2016, 69: 306-313. PMID: 28178592, DOI: 10.1016/j.pharep.2016.11.008.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCorpus StriatumDisease Models, AnimalGamma-Aminobutyric AcidGlutamic AcidHuntington DiseaseInterleukin-1betaInterleukin-6Lipid PeroxidationMaleMotor ActivityNeuroprotective AgentsNeurotransmitter AgentsOxidative StressQuinolinic AcidRatsRats, WistarRotarod Performance TestSertralineTumor Necrosis Factor-alphaVenlafaxine HydrochlorideConceptsMotor performanceQuinolinic acidAvailable drugsPro-inflammatory cytokine levelsNumerous neuroprotective propertiesAnti-inflammatory propertiesGrip strength testProgressive neurodegenerative disorderBDNF levelsCytokine levelsSymptomatic reliefNeuroprotective effectsRotarod testMonoamine levelsNeuroprotective propertiesStriatal atrophyNeurobehavioral deficitsNeurotransmitter levelsNeurotransmitter modulationGlutamatergic signalingRat striatumNeurochemical analysisBody weightDay 22Neurochemical levelsL-theanine, a Component of Green Tea Prevents 3-Nitropropionic Acid (3-NP)-Induced Striatal Toxicity by Modulating Nitric Oxide Pathway
Jamwal S, Kumar P. L-theanine, a Component of Green Tea Prevents 3-Nitropropionic Acid (3-NP)-Induced Striatal Toxicity by Modulating Nitric Oxide Pathway. Molecular Neurobiology 2016, 54: 2327-2337. PMID: 26957301, DOI: 10.1007/s12035-016-9822-5.Peer-Reviewed Original ResearchConceptsHuntington's diseaseStriatal toxicityL-NAMENeuroprotective potentialConcurrent treatmentProtective effectBody weightL-arginineL-theanineGABAergic medium spiny neuronsGreen tea preventsStriatal neurotransmitter levelsPro-inflammatory mediatorsPro-inflammatory cytokinesNitric oxide pathwayBlood-brain barrierMedium spiny neuronsNitric oxide productionL-theanine treatmentNeurotransmitter alterationsOxide pathwayBrain barrierSpiny neuronsNeurotransmitter levelsRat striatum
2015
Beneficial effects of lycopene against haloperidol induced orofacial dyskinesia in rats: Possible neurotransmitters and neuroinflammation modulation
Datta S, Jamwal S, Deshmukh R, Kumar P. Beneficial effects of lycopene against haloperidol induced orofacial dyskinesia in rats: Possible neurotransmitters and neuroinflammation modulation. European Journal Of Pharmacology 2015, 771: 229-235. PMID: 26712377, DOI: 10.1016/j.ejphar.2015.12.032.Peer-Reviewed Original ResearchConceptsOrofacial dyskinesiaHaloperidol treatmentChronic neuroleptic treatmentAbnormal involuntary movementsSevere side effectsNeuroinflammatory modulationNeuroleptic treatmentTardive dyskinesiaProtective effectInvoluntary movementsSide effectsDyskinesiaBiochemical parametersHaloperidolRatsTreatmentDaysLycopeneStriatumSpermidine ameliorates 3-nitropropionic acid (3-NP)-induced striatal toxicity: Possible role of oxidative stress, neuroinflammation, and neurotransmitters
Jamwal S, Kumar P. Spermidine ameliorates 3-nitropropionic acid (3-NP)-induced striatal toxicity: Possible role of oxidative stress, neuroinflammation, and neurotransmitters. Physiology & Behavior 2015, 155: 180-187. PMID: 26703234, DOI: 10.1016/j.physbeh.2015.12.015.Peer-Reviewed Original ResearchConceptsHuntington's diseaseStriatal toxicityStriatal neurotransmittersRat striatumMotor coordinationPro-inflammatory cytokine levelsOxidative stressPro-inflammatory mediatorsPotential neuroprotective effectsAnti-inflammatory propertiesGood experimental modelConfer neuroprotectionCytokine levelsNeuroinflammatory markersNeuroprotective effectsPresent studyNeurochemical analysisBody weightTherapeutic potentialNeurodegenerative disordersBiochemical parametersExperimental modelDecreased levelsNeurotransmittersSignificant alterationsPiperine Enhances the Protective Effect of Curcumin Against 3-NP Induced Neurotoxicity: Possible Neurotransmitters Modulation Mechanism
Singh S, Jamwal S, Kumar P. Piperine Enhances the Protective Effect of Curcumin Against 3-NP Induced Neurotoxicity: Possible Neurotransmitters Modulation Mechanism. Neurochemical Research 2015, 40: 1758-1766. PMID: 26160706, DOI: 10.1007/s11064-015-1658-2.Peer-Reviewed Original ResearchConceptsProtective effectPresence of piperineChronic treatmentMotor deficitsNeuroprotective effectsNeurochemical abnormalitiesAbstract3-Nitropropionic acidPresent studyInduced neurotoxicityMotor functionNeuroprotective activityBody weightMolecular alterationsBeneficial effectsHuntington's diseaseOxidative stressNatural polyphenolNeurotoxicityCurcuminPiperineRatsDiseaseAdministrationBehavioral parametersDaysProtective Effect of Spermidine Against Excitotoxic Neuronal Death Induced by Quinolinic Acid in Rats: Possible Neurotransmitters and Neuroinflammatory Mechanism
Jamwal S, Singh S, Kaur N, Kumar P. Protective Effect of Spermidine Against Excitotoxic Neuronal Death Induced by Quinolinic Acid in Rats: Possible Neurotransmitters and Neuroinflammatory Mechanism. Neurotoxicity Research 2015, 28: 171-184. PMID: 26078029, DOI: 10.1007/s12640-015-9535-y.Peer-Reviewed Original ResearchConceptsQuinolinic acidBody weightQA treatmentGABAergic medium spiny neuronsN-methyl-D-aspartate receptorsOxidative stressGABAergic neuronal lossPro-inflammatory levelsHyperkinetic movement disordersExcitotoxic cell deathAnti-inflammatory propertiesExcitotoxic neuronal deathMedium spiny neuronsReceptor antagonistic propertiesNeuroinflammatory mechanismsPossible neurotransmittersNeuroinflammatory markersNeuronal lossNeuroprotective effectsNeurotransmitter alterationsCatecholamine levelsCascade of eventsNeuronal deathSpiny neuronsMovement disorders
2014
Neuroprotective effect of hemeoxygenase-1/glycogen synthase kinase-3β modulators in 3-nitropropionic acid-induced neurotoxicity in rats
Khan A, Jamwal S, Bijjem K, Prakash A, Kumar P. Neuroprotective effect of hemeoxygenase-1/glycogen synthase kinase-3β modulators in 3-nitropropionic acid-induced neurotoxicity in rats. Neuroscience 2014, 287: 66-77. PMID: 25536048, DOI: 10.1016/j.neuroscience.2014.12.018.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBody WeightCorpus StriatumEncephalitisGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHeme Oxygenase-1HeminLipid PeroxidationLithium ChlorideMaleMetalloporphyrinsMotor ActivityNeuroprotective AgentsNeurotoxicity SyndromesNitritesNitro CompoundsOxidative StressPropionatesProtoporphyrinsRatsRats, WistarRotarod Performance TestSignal TransductionConceptsAdministration of heminHemeoxygenase-1GSK-3β activityN-methyl-D-aspartate receptorsOxidative stressPro-inflammatory mediatorsPresent studyHO-1 inhibitorGSK-3β pathwaySynthase kinase-3β pathwayDifferent neurodegenerative disordersHD-like symptomsProphylactic therapyNeuroprotective effectsPathophysiology of HDTin protoporphyrinMotor impairmentPharmacological modulationMotor coordinationBody weightLocomotor activityMolecular alterationsTherapeutic potentialOxidative burdenNeurodegenerative disorders