Search results for "gliosis"

showing 10 items of 37 documents

Neuroprotective action of diazepam at very low and moderate doses in Alzheimer's disease model rats

2018

Abstract Early manifestations of Alzheimer's disease (AD) include neuroinflammation, disrupted neurotransmission and cognitive deficits. Impairment of the GABAergic system is essentially involved in the pathogenesis of AD. Traditionally, agonists of GABAA receptors at doses above 1 mg/kg are known to possess memory impairing effects. However, we have previously found that GABAA receptor GABA site ligand muscimol at very low doses acted contrary – enhanced spatial learning/memory, as well as prevented neuroinflammation and augmented neurotransmission in AD model rats. Therefore, in the present study we focused on the assessment of the effects of non-sedative – very low (0.05 mg/kg) and moder…

Male0301 basic medicineAllosteric modulatormedicine.drug_classSynaptophysinNeurotransmissionPharmacologyHippocampusNeuroprotectionRandom Allocation03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicineAlzheimer DiseasemedicineAnimalsGliosisRats Wistargamma-Aminobutyric AcidCerebral CortexPharmacologyMemory DisordersBenzodiazepineDiazepamDose-Response Relationship DrugGlutamate DecarboxylaseGABAA receptorAcetylcholineNeuroprotective Agents030104 developmental biologyGene Expression RegulationMuscimolchemistryAstrocytesSynaptic plasticityGABAergic030217 neurology & neurosurgeryNeuropharmacology
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SETD7 mediates spinal microgliosis and neuropathic pain in a rat model of peripheral nerve injury

2019

Abstract Gene transcription regulation is critical for the development of spinal microgliosis and neuropathic pain after peripheral nerve injury. Using a model of chronic constriction injury (CCI) of the sciatic nerve, this study characterized the role of SET domain containing lysine methyltransferase 7 (SETD7) which monomethylates histone H3 lysine 4 (H3K4me1), a marker for active gene transcription. SETD7 protein expression in the spinal dorsal horn ipsilateral to nerve lesion was increased from one day to 14 days after CCI, concomitantly with the expression of inflammatory genes, Ccl2, Il-6 and Il-1β. The CCI-induced SETD7 expression was predominantly localized to microglia, as demonstra…

Male0301 basic medicineSpinal Cord Dorsal HornPathologymedicine.medical_specialtyImmunologyCCL2MicrogliosisRats Sprague-Dawley03 medical and health sciencesBehavioral Neuroscience0302 clinical medicinePeripheral Nerve InjuriesGanglia SpinalmedicineAnimalsGene knockdownMicrogliaEndocrine and Autonomic Systemsbusiness.industryHistone-Lysine N-MethyltransferaseNerve injurySciatic NerveSpineRats030104 developmental biologymedicine.anatomical_structureSpinal CordHyperalgesiaNeuropathic painPeripheral nerve injuryNeuralgiaFemaleMicrogliaSciatic nervemedicine.symptombusiness030217 neurology & neurosurgeryBrain, Behavior, and Immunity
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Administration of all‐ trans retinoic acid after experimental traumatic brain injury is brain protective

2020

BACKGROUND AND PURPOSE: All‐trans retinoic acid (ATRA) is a vitamin A metabolite, important in the developing and mature brain. Pre‐injury ATRA administration ameliorates ischaemic brain insults in rodents. This study examined the effects of post‐traumatic ATRA treatment in experimental traumatic brain injury (TBI). EXPERIMENTAL APPROACH: Male adult mice were subjected to the controlled cortical impact model of TBI or sham procedure and killed at 7 or 30 days post‐injury (dpi). ATRA (10 mg kg−1, i.p.) was given immediately after the injury and 1, 2 and 3 dpi. Neurological function and sensorimotor coordination were evaluated. Brains were processed for (immuno‐) histological, mRNA and protei…

Male0301 basic medicineTraumatic brain injuryRetinoic acidTretinoinPharmacologyHippocampal formationHMGB1Mice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineBrain Injuries TraumaticmedicineAnimalsInflammationPharmacologyMicrogliabiologybusiness.industryBrainmedicine.diseaseGranule cellResearch PapersAstrogliosis030104 developmental biologymedicine.anatomical_structurechemistryBlood-Brain BarrierApoptosisbiology.proteinbusiness030217 neurology & neurosurgeryBritish Journal of Pharmacology
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Clobetasol promotes neuromuscular plasticity in mice after motoneuronal loss via sonic hedgehog signaling, immunomodulation and metabolic rebalancing

2021

AbstractMotoneuronal loss is the main feature of amyotrophic lateral sclerosis, although pathogenesis is extremely complex involving both neural and muscle cells. In order to translationally engage the sonic hedgehog pathway, which is a promising target for neural regeneration, recent studies have reported on the neuroprotective effects of clobetasol, an FDA-approved glucocorticoid, able to activate this pathway via smoothened. Herein we sought to examine functional, cellular, and metabolic effects of clobetasol in a neurotoxic mouse model of spinal motoneuronal loss. We found that clobetasol reduces muscle denervation and motor impairments in part by restoring sonic hedgehog signaling and …

MaleCancer ResearchPhysiology129 StrainBiochemistryMiceDatabases GeneticMedicineMyocyteMotor NeuronsNeuronal PlasticitySkeletalSmoothened ReceptorHedgehog signaling pathwayMuscle atrophyMitochondriaAstrogliosisNeuroprotective AgentsMusclemedicine.symptomInflammation MediatorsSignal TransductionCholera ToxinMice 129 StrainhedgehogImmunologyMotor ActivityNeuroprotectionArticleDatabasesCellular and Molecular NeurosciencesmoothenedGeneticAnimalsHumansHedgehog ProteinsMuscle SkeletalHedgehogGlucocorticoidsMuscle DenervationQH573-671Animalbusiness.industryAmyotrophic Lateral SclerosisGlial biologyCell Biologymedicine.diseaseSaporinsSpineMitochondria MuscleDisease Models AnimalclobetasolinflammationCase-Control StudiesDisease ModelsDiseases of the nervous systemCytologySmoothenedbusinessEnergy MetabolismNeuroscienceOpen Field Test
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Giant axonal neuropathy and leukodystrophy

1991

Abstract An 11-year-old Persian boy, born to consanguineous parents, manifested a progressive gait abnormality beginning at 5 years of age. A severe cerebellar disorder developed with associated dysfunction of the peripheral nervous system, but no sign of mental impairment. The sensory and motor nerve conduction velocities were greatly reduced, especially in the lower extremities. Cerebrospinal fluid protein was normal. Computed tomography and magnetic resonance imaging revealed leukoencephalopathy, especially in the cerebellum, but also in periventricular areas. The diagnosis of giant axonal neuropathy was established by biopsy of the sural nerve. The few previous histologic examinations h…

MaleIntermediate FilamentsMotor nerveGenes RecessiveSural nerveCerebral VentriclesLeukoencephalopathyConsanguinityDevelopmental NeuroscienceCerebellummedicineHumansCerebellar disorderGliosisPeripheral NervesChildMyelin SheathSpinocerebellar DegenerationsGiant axonal neuropathybusiness.industryLeukodystrophyAnatomymedicine.diseaseMagnetic Resonance ImagingAxonsMicroscopy Electronmedicine.anatomical_structurenervous systemNeurologyPeripheral nervous systemPediatrics Perinatology and Child HealthGait abnormalityNeurology (clinical)medicine.symptomHereditary Sensory and Motor NeuropathybusinessPediatric Neurology
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Proteomic signature of the Dravet syndrome in the genetic Scn1a-A1783V mouse model.

2021

Abstract Background Dravet syndrome is a rare, severe pediatric epileptic encephalopathy associated with intellectual and motor disabilities. Proteomic profiling in a mouse model of Dravet syndrome can provide information about the molecular consequences of the genetic deficiency and about pathophysiological mechanisms developing during the disease course. Methods A knock-in mouse model of Dravet syndrome with Scn1a haploinsufficiency was used for whole proteome, seizure, and behavioral analysis. Hippocampal tissue was dissected from two- (prior to epilepsy manifestation) and four- (following epilepsy manifestation) week-old male mice and analyzed using LC-MS/MS with label-free quantificati…

MaleProteomics0301 basic medicineProteomeHippocampusEpilepsies MyoclonicHaploinsufficiencyScn1aHippocampusSynaptic TransmissionElevated Plus Maze TestEpilepsyMice0302 clinical medicineTandem Mass Spectrometry11-beta-Hydroxysteroid Dehydrogenase Type 1Genetic epilepsyCarbon-Nitrogen LigasesGene Knock-In TechniquesGliosisNeuronal PlasticityBehavior AnimalEpileptic encephalopathyImmunohistochemistryAstrogliosisNeurologyProteomeDisease ProgressionFemaleHaploinsufficiencySignal TransductionRC321-571Dopamine and cAMP-Regulated Phosphoprotein 32Neovascularization PhysiologicNeurosciences. Biological psychiatry. NeuropsychiatryBiologyNitric Oxide03 medical and health sciencesDravet syndromemedicineAnimalsHyperthermiaSocial Behaviorras-GRF1Proteomic Profilingmedicine.diseaseVascular Endothelial Growth Factor Receptor-2NAV1.1 Voltage-Gated Sodium ChannelDisease Models Animal030104 developmental biologyRotarod Performance TestSynaptic plasticityEpileptic Encephalopathy ; Genetic Epilepsy ; Mice ; Proteome ; Scn1aCalcium-Calmodulin-Dependent Protein Kinase Type 2Open Field TestNeuroscience030217 neurology & neurosurgeryChromatography Liquid
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Adipocyte cannabinoid CB1 receptor deficiency alleviates high fat diet-induced memory deficit, depressive-like behavior, neuroinflammation and impair…

2019

Abstract Background Obesity is a low-grade inflammation condition that facilitates the development of numerous comorbidities and the dysregulation of brain homeostasis. Additionally, obesity also causes distinct behavioral alterations both in humans and rodents. Here, we investigated the effect of inducible genetic deletion of the cannabinoid type 1 receptor (CB1) in adipocytes (Ati-CB1-KO mice) on obesity-induced memory deficits, depressive-like behavior, neuroinflammation and adult neurogenesis. Methods Behavioral, mRNA expression and immunohistochemical studies were performed in Ati-CB1-KO mice and corresponding wild-type controls under standard and high-fat diet. Results Adipocyte-speci…

Malemedicine.medical_specialtyCannabinoid receptorNeurogenesisEndocrinology Diabetes and Metabolismmedicine.medical_treatmentInflammationDiet High-FatMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineEndocrinologyNeural Stem CellsNeuritisReceptor Cannabinoid CB1AdipocyteInternal medicineAdipocytesmedicineAnimalsBiological PsychiatryNeuroinflammationMice KnockoutMemory DisordersBehavior AnimalDepressionEndocrine and Autonomic Systemsbusiness.industryNeurogenesisBrain030227 psychiatryAdult Stem CellsPsychiatry and Mental healthEndocrinologynervous systemchemistryGliosisOrgan SpecificityCannabinoidmedicine.symptombusinessGene Deletion030217 neurology & neurosurgeryHomeostasisPsychoneuroendocrinology
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Cytopathologic and neurochemical correlates of progression to motor/cognitive impairment in SIV-infected rhesus monkeys.

1994

Neurochemical, pathologic, virologic, and histochemical correlates of simian immunodeficiency virus (SIV)-associated central nervous system (CNS) dysfunction were assessed serially or at necropsy in rhesus monkeys that exhibited motor and cognitive deficits after SIV infection. Some infected monkeys presented with signs of acquired immunodeficiency disease (AIDS) at the time of sacrifice. Seven of eight animals exhibited motor skill impairment which was associated with elevated quinolinic acid in cerebrospinal fluid (CSF). Examination of the brains revealed diffuse increases in glial fibrillary acidic protein immunoreacti vity in cerebral cortex in all animals, regardless of evidence of imm…

MalevirusesCentral nervous systemSimian Acquired Immunodeficiency SyndromeMotor Activitymedicine.disease_causeVirusPathology and Forensic MedicineCentral nervous system diseaseCellular and Molecular Neurosciencechemistry.chemical_compoundCerebrospinal fluidCognitionGlial Fibrillary Acidic ProteinmedicineAnimalsCerebral CortexGlial fibrillary acidic proteinbiologyBrainGeneral MedicineSimian immunodeficiency virusQuinolinic Acidmedicine.diseaseMacaca mulattaAstrogliosismedicine.anatomical_structureNeurologychemistrySpinal CordImmunologybiology.proteinSimian Immunodeficiency VirusNeurology (clinical)PsychologyCognition DisordersQuinolinic acidJournal of neuropathology and experimental neurology
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Neuronal injury in chronic CNS inflammation.

2010

Introduction Multiple sclerosis (MS) is the most common chronic inflammatory disease of the central nervous system which is characterized by inflammatory demyelination and neurodegeneration. Neurological symptoms include sensory disturbances, optic neuritis, limb weakness, ataxia, bladder dysfunction, cognitive deficits and fatigue. Pathophysiology The inflammation process with MS is promoted by several inflammatory cytokines produced by the immune cells themselves and local resident cells like activated microglia. Consecutive damaging pathways involve the transmigration of activated B lymphocytes and plasma cells, which synthesize antibodies against the myelin sheath, boost the immune atta…

Multiple SclerosisInflammationNeuroprotectionSeverity of Illness IndexProinflammatory cytokineCentral Nervous System DiseasesmedicineAnimalsHumansRemyelinationNeuroinflammationInflammationNeuronsMicrogliabusiness.industryMultiple sclerosismedicine.diseaseAstrogliosisAnesthesiology and Pain Medicinemedicine.anatomical_structureNeuroprotective AgentsImmunologyChronic DiseaseMicrogliamedicine.symptomInflammation MediatorsbusinessBest practiceresearch. Clinical anaesthesiology
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Regulation of cholesterol metabolism in the retina under experimental conditions associated with glaucoma

2019

Cholesterol is a lipid found in every animal cell and is necessary for its survival. Among its multiple roles in the body, it is a component of cell membranes that is crucial for the maintenance of their structure and fluidity and is thus implicated in the modulation of many signalling pathways. Neurons are especially dependant on cholesterol input since the proper composition of their plasma membrane is required for vesicular exocytosis of neurotransmitters and transduction of the post-synaptic signal. It has been shown that both an excess and a lack of cholesterol is neurotoxic. Moreover, many neurodegenerative diseases, such as Alzheimer’s or Huntington’s disease, have been associated wi…

Müller cellsInflammation24(S)-Hydroxycholesterol24(S)-HydroxycholestérolGlioseCellules de MüllerLaser photocoagulationGliosisHyperpression oculaireOcular hypertensionPhotocoagulation laser[SDV.BBM.BC] Life Sciences [q-bio]/Biochemistry Molecular Biology/Biochemistry [q-bio.BM][SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biomolecules [q-bio.BM]
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