Search results for "NBQX"

showing 3 items of 3 documents

Phencyclidine-induced disruption of oscillatory activity in prefrontal cortex: Effects of antipsychotic drugs and receptor ligands

2016

The non-competitive NMDA receptor (NMDA-R) antagonist phencyclidine (PCP) markedly disrupts thalamocortical activity, increasing excitatory neuron discharge and reducing low frequency oscillations (LFO, <4Hz) that temporarily group neuronal discharge. These actions are mainly driven by PCP interaction with NMDA-R in GABAergic neurons of the thalamic reticular nucleus and likely underlie PCP psychotomimetic activity. Here we report that classical (haloperidol, chlorpromazine, perphenazine) and atypical (clozapine, olanzapine, quetiapine, risperidone, ziprasidone, aripripazole) antipsychotic drugs - but not the antidepressant citalopram - countered PCP-evoked fall of LFO in the medial prefron…

Male0301 basic medicineOscillationsmedicine.drug_classDopamine AgentsAtypical antipsychoticPhencyclidineKainate receptorPharmacologyNeurotransmissionPrefrontal cortex03 medical and health scienceschemistry.chemical_compoundSerotonin Agents0302 clinical medicineHistamine AgentsmedicineAnimalsPharmacology (medical)NMDA receptor antagonistsAntipsychotic drugsRats WistarChlorpromazineEvoked PotentialsPhencyclidineBiological PsychiatryPharmacologyRacloprideAnalysis of VarianceDose-Response Relationship DrugFourier AnalysisChemistryElectroencephalographyPsychotomimeticRatsPsychiatry and Mental health030104 developmental biologyNeurologynervous systemSchizophreniaNBQXNeurology (clinical)Excitatory Amino Acid AntagonistsNeuroscience030217 neurology & neurosurgeryAntipsychotic Agentsmedicine.drug
researchProduct

Molecular and functional interactions between tumor necrosis factor-alpha receptors and the glutamatergic system in the mouse hippocampus: Implicatio…

2009

Tumor necrosis factor (TNF)-alpha is a proinflammatory cytokine acting on two distinct receptor subtypes, namely p55 and p75 receptors. TNF-alpha p55 and p75 receptor knockout mice were previously shown to display a decreased or enhanced susceptibility to seizures, respectively, suggesting intrinsic modifications in neuronal excitability. We investigated whether alterations in glutamate system function occur in these naive knockout mice with perturbed cytokine signaling that could explain their different propensity to develop seizures. Using Western blot analysis of hippocampal homogenates, we found that p55(-/-) mice have decreased levels of membrane GluR3 and NR1 glutamate receptor subuni…

Malemedicine.medical_specialtyReceptors Kainic acidMicrodialysisAction PotentialsGlutamic AcidKainate receptorAMPA receptorIn Vitro TechniquesBiologyHippocampusReceptors N-Methyl-D-Aspartateelectrophysiology microiontophoresisSettore BIO/09 - FisiologiaMicechemistry.chemical_compoundGlutamatergicReceptors Kainic AcidSeizuresInternal medicinemedicineAnimalsReceptors Tumor Necrosis Factor Type IIReceptors AMPAMice KnockoutNeuronsInflammationTumor Necrosis Factor-alphaGeneral NeuroscienceGlutamate receptorProtein SubunitsEndocrinologymedicine.anatomical_structureReceptors Glutamatenervous systemchemistryReceptors Tumor Necrosis Factor Type IMetabotropic glutamate receptorAstrocytesCytokinesNMDA receptorNBQXDisease SusceptibilityAstrocyte
researchProduct

The effects of glutamate receptor antagonists on cerebellar granule cell survival and development.

2007

N-Methyl-d-aspartate (NMDA) receptor stimulation promotes neuronal survival and differentiation under both in vitro and in vivo conditions. We studied the effects of various NMDA receptor antagonists acting at different NMDA receptor binding sites and non-NMDA receptor antagonists on the development and survival of cerebellar granule cell (CGC) culture. Only three of the drugs tested induced neurotoxicity-MK-801 (non-competitive NMDA channel blocking antagonist), ifenprodil (an antagonist of the NR2B site and polyamine site of the NMDA receptor) and L-701.324 (full antagonist at glycine site), while CGP-37849 (a competitive NMDA antagonist), (+)-HA-966 (a partial agonist of the glycine site…

N-MethylaspartateTime FactorsNeuriteCell SurvivalGlutamic AcidTetrazolium SaltsAMPA receptorPharmacologyBiologyToxicologyNeuroprotectionchemistry.chemical_compoundCerebellumIfenprodilExcitatory Amino Acid AgonistsIn Situ Nick-End LabelingAnimalsDrug InteractionsRats WistarCells CulturedNeuronsAnalysis of VarianceCell DeathDose-Response Relationship DrugGeneral NeuroscienceGlutamic acidRatsThiazolesnervous systemchemistryBiochemistryAnimals NewbornCompetitive antagonistNMDA receptorNBQXExcitatory Amino Acid AntagonistsNeurotoxicology
researchProduct