Search results for "bicuculline"

showing 10 items of 40 documents

Mild systemic inflammation and moderate hypoxia transiently alter neuronal excitability in mouse somatosensory cortex

2016

During the perinatal period, the brain is highly vulnerable to hypoxia and inflammation, which often cause white matter injury and long-term neuronal dysfunction such as motor and cognitive deficits or epileptic seizures. We studied the effects of moderate hypoxia (HYPO), mild systemic inflammation (INFL), or the combination of both (HYPO + INFL) in mouse somatosensory cortex induced during the first postnatal week on network activity and compared it to activity in SHAM control animals. By performing in vitro electrophysiological recordings with multi-electrode arrays from slices prepared directly after injury (P8–10), one week after injury (P13–16), or in young adults (P28–30), we investig…

Male0301 basic medicineAction PotentialsKainate receptorStimulationPotassium ChlorideMicechemistry.chemical_compound0302 clinical medicineHypoxia6-Cyano-7-nitroquinoxaline-23-dioneNeuronsAge FactorsInterleukin-1βElectrophysiologyEpileptiform activityNeurologyAnesthesiaCNQXNMDA receptorFemalemedicine.symptommedicine.drugmedicine.medical_specialtyAMPA receptorIn Vitro TechniquesBiologyBicucullineMulti-electrode arrayArticlelcsh:RC321-57103 medical and health sciencesInternal medicinemedicineAnimalsGABA-A Receptor Antagonistslcsh:Neurosciences. Biological psychiatry. NeuropsychiatryInflammationSystemic inflammationSomatosensory CortexHypoxia (medical)BicucullineBarrel cortexMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinology2-Amino-5-phosphonovalerateGene Expression Regulationchemistrynervous systemExploratory BehaviorExcitatory Amino Acid Antagonists030217 neurology & neurosurgeryNeurobiology of Disease
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GABA receptors are involved in the modulation of the release of 5-hydroxytryptamine from the vascularly perfused small intestine of the guinea-pig

1989

Isolated small intestinal segments of the guinea-pig were perfused arterially and the release of 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) into the portal venous effluent was determined by HPLC with electrochemical detection. Test substances were applied intraarterially. Muscimol (1 microM) time dependently first increased then decreased the release of 5-HT and 5-HIAA. The stimulatory effect was prevented by tetrodotoxin (TTx) or scopolamine, indicating that it was mediated by the release of acetylcholine. Bicuculline concentration dependently decreased (1 microM) or increased (10, 50 microM) the release of 5-HT and 5-HIAA, indicating that endogenous GABA also activ…

MaleBaclofenSerotoninmedicine.medical_specialtyGuinea PigsTetrodotoxinIn Vitro TechniquesBiologyGABAB receptorBicucullineInhibitory postsynaptic potential5-Hydroxytryptophanchemistry.chemical_compoundInternal medicineIntestine SmallmedicineAnimalsReceptorPharmacologyMuscimolGABAA receptorOxotremorineMuscle SmoothHydroxyindoleacetic AcidBicucullineReceptors GABA-APerfusionEndocrinologynervous systemMuscimolchemistryFemaleSerotoninAcetylcholinemedicine.drugEuropean Journal of Pharmacology
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A repetitive intracortical microstimulation pattern induces long-lasting synaptic depression in brain slices of the rat primary somatosensory cortex.

2000

Repetitive intracortical microstimulation (ICMS) applied to the rat primary somatosensory cortex (SI) in vivo was reported to induce reorganization of receptive fields and cortical maps. The present study was designed to exam- ine the effect of such an ICMS pattern applied to layer IV of brain slices containing SI on the efficacy of synaptic in- put to layer II/III. Effects of ICMS on the synaptic strength was quantified for the first synaptic component ( s1) of cor- tical field potentials (FPs) recorded from layer II/III of SI. FPs were evoked by stimulation in layer IV. The pattern of ICMS was identical to that used in vivo. However, stimula- tion intensity had to be raised to induce an a…

MaleLong-Term PotentiationNeurotransmissionIn Vitro TechniquesInhibitory postsynaptic potentialBicucullineReceptors N-Methyl-D-AspartateGABA AntagonistsRats Sprague-DawleymedicineAnimalsReceptors AMPASynaptic potentialNeuronal PlasticityChemistryGeneral NeuroscienceLong-term potentiationSomatosensory CortexBicucullineElectric StimulationRatsElectrophysiologyembryonic structuresSynaptic plasticitySynapsesExcitatory postsynaptic potentialNeuroscienceMicroelectrodesmedicine.drugExperimental brain research
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Opposite motor responses elicited by ethanol in the posterior VTA: The role of acetaldehyde and the non-metabolized fraction of ethanol

2013

Recent electrophysiological evidence suggests that ethanol simultaneously exerts opposite effects on the activity of dopamine (DA) neurons in the ventral tegmental area (VTA) through two parallel mechanisms, one promoting and the other reducing the GABA release onto VTA DA neurons. Here we explore the possible behavioural implications of these findings by investigating the role displayed by acetaldehyde (the main metabolite of ethanol) and the non-metabolized fraction of ethanol in motor activity of rats. We analyse the appearance of motor activation or depression after intra-VTA administration of ethanol in rats subjected to different pharmacological pre-treatments designed to preferential…

MaleMicroinjectionsMetaboliteGABA(A) receptorsAcetaldehydePharmacologyMotor ActivityNon-metabolized fraction of ethanolBicucullineCellular and Molecular Neurosciencechemistry.chemical_compoundDopaminemedicineAnimalsGABA-A Receptor AntagonistsEnzyme InhibitorsRats WistarPharmacologyEthanolDose-Response Relationship DrugEthanolChemistryGABAA receptorVentral Tegmental AreaAcetaldehydeCentral Nervous System DepressantsBicucullineRatsVentral tegmental areaElectrophysiologymedicine.anatomical_structureBiochemistrynervous systemCyanamideVTAmedicine.drug
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Role of GABAergic antagonism in the neuroprotective effects of bilobalide

2006

Bilobalide, a constituent of Ginkgo biloba, has neuroprotective properties. Its mechanism of action is unknown but it was recently found to block GABA(A) receptors. The goal of this study was to test the potential role of a GABAergic mechanism for the neuroprotective activity of bilobalide. In rat hippocampal slices exposed to NMDA, release of choline indicates breakdown of membrane phospholipids. NMDA-induced choline release was almost completely blocked in the presence of bilobalide (10 microM) and under low-chloride conditions. Bicuculline (100 microM), a competitive antagonist at GABA(A) receptors, reduced NMDA-induced choline release to a small extent (-23%). GABA (100 microM) partiall…

MaleN-MethylaspartateBrain EdemaCyclopentanesIn Vitro TechniquesPharmacologyBicucullineInhibitory postsynaptic potentialHippocampusArticlegamma-Aminobutyric acidCholineGABA AntagonistsRats Sprague-Dawleychemistry.chemical_compoundBilobalideExcitatory Amino Acid AgonistsmedicineAnimalsPicrotoxinDrug InteractionsFuransMolecular Biologygamma-Aminobutyric AcidChemistryGABAA receptorGeneral NeuroscienceBicucullineGABA receptor antagonistBridged Bicyclo Compounds HeterocyclicRatsGinkgolidesNeuroprotective Agentsnervous systemNonlinear DynamicsMechanism of actionArea Under CurveGABAergicNeurology (clinical)medicine.symptomSynaptosomesDevelopmental Biologymedicine.drugBrain Research
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Lateral habenula and hippocampus: A complex interaction raphe cells-mediated

1997

The study has shown an excitatory influence exerted by lateral habenula (LH) on hippocampal pyramidal cells. The modulatory influence is paradoxically serotonine-mediated; in fact all LH stimulation effects were abolished by intrahippocampal iontophoretic methysergide application. The data suggest the involvement of dorsal raphe nucleus. In fact, the dorsal raphe nucleus stimulation caused on hippocampus an expected inhibitory effect antagonized by intrahippocampal iontophoretic methysergide application. In the context of this neural structure we have highlighted a disinhibitory relation between two types of cells: slow serotonergic efferent neurones and fast GABAergic interneurones. The di…

MaleN-MethylaspartateMethysergideCell CommunicationBicucullineGABA AntagonistsDorsal raphe nucleusmedicineAnimalsRats WistarBiological PsychiatryNeuronsHabenulaRapheChemistryPyramidal CellsIontophoresisBicucullineGABA receptor antagonistElectric StimulationRatsPsychiatry and Mental healthHabenula2-Amino-5-phosphonovaleratenervous systemNeurologyRaphe NucleiGABAergicNeurology (clinical)Raphe nucleiNeurosciencemedicine.drugJournal of Neural Transmission
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Intensity of GABA-evoked responses is modified by nitric oxide-active compounds in the subthalamic nucleus of the rat: a microiontophoretic study.

2009

We have previously described modulatory effects of nitric oxide (NO)-active drugs on subthalamic nucleus (STN) neurons. In this study, the effects of microiontophoretically applied NO-active compounds on GABA-evoked responses were investigated in subthalamic neurons extracellularly recorded from anesthetized rats: 45 of 62 cells were excited by S-nitroso-glutathione (SNOG), an NO donor, whereas 28 of 43 neurons were inhibited by N-nitro-L-arginine methyl ester (L-NAME), a NOS inhibitor. Nearly all neurons responding to SNOG and/or L-NAME showed significant inhibitory responses to the administration of iontophoretic GABA. In these cells, the changes induced by NO-active drugs in the magnitud…

MaleNOS inhibitormedicine.drug_classBiophysicsAction PotentialsGlutamic AcidPharmacologyNeurotransmissionInhibitory postsynaptic potentialBicucullineNitric OxideSettore BIO/09 - FisiologiaNitric oxideGABA AntagonistsCellular and Molecular Neurosciencechemistry.chemical_compoundSubthalamic NucleusmedicineAnimalsDrug InteractionsNitric Oxide DonorsEnzyme InhibitorsRats Wistargamma-Aminobutyric AcidNeuronssubthalamic nucleus GABA SNOG L-NAMEIontophoresisBicucullineIontophoresisReceptor antagonistElectric StimulationRatsSubthalamic nucleusNG-Nitroarginine Methyl Esternervous systemchemistryS-Nitrosoglutathionemedicine.drugJournal of neuroscience research
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The gamma(2)-MSH peptide mediates a central analgesic effect via a GABA-ergic mechanism that is independent from activation of melanocortin receptors.

2001

Using the latency for tail-flick after thermal stimulation we have assessed the effects of alpha-, gamma(1)- and gamma(2)-MSH on nociceptive threshold in the mice. Intracisternal injections of gamma(2)-MSH induced a distinct analgesia, while gamma(1)-MSH in the same doses gave only a minor analgesia. Intracisternal alpha-MSH instead gave a short-term hyperalgesia. The effect of gamma(2)-MSH was not blocked by any of the MC(4)/MC(3)receptor antagonist HS014, naloxone or by the prior intracisternal administrations of gamma(1)-MSH. However, the gamma(2)-MSH analgesic response was completely attenuated by treating animals with the GABA(A)antagonist bicuculline. The gamma(2)-MSH analgesic effect…

MaleNarcotic Antagonists(+)-NaloxonePharmacologyGABA Antagonistschemistry.chemical_compoundMiceEndocrinologyDrug Interactionsgamma-Aminobutyric AcidAnalgesicsMice Inbred BALB Cintegumentary systemMuscimolNaloxoneReceptors MelanocortinNociceptorsGeneral MedicineReceptor antagonistNeurologyHyperalgesiamedicine.symptomhormones hormone substitutes and hormone antagonistsmedicine.drugPain ThresholdTailendocrine systemmedicine.medical_specialtyanimal structuresmedicine.drug_classCatalepsyBicucullinePeptides CyclicCellular and Molecular Neurosciencegamma-MSHMelanocortin receptorInternal medicinemedicineAnimalsGABA ModulatorsGABA AgonistsCatalepsyDiazepamEthanolEndocrine and Autonomic SystemsAntagonistCentral Nervous System DepressantsBicucullinemedicine.diseaseEndocrinologyMuscimolchemistryReceptors Corticotropinalpha-MSHNeuropeptides
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Interaction Between Uridine and GABA-Mediated Inhibitory Transmission: Studies In Vivo and In Vitro

1985

Na+-independent [3H]gamma-aminobutyric acid (GABA) binding to membrane preparations from frontal cortex, hippocampus, and thalamus is competitively inhibited by the in vitro addition of a naturally occurring pyrimidinic compound, uridine. Moreover, the intraperitoneal injection of uridine produces a dose-related decrease in the cerebellar content of cyclic GMP and antagonizes its increase elicited by bicuculline. The pyrimidinic compound also shows an antagonism toward bicuculline-induced seizures. The relationship between the anti-convulsant actions of uridine and GABA-mediated inhibitory neurotransmission is discussed in terms of an activation of GABA receptor function by the naturally oc…

MaleSynaptic MembranesNeurotransmissionPharmacologyBicucullineInhibitory postsynaptic potentialHippocampusSynaptic Transmissiongamma-Aminobutyric acidchemistry.chemical_compoundThalamusGABA receptorSeizuresIn vivomedicineAnimalsCyclic GMPUridinegamma-Aminobutyric AcidNeurotransmitter AgentsBicucullineReceptors GABA-AUridineIn vitroFrontal LobeRatsnervous systemNeurologychemistryBiochemistryNeurology (clinical)medicine.drugEpilepsia
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Homogenous glycine receptor expression in cortical plate neurons and cajal-retzius cells of neonatal rat cerebral cortex

2004

Glycinergic membrane responses have been described in cortical plate neurons (CPn) and Cajal-Retzius cells (CRc) during early neocortical development. In order to elucidate the functional properties and molecular identity of glycine receptors in these two neuronal cell types, we performed whole-cell patch-clamp recordings and subsequent single-cell multiplex reverse transcriptase-polymerase chain reaction (RT-PCR) analyses on visually identified neurons in tangential and coronal slices as well as in situ hybridizations of coronal slices from neonatal rat cerebral cortex (postnatal days 0-4). In both CPn and CRc the glycinergic agonists glycine, beta-alanine and taurine induced inward curren…

Malemedicine.drug_classBiologyMembrane PotentialsGABA Antagonistschemistry.chemical_compoundReceptors GlycinemedicineAnimalsPatch clampRats WistarReceptorGlycine receptorCerebral CortexNeuronsDose-Response Relationship DrugGeneral NeuroscienceGene Expression Regulation DevelopmentalStrychnineBicucullineReceptor antagonistMolecular biologyRatsAnimals NewbornchemistryBiochemistryGlycineNMDA receptorExcitatory Amino Acid Antagonistsmedicine.drugNeuroscience
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