0000000000082230

AUTHOR

Evanthia Mergia

showing 4 related works from this author

Presynaptic nitric oxide/cGMP facilitates glutamate release via hyperpolarization-activated cyclic nucleotide-gated channels in the hippocampus

2011

In hippocampal neurons, synaptic transmission is affected by a variety of modulators, including nitric oxide (NO), which was proposed as a retrograde messenger as long as two decades ago. NO signals via two NO-sensitive guanylyl cyclases (NO-GCs) (NO-GC1 and NO-GC2) and the subsequent increase in cGMP. Lack of long-term potentiation in mice deficient in either one of the two NO-GCs demonstrates the involvement of both NO-GCs in synaptic transmission. However, the physiological consequences of NO/cGMP and the cellular mechanisms involved are unknown. Here, we analyzed glutamatergic synaptic transmission, most likely reflecting glutamate release, in the hippocampal CA1 region of NO-GC knockou…

General NeuroscienceGlutamate receptorLong-term potentiationHyperpolarization (biology)BiologyNeurotransmissionNitric oxideCell biologychemistry.chemical_compoundGlutamatergicBiochemistrychemistryRetrograde signalingSoluble guanylyl cyclaseEuropean Journal of Neuroscience
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Nitric oxide/cGMP signaling via guanylyl cyclase isoform 1 modulates glutamate and GABA release in somatosensory cortex of mice

2017

Abstract In hippocampus, two guanylyl cyclases (NO-GC1 and NO-GC2) are involved in the transduction of the effects of nitric oxide (NO) on synaptic transmission. However, the respective roles of the NO-GC isoforms on synaptic transmission are less clear in other regions of the brain. In the present study, we used knock-out mice deficient for the NO-GC1 isoform (NO-GC1 KO) to analyze its role in the glutamatergic and GABAergic neurotransmission at pyramidal neurons in layers II/III of somatosensory cortex. NO-GC1 KO slices revealed reduced frequencies of miniature excitatory- and inhibitory-postsynaptic currents, increased paired-pulse ratios and decreased input–output curves of evoked signa…

0301 basic medicineendocrine systemgenetic structuresGlutamic AcidReceptors Cell SurfaceAMPA receptorBiologyNeurotransmissionNitric OxideInhibitory postsynaptic potentialHippocampusSynaptic Transmission03 medical and health sciencesGlutamatergicSoluble Guanylyl Cyclase0302 clinical medicineAnimalsCyclic GMPgamma-Aminobutyric AcidMice KnockoutGeneral NeuroscienceGlutamate receptorSomatosensory CortexCell biology030104 developmental biologyGuanylate CyclaseSynapsesExcitatory postsynaptic potentialNMDA receptorGABAergicNeuroscience030217 neurology & neurosurgeryNeuroscience
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Nitric Oxide/Cyclic Guanosine Monophosphate Signaling via Guanylyl Cyclase Isoform 1 Mediates Early Changes in Synaptic Transmission and Brain Edema …

2021

Traumatic brain injury (TBI) often induces structural damage, disruption of the blood-brain barrier (BBB), neurodegeneration, and dysfunctions of surviving neuronal networks. Nitric oxide (NO) signaling has been suggested to affect brain functions after TBI. The NO exhibits most of its biological effects by activation of the primary targets-guanylyl cyclases (NO-GCs), which exists in two isoforms (NO-GC1 and NO-GC2), and the subsequently produced cyclic guanosine monophosphate (cGMP). However, the specific function of the NO-NO-GCs-cGMP pathway in the context of brain injury is not fully understood. To investigate the specific role of the isoform NO-GC1 early after brain injuries, we perfor…

Gene isoform030506 rehabilitationTraumatic brain injuryBrain EdemaReceptors Cell SurfaceNeurotransmissionBlood–brain barrierNitric OxideSynaptic TransmissionNitric oxide03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineBrain Injuries TraumaticmedicinePremovement neuronal activityAnimalsCyclic guanosine monophosphateCyclic GMPMice KnockoutNeurodegenerationSomatosensory Cortexmedicine.diseaseIsoenzymesmedicine.anatomical_structurenervous systemchemistryGuanylate CyclaseNeurology (clinical)0305 other medical scienceNeuroscience030217 neurology & neurosurgerySignal TransductionJournal of neurotrauma
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Postsynaptic NO/cGMP Increases NMDA Receptor Currents via Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels in the Hippocampus

2013

The nitric oxide (NO)/cyclic guanosine monophosphate (cGMP) signaling cascade participates in the modulation of synaptic transmission. The effects of NO are mediated by the NO-sensitive cGMP-forming guanylyl cyclases (NO-GCs), which exist in 2 isoforms with indistinguishable regulatory properties. The lack of long-term potentiation (LTP) in knock-out (KO) mice deficient in either one of the NO-GC isoforms indicates the contribution of both NO-GCs to LTP. Recently, we showed that the NO-GC1 isoform is located presynaptically in glutamatergic neurons and increases the glutamate release via hyperpolarization-activated cyclic nucleotide (HCN)-gated channels in the hippocampus. Electrophysiologi…

Patch-Clamp TechniquesCognitive NeuroscienceLong-Term PotentiationIn Vitro TechniquesNeurotransmissionNitric OxideReceptors N-Methyl-D-AspartateMiceCellular and Molecular Neurosciencechemistry.chemical_compoundCyclic nucleotidePostsynaptic potentialHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsHCN channelAnimalsAnesthetics LocalCA1 Region HippocampalCyclic GMPCyclic guanosine monophosphateMice KnockoutNeuronsbiologyLidocaineTetraethylammoniumLong-term potentiationHyperpolarization (biology)Electric StimulationPyrimidinesAnimals Newbornnervous systemchemistryGuanylate CyclaseBiophysicsbiology.proteinNMDA receptorExcitatory Amino Acid AntagonistsNeuroscienceCerebral Cortex
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