6533b858fe1ef96bd12b6e0f

RESEARCH PRODUCT

Nitric Oxide/Cyclic Guanosine Monophosphate Signaling via Guanylyl Cyclase Isoform 1 Mediates Early Changes in Synaptic Transmission and Brain Edema Formation after Traumatic Brain Injury.

Thomas MittmannDoris KoeslingQi WangEvanthia Mergia

subject

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 Transduction

description

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 performed an

yearjournalcountryeditionlanguage
2021-01-12Journal of neurotrauma
10.1089/neu.2020.7364https://pubmed.ncbi.nlm.nih.gov/33427032