title: [Brain repair after ischemic stroke: role of neurotransmitters in post-ischemic neurogenesis].
abstract: BACKGROUND
  Brain ischemia and reperfusion produce alterations in the microenvironment of the parenchyma, including ATP depletion, ionic homeostasis alterations, inflammation, release of multiple cytokines and abnormal release of neurotransmitters. As a consequence, the induction of proliferation and migration of neural stem cells towards the peri-infarct region occurs.
  
  
  METHODS
  The success of new neurorestorative treatments for damaged brain implies the need to know, with greater accuracy, the mechanisms in charge of regulating adult neurogenesis, both under physiological and pathological conditions. Recent evidence demonstrates that many neurotransmitters, glutamate in particular, control the subventricular zone, thus being part of the complex signalling network that influences the production of new neurons.
  
  
  CONCLUSIONS
  Neurotransmitters provide a link between brain activity and subventricular zone neurogenesis. Therefore, a deeper knowledge of the role of neurotransmitters systems, such as glutamate and its transporters, in adult neurogenesis, may provide a valuable tool to be used as a neurorestorative therapy in this pathology.
authors.affiliation: Departamento de Bioquímica y Biología Molecular II, Facultad de Farmacia, Universidad Complutense de Madrid, España.
authors.forename: Eduardo
authors.initials: E
authors.lastname: Sánchez-Mendoza
authors.forename: Víctor
authors.initials: V
authors.lastname: Bellver-Landete
authors.forename: María Pilar
authors.initials: MP
authors.lastname: González
authors.forename: José Joaquín
authors.initials: JJ
authors.lastname: Merino
authors.forename: Ricardo
authors.initials: R
authors.lastname: Martínez-Murillo
authors.forename: María Jesús
authors.initials: MJ
authors.lastname: Oset-Gasque
mesh_terms: D053687:Adult Stem Cells / Q000502:physiology; D000818:Animals; D001921:Brain / Q000502:physiology*; D001925:Brain Damage, Chronic / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control; D002545:Brain Ischemia / Q000188:drug therapy / Q000503:physiopathology*; D015687:Cell Hypoxia; D002465:Cell Movement; D050491:Glutamate Plasma Membrane Transport Proteins / Q000502:physiology; D018698:Glutamic Acid / Q000502:physiology; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins / Q000502:physiology; D047908:Intracellular Signaling Peptides and Proteins / Q000502:physiology; D008959:Models, Neurological; D009419:Nerve Tissue Proteins / Q000502:physiology; D058953:Neural Stem Cells / Q000502:physiology; D055495:Neurogenesis / Q000502:physiology*; D018377:Neurotransmitter Agents / Q000502:physiology* / Q000627:therapeutic use; D017978:Receptors, Growth Factor / Q000502:physiology; D017981:Receptors, Neurotransmitter / Q000502:physiology; D012038:Regeneration / Q000502:physiology*; D015427:Reperfusion Injury / Q000503:physiopathology; D014157:Transcription Factors / Q000502:physiology
chemical_list: D050491:Glutamate Plasma Membrane Transport Proteins; D036341:Intercellular Signaling Peptides and Proteins; D047908:Intracellular Signaling Peptides and Proteins; D009419:Nerve Tissue Proteins; D018377:Neurotransmitter Agents; D017978:Receptors, Growth Factor; D017981:Receptors, Neurotransmitter; D014157:Transcription Factors; D018698:Glutamic Acid