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Intraventricular haemorrhage in premature infants: the role of immature neuronal salt and water transport.
Bahari, Fatemeh; Dzhala, Volodymyr; Balena, Trevor; Lillis, Kyle P; Staley, Kevin J.
Afiliación
  • Bahari F; Department of Neurology, Massachusetts General Hospital, Boston, MA 02114, USA.
  • Dzhala V; Department of Neurology, Harvard Medical School, Boston, MA 02115, USA.
  • Balena T; Department of Neurology, Massachusetts General Hospital, Boston, MA 02114, USA.
  • Lillis KP; Department of Neurology, Harvard Medical School, Boston, MA 02115, USA.
  • Staley KJ; Department of Neurology, Massachusetts General Hospital, Boston, MA 02114, USA.
Brain ; 147(9): 3216-3233, 2024 Sep 03.
Article en En | MEDLINE | ID: mdl-38815055
ABSTRACT
Intraventricular haemorrhage is a common complication of premature birth. Survivors are often left with cerebral palsy, intellectual disability and/or hydrocephalus. Animal models suggest that brain tissue shrinkage, with subsequent vascular stretch and tear, is an important step in the pathophysiology, but the cause of this shrinkage is unknown. Clinical risk factors for intraventricular haemorrhage are biomarkers of hypoxic-ischaemic stress, which causes mature neurons to swell. However, immature neuronal volume might shift in the opposite direction in these conditions. This is because immature neurons express the chloride, salt and water transporter NKCC1, which subserves regulatory volume increases in non-neural cells, whereas mature neurons express KCC2, which subserves regulatory volume decreases. When hypoxic-ischaemic conditions reduce active ion transport and increase the cytoplasmic membrane permeability, the effects of these transporters are diminished. Consequentially, mature neurons swell (cytotoxic oedema), whereas immature neurons might shrink. After hypoxic-ischaemic stress, in vivo and in vitro multi-photon imaging of perinatal transgenic mice demonstrated shrinkage of viable immature neurons, bulk tissue shrinkage and blood vessel displacement. Neuronal shrinkage was correlated with age-dependent membrane salt and water transporter expression using immunohistochemistry. Shrinkage of immature neurons was prevented by prior genetic or pharmacological inhibition of NKCC1 transport. These findings open new avenues of investigation for the detection of acute brain injury by neuroimaging, in addition to prevention of neuronal shrinkage and the ensuing intraventricular haemorrhage, in premature infants.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Recien Nacido Prematuro / Miembro 2 de la Familia de Transportadores de Soluto 12 / Neuronas Límite: Animals / Humans / Newborn Idioma: En Revista: Brain Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Recien Nacido Prematuro / Miembro 2 de la Familia de Transportadores de Soluto 12 / Neuronas Límite: Animals / Humans / Newborn Idioma: En Revista: Brain Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido