The benzodiazepine Midazolam mitigates the breathing defects of Mecp2-deficient mice

Respir Physiol Neurobiol. 2011 Jun 30;177(1):56-60. doi: 10.1016/j.resp.2011.02.002. Epub 2011 Feb 22.

Abstract

Rett syndrome is a severe neurodevelopmental disease caused by mutations of the transcriptional repressor methyl-CpG-binding protein 2 (MeCP2) that induce complex, disabling symptoms, including breathing symptoms. Males of Mecp2-deficient mice (Mecp2(-/y)) normally breathe at birth but develop first altered breathing regulations, thereafter erratic breathing with severe apnoeas, aggravating until respiratory distress and premature death. Mecp2(-/y) mice also develop early GABA deficits. To examine whether GABA deficits contributed to breathing defects of Mecp2(-/y) mice, mice were subjected to acute administration of Midazolam, a benzodiazepine of clinical use known to enhance GABA effects. For the first time, we showed that Midazolam abolished, although transiently, the breathing defects of Mecp2(-/y) mice, confirming a crucial role of GABA deficits in their breathing defects.

MeSH terms

  • Animals
  • Benzodiazepines / pharmacology
  • Disease Models, Animal
  • GABA Agonists / pharmacology*
  • Methyl-CpG-Binding Protein 2 / deficiency
  • Methyl-CpG-Binding Protein 2 / genetics
  • Mice
  • Mice, Knockout
  • Midazolam / pharmacology*
  • Rett Syndrome / genetics
  • Rett Syndrome / metabolism*
  • Rett Syndrome / physiopathology
  • gamma-Aminobutyric Acid / metabolism*

Substances

  • GABA Agonists
  • Mecp2 protein, mouse
  • Methyl-CpG-Binding Protein 2
  • Benzodiazepines
  • gamma-Aminobutyric Acid
  • Midazolam