Enhanced Hypoxia Susceptibility in Hippocampal Slices From a Mouse Model of Rett Syndrome
Abstract
Rett syndrome is a neurodevelopmental disorder caused by mutations in the X-chromosomal MECP2 gene encoding for the transcriptional regulator methyl CpG binding protein 2 (MeCP2). Rett patients suffer from episodic respiratory irregularities and reduced arterial oxygen levels. To elucidate whether such intermittent hypoxic episodes induce adaptation/preconditioning of the hypoxia-vulnerable hippocampal network, we analyzed its responses to severe hypoxia in adult Rett mice. The occurrence of hypoxia-induced spreading depression (HSD)—an experimental model for ischemic stroke—was hastened in Mecp2− /y males. The extracellular K+ rise during HSD was attenuated in Mecp2− /y males and the input resistance of CA1 pyramidal neurons decreased less before HSD onset. CA1 pyramidal neurons were smaller and more densely packed, but the cell swelling during HSD was unaffected. The intrinsic optical signal and the propagation of HSD were similar among the different genotypes. Basal synaptic function was intact, but Mecp2− /y males showed reduced paired-pulse facilitation and higher field potential/fiber volley ratios, but no increased seizure susceptibility. Synaptic failure during hypoxia was complete in all genotypes and the final degree of posthypoxic synaptic recovery indistinguishable. Cellular ATP content was normal in Mecp2− /y males, but their hematocrit was increased as was HIF-1α expression throughout the brain. This is the first study showing that in Rett syndrome, the susceptibility of telencephalic neuronal networks to hypoxia is increased; the underlying molecular mechanisms apparently involve disturbed K+ channel function. Such an increase in hypoxia susceptibility may potentially contribute to the vulnerability of male Rett patients who are either not viable or severely disabled.
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Studies of animal models suggest that genetic defects in synaptic function may alter sensitivity to the environment.
“studies of animal models have suggested that genetic defects in synaptic function may alter sensitivity to the environment.”
From Autism risk factors: genes, environment, and gene-environment interactions (2012) · cites this paper as [98]
Hippocampal slices from MecP2-deficient mice are more susceptible to hypoxia.
“Another study reported that the hippocampal slices from MecP2- deficient mice are more susceptible to hypoxia.98”
From Autism risk factors: genes, environment, and gene-environment interactions (2012) · cites this paper as [98]
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Brain Poster Session: Experimental Stroke and Cerebral Ischemia
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- Authors
- Fischer, M., Reuter, J., Gerich, F. J., Hildebrandt, B., Hägele, S., Katschinski, D., & Müller, M.
- Affiliations
- University of Göttingen (DE)
- Venue
- Journal of Neurophysiology
- Publisher
- American Physiological Society
- Published
- 2009-02
- Volume
- 101
- Issue
- 2
- Pages
- 1016-1032
- ISSN
- 0022-3077 (ISSN-L)
- 1522-1598
- OpenAlex
- W2153195998
- Cited by
- 65
- References
- 78
- Citations by year
- 2025: 3 · 2024: 2 · 2023: 5 · 2022: 6 · 2021: 6 · 2020: 2 · 2019: 3 · 2018: 1 · 2017: 4 · 2016: 4 · 2015: 4 · 2014: 6 · 2013: 5 · 2012: 6
- FWCI
- 1.52
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neurophysiology (publishedVersion)
- PubMed (publishedVersion)
- GRO (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Neuroscience of respiration and sleep
- Health Sciences › Medicine › Psychiatry and Mental health › Migraine and Headache Studies
- Keywords
- Rett syndrome, MeCP2, cortical spreading depression, ischemic stroke, hippocampus, CA1 pyramidal neurons, potassium channel dysfunction, extracellular potassium, input resistance, synaptic failure, HIF-1α, hematocrit, neurodevelopmental disorders
- MeSH terms
- Adenosine Triphosphate, Quaternary Ammonium Compounds, Animals, Hypoxia, Bicuculline, Disease Models, Animal, Disease Susceptibility, Edema, Electric Stimulation, Evoked Potentials, Exons, Female, Hippocampus, Male, Mice, Inbred C57BL, Potassium, Reaction Time, Sex Factors, Rett Syndrome, 4-Aminopyridine, Mice, Knockout, GABA Antagonists, Excitatory Postsynaptic Potentials, Potassium Channel Blockers, Mice, Methyl-CpG-Binding Protein 2, Hypoxia-Inducible Factor 1, alpha Subunit, In Vitro Techniques
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