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Reduced Gamma Oscillations in a Mouse Model of Intellectual Disability: A Role for Impaired Repetitive Neurotransmission?
The findings suggest that the intellectual disability due to mutations of oligophrenin-1 results from a synaptopathy and consequent network malfunction, providing a plausible mechanism for the learning disabilities, and raise the prospect of drug treatments for affected individuals.
Rapid reversal of impaired inhibitory and excitatory transmission but not spine dysgenesis in a mouse model of mental retardation
- Andrew D. Powell, Kalbinder K. Gill, John Gordon Ralph Jefferys
- BiologyJournal of Physiology
- 1 February 2012
It is shown that, in addition to the misshaped dendritic spines, these mice have abnormal physiology in the inability of both excitatory and inhibitory inputs to operate repetitively as they need to in many aspects of normal brain function.
Chemical genetic identification of GAK substrates reveals its role in regulating Na+/K+-ATPase
It is shown that the sodium potassium pump α-subunit Atp1a3 is a GAK target and that GAK regulates Na+/K+-ATPase trafficking to the plasma membrane, suggesting a modulatory role for GAK via phosphoregulation of substrates such as Atp 1a3 during cargo trafficking.
Pathophysiology of a mouse model of X-linked mental retardation
- Kalbinder K. Gill
- 1 December 2013
The loss of several previously reported phenotypes, including, altered inhibitory transmission, gamma oscillations and vesicle dynamics, suggests that the Ophn1 mouse model of MR may be susceptible to genetic drift.