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Altered Astrocyte-Neuron Interactions and Epileptogenesis in Tuberous Sclerosis Complex Disorder

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Technical Report,01 Jun 2012,31 May 2016

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Columbia University New York United States

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The original goals were to explore potential mechanisms underlying epileptogenesis in Tuberous Sclerosis Complex TSC disease, with a focus on altered astrocyte-neuronal interactions caused by astrocyte-specific TSC deficiency. Astrocytes may contribute to abnormal neuronal excitability through mechanisms including glutamate uptake, potassium buffering and other means that alter expression and function of synaptic receptors for glutamate, or by altering the number of synapses. We chose to use a mouse GFAP mGFAP promoter sequence directing expression of a Cre-recombinase in most astrocytes and a subpopulation of the adult stem cells in the subventricular zone. We unexpectedly found, however, that there are indeed recombinant neurons that are derived from mGFAPcre expressing progenitors and are deficient for TSC1. We have compared directly and in the same brain region the effect of neuronal-intrinsic mTOR activation on the morphology and physiological functions of wild-type and recombinant neurons, as well as the effects of Tsc1-deficient astrocytes on neuronal morphology and neuronal activity associated with seizures.

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