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Double agent mTOR.

Steve C Danzer

    Epilepsy Currents
    |March 7, 2019
    PubMed
    Summary

    Remodeling of cortical inhibition, specifically involving somatostatin-interneurons, prevents motor seizures in generalized epilepsy. mTORC1-dependent pathways are crucial, and their inhibition can worsen seizures.

    Area of Science:

    • Neuroscience
    • Epilepsy Research
    • Cellular and Network Physiology

    Background:

    • Deletions in CACNA1A cause epilepsy and ataxia.
    • Cacna1a deletion in medial ganglionic eminence-derived interneurons impairs cortical inhibition and leads to generalized seizures.
    • Parvalbumin-expressing interneurons (PV-INs) are critical for cortical inhibition, unlike somatostatin-expressing interneurons (SOM-INs).

    Purpose of the Study:

    • To investigate the specific cellular and network consequences of Cacna1a deletion in PV-INs.
    • To understand the role of PV-INs in generalized epilepsy and seizure prevention.
    • To explore the impact of compensatory inhibitory mechanisms on seizure phenotypes.

    Main Methods:

    • Generated PVCre;Cacna1ac/c mutant mice with conditional Cacna1a deletion in PV neurons.

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  • Utilized immunohistochemistry, in vitro electrophysiology, 2-photon imaging, and in vivo video-electroencephalography.
  • Assessed cortical cellular and network outcomes, including inhibitory circuit remodeling.

    • Main Results:

    • PVCre;Cacna1ac/c mice showed reduced perisomatic inhibition but rare motor seizures, unlike Nkx2.1Cre;Cacna1ac/c mice.
    • A net increase in cortical inhibition occurred due to SOM-IN axon sprouting and enhanced dendritic inhibition.
    • This compensatory mechanism, dependent on mechanistic target of rapamycin complex 1 (mTORC1), prevented motor seizures; mTORC1 inhibition increased seizures.

    Conclusions:

    • Cortical inhibition remodeling, particularly an mTOR-dependent gain in dendritic inhibition, dictates the seizure phenotype in generalized epilepsy.
    • mTOR inhibition can be detrimental in certain epilepsies, highlighting the complexity of therapeutic interventions.
    • Targeting SOM-INs or related pathways may offer novel strategies for seizure control.