Tsc1 represses parvalbumin expression and fast-spiking properties in somatostatin lineage cortical interneurons

Ruchi Malik, Emily Ling-Lin Pai, Anna N Rubin, April M Stafford, Kartik Angara, Petros Minasi, John L. Rubenstein, Vikaas S Sohal () and Daniel Vogt ()
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Ruchi Malik: Department of Psychiatry and UCSF Weill Institute for Neurosciences
Emily Ling-Lin Pai: Department of Psychiatry and UCSF Weill Institute for Neurosciences
Anna N Rubin: Department of Psychiatry and UCSF Weill Institute for Neurosciences
April M Stafford: Department of Pediatrics and Human Development
Kartik Angara: Department of Pediatrics and Human Development
Petros Minasi: Department of Psychiatry and UCSF Weill Institute for Neurosciences
John L. Rubenstein: Department of Psychiatry and UCSF Weill Institute for Neurosciences
Vikaas S Sohal: Department of Psychiatry and UCSF Weill Institute for Neurosciences
Daniel Vogt: Department of Pediatrics and Human Development

Nature Communications, 2019, vol. 10, issue 1, 1-16

Abstract: Abstract Medial ganglionic eminence (MGE)-derived somatostatin (SST)+ and parvalbumin (PV)+ cortical interneurons (CINs), have characteristic molecular, anatomical and physiological properties. However, mechanisms regulating their diversity remain poorly understood. Here, we show that conditional loss of the Tuberous Sclerosis Complex (TSC) gene, Tsc1, which inhibits the mammalian target of rapamycin (MTOR), causes a subset of SST+ CINs, to express PV and adopt fast-spiking (FS) properties, characteristic of PV+ CINs. Milder intermediate phenotypes also occur when only one allele of Tsc1 is deleted. Notably, treatment of adult mice with rapamycin, which inhibits MTOR, reverses the phenotypes. These data reveal novel functions of MTOR signaling in regulating PV expression and FS properties, which may contribute to TSC neuropsychiatric symptoms. Moreover, they suggest that CINs can exhibit properties intermediate between those classically associated with PV+ or SST+ CINs, which may be dynamically regulated by the MTOR signaling.

Date: 2019
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DOI: 10.1038/s41467-019-12962-4

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