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Using gene knockouts, phosphoproteomics, and electrophysiology we show PTEN regulates neuronal growth and intrinsic excitability through separable downstream mechanisms.\n                  <jats:italic>Pten<\/jats:italic>\n                  loss induces cellular hypertrophy, increased excitatory synaptic input, reduced fast afterhyperpolarization, and burst firing. Deleting the mTORC1 scaffold,\n                  <jats:italic>Raptor,<\/jats:italic>\n                  rescues overgrowth and synaptic input but fails to normalize firing, while deleting\n                  <jats:italic>Akt<\/jats:italic>\n                  or the mTORC2 scaffold,\n                  <jats:italic>Rictor,<\/jats:italic>\n                  restores firing without rescuing growth. This dissociation identifies an AKT-mTORC2 mechanism that regulates voltage-gated calcium and BK potassium channels to set spike repolarization and burst firing.\n                  <jats:italic>In vivo<\/jats:italic>\n                  ,\n                  <jats:italic>Pten<\/jats:italic>\n                  knockout produces altered network synchrony, lethal seizures, and impaired object and location behavior;\n                  <jats:italic>Raptor<\/jats:italic>\n                  co-deletion display non-lethal hyperexcitability with improved object-location coupling. The biological and pathophysiological significance of these mechanisms is demonstrated by overlap of the PTEN-regulated phosphoproteome with ASD and epilepsy.\n                <\/jats:p>","DOI":"10.64898\/2026.06.22.733785","type":"posted-content","created":{"date-parts":[[2026,6,26]],"date-time":"2026-06-26T19:10:29Z","timestamp":1782501029000},"source":"Crossref","is-referenced-by-count":0,"title":["Scaling of Neuronal Growth and Excitability Through Separable mTORC1 and mTORC2 Pathways"],"prefix":"10.64898","author":[{"given":"Asan F","family":"Abdulkareem","sequence":"first","affiliation":[{"name":"Department of Neurobiology, Heersink School of Medicine, University of Alabama at Birmingham, Birmingham, AL"},{"name":"Department of Molecular and Systems Biology, Geisel School of Medicine, Dartmouth College, Hanover, NH"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Noah H","family":"Elste","sequence":"additional","affiliation":[{"name":"Department of Neurological Sciences, Larner College of Medicine, University of Vermont, Burlington VT"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rain","family":"Younger","sequence":"additional","affiliation":[{"name":"Department of Neurological Sciences, Larner College of Medicine, University of Vermont, Burlington VT"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mackenzi L","family":"Prina","sequence":"additional","affiliation":[{"name":"Department of Neurobiology, Heersink School of Medicine, University of Alabama at Birmingham, Birmingham, AL"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Evan","family":"Dennis","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery, Massachusetts General Hospital & Harvard Medical School, Boston, MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jessica","family":"Urbanczyk","sequence":"additional","affiliation":[{"name":"Fralin Biomedical Research Institute, Virginia Tech, 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