{
  "abstract": "Kcnb1-null mice exhibit hypoleptinemia, disrupted Kcnb1-integrin-K⁺ channel complex (IKC) interactions with the leptin receptor (LepR) in proopiomelanocortin neurons, and broad neurodevelopmental and cognitive abnormalities. Because leptin is neurotrophic and IKC-LepR assemblies are present in neocortex, we tested whether leptin modifies these phenotypes. Early-life leptin supplementation partially improved behavioral and cognitive deficits and more strongly corrected anatomical and neuronal abnormalities. In null cortical neurons, leptin normalized dendritic overgrowth and F-actin dynamics through LepR- and integrin-dependent mechanisms. WT animals and neurons showed modest leptin responses; however, integrin manipulation unmasked leptin sensitivity, whereas LepR blockade induced null-like defects without exogenous leptin. These findings support a dual-mode model in which LepR signaling is regulated by both ligand availability and IKC-dependent mechanisms, identifying IKC-LepR coupling as a molecular interface linking endocrine signaling to neocortical development.",
  "abstract_shown": true,
  "affiliations": [],
  "article_type": "Article",
  "arxiv": null,
  "author_total": 10,
  "authors": [
    {
      "name": "Elena Forzisi",
      "orcid": "0000-0002-3271-7052"
    },
    {
      "name": "Anika Gaur"
    },
    {
      "name": "Aniket Gaur"
    },
    {
      "name": "Maria del Carmen Medranda"
    },
    {
      "name": "Rachel Philip"
    },
    {
      "name": "Srishti Anand"
    },
    {
      "name": "Clotilde Impaloni",
      "orcid": "0009-0008-7694-0740"
    },
    {
      "name": "Kiarah Leonard",
      "orcid": "0000-0002-5546-1352"
    },
    {
      "name": "Srinidi Venkateswaran"
    },
    {
      "name": "Federico Sesti",
      "orcid": "0000-0002-2761-9693"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/e2x93cagd8zdr.bib",
  "cited_by": 0,
  "doi": "10.1016/j.isci.2026.117851",
  "fulltext_url": "https://europepmc.org/articles/PMC13677428",
  "id": "e2x93cagd8zdr",
  "issns": [
    "2589-0042"
  ],
  "landing_url": "https://www.cell.com/iscience/fulltext/S2589-0042(26)03232-3",
  "language": "eng",
  "licence": "CC-BY-NC-ND-4.0",
  "licence_label": "CC BY-NC-ND 4.0",
  "licence_source": "article",
  "licence_url": "http://creativecommons.org/licenses/by-nc-nd/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "heading",
      "Cellular neuroscience"
    ],
    [
      "heading",
      "Molecular neuroscience"
    ],
    [
      "heading",
      "Neuroscience"
    ],
    [
      "openalex",
      "2807|Regulation of Appetite and Obesity"
    ]
  ],
  "openalex": "W7221164007",
  "pdf_url": "https://europepmc.org/articles/PMC13677428?pdf=render",
  "pmcid": "PMC13677428",
  "pmid": "42898164",
  "published": "2026-10-08",
  "publisher": "Elsevier BV",
  "ris": "https://research.draconitic.com/paper/e2x93cagd8zdr.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T12:17:16Z",
      "native_id": "10.1016/j.isci.2026.117851",
      "source": "feed-cell",
      "url": "https://www.cell.com/iscience/fulltext/S2589-0042(26)03232-3"
    },
    {
      "first_seen": "2026-10-30T12:17:49Z",
      "native_id": "10.1016/j.isci.2026.117851",
      "source": "crossref",
      "url": "https://linkinghub.elsevier.com/retrieve/pii/S2589004226032323"
    },
    {
      "first_seen": "2026-10-30T12:19:37Z",
      "native_id": "MED:42898164",
      "source": "europepmc",
      "url": "https://europepmc.org/article/MED/42898164"
    }
  ],
  "subjects": [
    {
      "field": "biology",
      "origin": "heading:Neuroscience",
      "subfield": "neuroscience"
    }
  ],
  "title": "The IKC-leptin axis functions as a molecular bridge between neurodevelopment and endocrine signaling",
  "title_text": "The IKC-leptin axis functions as a molecular bridge between neurodevelopment and endocrine signaling",
  "type": "peer-reviewed",
  "updated_at": "2026-10-30T12:19:37Z",
  "url": "https://research.draconitic.com/paper/e2x93cagd8zdr",
  "venue": "iScience",
  "versions": []
}