Version history

{
  "scope": "human genetics and mouse models (review)",
  "claim_text": "Loss-of-function mutations in SCN1A encoding Nav1.1 cause Dravet syndrome through disruption of excitatory/inhibitory balance, as Nav1.1 is essential for high-frequency action potential generation specifically in inhibitory interneurons.",
  "raw_fields": {
    "n": 0,
    "doi": "10.1016/j.yebeh.2011.11.022",
    "claim": "Loss-of-function mutations in SCN1A encoding Nav1.1 cause Dravet syndrome through disruption of excitatory/inhibitory balance, as Nav1.1 is essential for high-frequency action potential generation specifically in inhibitory interneurons.",
    "evidence": "Rare loss-of-function SCN1A mutations cause developmental and epileptic encephalopathies including Dravet syndrome; common SCN1A variants are risk factors for epilepsy.",
    "effect_size": "Nav1.1 critical for high-frequency AP generation in inhibitory interneurons",
    "text_access": "abstract_only",
    "study_system": "human genetics and mouse models (review)",
    "replication_status": "independently_replicated",
    "claim_source_sentence": "Nav1.1 voltage-gated sodium channels encoded by the SCN1A gene are critical to high frequency action potential generation in inhibitory interneurons and so play a crucial role in maintaining the excitatory-inhibitory balance in the brain.",
    "replication_evidence_dois": [
      "10.1523/jneurosci.5270-06.2007",
      "10.1073/pnas.1411131111"
    ],
    "effect_size_source_sentence": "Nav1.1 voltage-gated sodium channels encoded by the SCN1A gene are critical to high frequency action potential generation in inhibitory interneurons."
  },
  "section_id": "section_05_evidence_package",
  "source_url": "https://github.com/AllenNeuralDynamics/ComputationalReviewPV/blob/df9fc7e8d455b084152c9d713558dae0013cef21/evidence/section_05_evidence_package.json",
  "effect_size": "Nav1.1 critical for high-frequency AP generation in inhibitory interneurons",
  "review_repo": "ComputationalReviewPV",
  "section_ref": "wiki_page:computationalreviewpv-05",
  "source_kind": "review_finding",
  "source_path": "evidence/section_05_evidence_package.json",
  "source_refs": [
    "paper:paper-08cd52ae3e4e"
  ],
  "source_span": "Nav1.1 voltage-gated sodium channels encoded by the SCN1A gene are critical to high frequency action potential generation in inhibitory interneurons and so play a crucial role in maintaining the excitatory-inhibitory balance in the brain.",
  "study_system": "human genetics and mouse models (review)",
  "evidence_refs": [
    {
      "ref": "paper:paper-08cd52ae3e4e"
    }
  ],
  "section_title": "Intrinsic Electrophysiology: The Fast-Spiking Phenotype and Its Variants",
  "source_policy": {
    "mode": "public_source_pointer_with_short_context",
    "notes": [
      "Local review repositories are read-only inputs.",
      "SciDEX stores paper metadata, structured evidence, file pointers, and short citation contexts; it does not copy full review prose."
    ],
    "source_commit_sha": "df9fc7e8d455b084152c9d713558dae0013cef21",
    "source_repository_url": "https://github.com/AllenNeuralDynamics/ComputationalReviewPV"
  },
  "evidence_summary": "Rare loss-of-function SCN1A mutations cause developmental and epileptic encephalopathies including Dravet syndrome; common SCN1A variants are risk factors for epilepsy.",
  "review_bundle_ref": "analysis_bundle:ab-e6261c8263e7",
  "replication_status": "independently_replicated",
  "review_package_ref": "analysis_bundle:ab-e6261c8263e7",
  "source_artifact_ref": "wiki_page:computationalreviewpv-05",
  "origin_url": "https://github.com/AllenNeuralDynamics/ComputationalReviewPV/blob/df9fc7e8d455b084152c9d713558dae0013cef21/evidence/section_05_evidence_package.json",
  "commit_sha": "df9fc7e8d455b084152c9d713558dae0013cef21",
  "created_by": "persona-jerome-lecoq-gbo-neuroscience",
  "repository_url": "https://github.com/AllenNeuralDynamics/ComputationalReviewPV"
}