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- Live5/17/2026, 4:35:28 PM
daf5305b4f0cContent snapshot
{ "scope": "mouse Nav1.1-R1648H knock-in model, multiple brain regions", "claim_text": "The key mechanism of interneuron dysfunction in an SCN1A epilepsy mutation is a deficit of action potential initiation at the axon initial segment, not changes in somatic Na+ channels, with the deficit increasing with firing duration suggesting enhanced slow inactivation.", "raw_fields": { "n": 0, "doi": "10.1523/jneurosci.0721-14.2014", "claim": "The key mechanism of interneuron dysfunction in an SCN1A epilepsy mutation is a deficit of action potential initiation at the axon initial segment, not changes in somatic Na+ channels, with the deficit increasing with firing duration suggesting enhanced slow inactivation.", "evidence": "Multisystem analysis of SCN1A R1648H knock-in mice showing ubiquitous interneuron hypoexcitability in thalamus, cortex, and hippocampus without changes in excitatory neurons.", "effect_size": "ubiquitous interneuron hypoexcitability across thalamus, cortex, hippocampus; no changes in excitatory neurons", "text_access": "abstract_only", "study_system": "mouse Nav1.1-R1648H knock-in model, multiple brain regions", "replication_status": "independently_replicated", "claim_source_sentence": "Instead, the key mechanism of interneuron dysfunction was a deficit of action potential initiation at the axon initial segment that was identified by analyzing action potential firing. This deficit increased with the duration of firing periods.", "replication_evidence_dois": [ "10.1073/pnas.1411131111" ], "effect_size_source_sentence": "We found a ubiquitous hypoexcitability of interneurons in thalamus, cortex, and hippocampus, without detectable changes in excitatory neurons." }, "section_id": "section_05_evidence_package", "source_url": "https://github.com/AllenNeuralDynamics/ComputationalReviewPV/blob/df9fc7e8d455b084152c9d713558dae0013cef21/evidence/section_05_evidence_package.json", "effect_size": "ubiquitous interneuron hypoexcitability across thalamus, cortex, hippocampus; no changes in excitatory neurons", "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-7a06f96aaed3" ], "source_span": "Instead, the key mechanism of interneuron dysfunction was a deficit of action potential initiation at the axon initial segment that was identified by analyzing action potential firing. This deficit increased with the duration of firing periods.", "study_system": "mouse Nav1.1-R1648H knock-in model, multiple brain regions", "evidence_refs": [ { "ref": "paper:paper-7a06f96aaed3" } ], "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": "Multisystem analysis of SCN1A R1648H knock-in mice showing ubiquitous interneuron hypoexcitability in thalamus, cortex, and hippocampus without changes in excitatory neurons.", "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" }