Details

scope
mouse Scn1a+/- Dravet syndrome model, longitudinal P16-P35+
section_id
section_05_evidence_package
source_url
https://github.com/AllenNeuralDynamics/ComputationalReviewPV/blob/df9fc7e8d455b084152c9d713558dae0013cef21/evidence/section_05_evidence_package.json
effect_size
impaired spike generation at P16-21 normalizes by P35; synaptic transmission dysfunction persists
review_repo
ComputationalReviewPV
section_ref
wiki_page:computationalreviewpv-05
source_kind
review_finding
source_path
evidence/section_05_evidence_package.json
study_system
mouse Scn1a+/- Dravet syndrome model, longitudinal P16-P35+
section_title
Intrinsic Electrophysiology: The Fast-Spiking Phenotype and Its Variants
evidence_summary
Longitudinal assessment showed impaired spike generation in all Scn1a+/- mice at P16-21, with normalization by P35 in surviving mice. However, PV-IN synaptic transmission remains dysfunctional even at P35+.
review_bundle_ref
analysis_bundle:ab-e6261c8263e7
replication_status
replication_unknown
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
Raw fields (6)
claim_text
PV interneuron dysfunction in Dravet syndrome is dynamic: combined abnormalities of spike generation and axonal propagation drive early disease severity, while ongoing dysfunction of synaptic transmission contributes to chronic pathology even after spike generation normalizes.
raw_fields
{
  "n": 0,
  "doi": "10.1016/j.celrep.2022.110580",
  "claim": "PV interneuron dysfunction in Dravet syndrome is dynamic: combined abnormalities of spike generation and axonal propagation drive early disease severity, while ongoing dysfunction of synaptic transmission contributes to chronic pathology even after spike generation normalizes.",
  "evidence": "Longitudinal assessment showed impaired spike generation in all Scn1a+/- mice at P16-21, with normalization by P35 in surviving mice. However, PV-IN synaptic transmission remains dysfunctional even at P35+.",
  "effect_size": "impaired spike generation at P16-21 normalizes by P35; synaptic transmission dysfunction persists",
  "text_access": "fulltext",
  "study_system": "mouse Scn1a+/- Dravet syndrome model, longitudinal P16-P35+",
  "replication_status": "replication_unknown",
  "claim_source_sentence": "These results demonstrate dynamic dysfunction in Dravet syndrome: combined abnormalities of PV-IN spike generation and propagation drives early disease severity, while ongoing dysfunction of synaptic transmission contributes to chronic pathology.",
  "replication_evidence_dois": [],
  "effect_size_source_sentence": "impaired spike generation in all Scn1a+/- mice at postnatal days (P) 16-21, whether deceased prior or surviving to P35, with normalization by P35 in surviving mice."
}
source_refs
[
  "paper:paper-d4a202dd1651"
]
source_span
These results demonstrate dynamic dysfunction in Dravet syndrome: combined abnormalities of PV-IN spike generation and propagation drives early disease severity, while ongoing dysfunction of synaptic transmission contributes to chronic pathology.
evidence_refs
[
  {
    "ref": "paper:paper-d4a202dd1651"
  }
]
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"
}

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