Repeated methamphetamine administration produces cognitive deficits through aug…

Repeated methamphetamine administration produces cognitive deficits through augmentation of GABAergic synaptic transmission in the prefrontal cortex — Methamphetamine (METH) abuse is associated with the emergence of cognitive deficits and hypofrontality, a pathophysiological marker of many neuropsychiatric dis

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  "n": 0,
  "doi": "10.1038/s41386-022-01371-9",
  "claim": "Repeated methamphetamine administration produces cognitive deficits through augmentation of GABAergic synaptic transmission in the prefrontal cortex — Methamphetamine (METH) abuse is associated with the emergence of cognitive deficits and hypofrontality, a pathophysiological marker of many neuropsychiatric dis",
  "title": null,
  "cite_key": "Armentaresendiz2022",
  "evidence": "Reported in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology (2022); from Body of abstract.",
  "effect_size": "7",
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  "study_system": "rat",
  "_source_cluster": "cluster_05_synaptic_connectivity",
  "replication_status": "replication_unknown",
  "_source_cluster_index": 308,
  "claim_source_sentence": "Methamphetamine (METH) abuse is associated with the emergence of cognitive deficits and hypofrontality, a pathophysiological marker of many neuropsychiatric disorders that is produced by altered balance of local excitatory and inhibitory synaptic transmission.",
  "replication_evidence_dois": [],
  "effect_size_source_sentence": "Using PV-Cre transgenic rats that went through a METH sensitization regime or saline (SAL) followed by 7-10 days of home cage abstinence combined with cognitive tests, chemogenetic experiments, and whole-cell patch recordings on the prelimbic prefrontal cortex (PFC), we investigated the cellular and synaptic mechanisms underlying METH-induce hypofrontality."
}

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Methamphetamine (METH) abuse is associated with the emergence of cognitive deficits and hypofrontality, a pathophysiological marker of many neuropsychiatric disorders that is produced by altered balance of local excitatory and inhibitory synaptic transmission.

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