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@ARTICLE{Pinky:265942,
      author       = {Pinky, Priyanka D and Bloemer, Jenna and Smith, Warren D
                      and Du, Yifeng and Heslin, Ryan T and Setti, Sharay E and
                      Pfitzer, Jeremiah C and Chowdhury, Kawsar and Hong, Hao and
                      Bhattacharya, Subhrajit and Dhanasekaran, Muralikrishnan and
                      Dityatev, Alexander and Reed, Miranda N and Suppiramaniam,
                      Vishnu},
      title        = {{P}renatal {C}annabinoid {E}xposure {E}licits {M}emory
                      {D}eficits {A}ssociated with {R}educed {PSA}-{NCAM}
                      {E}xpression, {A}ltered {G}lutamatergic {S}ignaling, and
                      {A}daptations in {H}ippocampal {S}ynaptic {P}lasticity.},
      journal      = {Cells},
      volume       = {12},
      number       = {21},
      issn         = {2073-4409},
      address      = {Basel},
      publisher    = {MDPI},
      reportid     = {DZNE-2023-01065},
      pages        = {2525},
      year         = {2023},
      abstract     = {Cannabis is now one of the most commonly used illicit
                      substances among pregnant women. This is particularly
                      concerning since developmental exposure to cannabinoids can
                      elicit enduring neurofunctional and cognitive alterations.
                      This study investigates the mechanisms of learning and
                      memory deficits resulting from prenatal cannabinoid exposure
                      (PCE) in adolescent offspring. The synthetic cannabinoid
                      agonist WIN55,212-2 was administered to pregnant rats, and a
                      series of behavioral, electrophysiological, and
                      immunochemical studies were performed to identify potential
                      mechanisms of memory deficits in the adolescent offspring.
                      Hippocampal-dependent memory deficits in adolescent PCE
                      animals were associated with decreased long-term
                      potentiation (LTP) and enhanced long-term depression (LTD)
                      at hippocampal Schaffer collateral-CA1 synapses, as well as
                      an imbalance between GluN2A- and GluN2B-mediated signaling.
                      Moreover, PCE reduced gene and protein expression of neural
                      cell adhesion molecule (NCAM) and polysialylated-NCAM
                      (PSA-NCAM), which are critical for GluN2A and GluN2B
                      signaling balance. Administration of exogenous PSA abrogated
                      the LTP deficits observed in PCE animals, suggesting PSA
                      mediated alterations in GluN2A- and GluN2B- signaling
                      pathways may be responsible for the impaired hippocampal
                      synaptic plasticity resulting from PCE. These findings
                      enhance our current understanding of how PCE affects memory
                      and how this process can be manipulated for future
                      therapeutic purposes.},
      keywords     = {Humans / Rats / Female / Animals / Pregnancy / Adolescent /
                      Neural Cell Adhesion Molecules: metabolism / Cannabinoids:
                      pharmacology / Cannabinoids: metabolism / Neuronal
                      Plasticity: physiology / Hippocampus: metabolism / Memory
                      Disorders: metabolism / adolescence (Other) / behavior
                      (Other) / cannabinoid (Other) / developmental (Other) /
                      glutamate (Other) / marijuana (Other) / memory (Other) /
                      prenatal (Other) / synaptic plasticity (Other) / polysialyl
                      neural cell adhesion molecule (NLM Chemicals) / Neural Cell
                      Adhesion Molecules (NLM Chemicals) / Cannabinoids (NLM
                      Chemicals)},
      cin          = {AG Dityatev},
      ddc          = {570},
      cid          = {I:(DE-2719)1310007},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC10648717},
      pubmed       = {pmid:37947603},
      doi          = {10.3390/cells12212525},
      url          = {https://pub.dzne.de/record/265942},
}