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@INPROCEEDINGS{DasPinky:154226,
      author       = {Das Pinky, Priyanka and Bloemer, Jenna and Du, Yifeng and
                      Setti, Sharay E. and Heslin, Ryan T. and Smith, Warren D.
                      and Dityatev, Alexander and Reed, Miranda N. and
                      Suppiramaniam, Vishnu},
      title        = {{P}renatal {C}annabinoid {E}xposure {M}ediated {C}ognitive
                      {D}eficits in the {O}ffspring: {E}lucidation of the
                      {M}echanism and {I}dentifying {T}herapeutic {T}argets},
      journal      = {The FASEB journal},
      volume       = {34},
      number       = {S1},
      issn         = {1530-6860},
      reportid     = {DZNE-2021-00087},
      pages        = {1 - 1},
      year         = {2020},
      abstract     = {Cannabinoid is currently one of the most commonly used
                      recreational drugs in the world with an approximate user of
                      22.2 million. As more and more states in the US are
                      legalizing the use of cannabinoid, the rate of cannabinoid
                      use is increasing specially in pregnant women. The active
                      ingredient of cannabis is delta‐9‐tetrahydrocannabinol
                      (THC) which can cross blood placental barrier and may cause
                      enduring alterations in synaptic circuitry of the fetal
                      brain. The aim of our study is to investigate the mechanism
                      of learning and memory deficits in case of prenatal
                      cannabinoid exposure (PCE) in the adolescent offspring. An
                      osmotic pump filled with either vehicle or the cannabinoid
                      receptor full agonist WIN55,212‐2 (2 mg/kg body
                      weight/day) was implanted subcutaneously in Gestational
                      Day‐3 to deliver the drug at a constant rate until the
                      pups were born. Open field test was performed to see the
                      effect of PCE on locomotor activity which revealed no
                      abnormality in the general motor activity. Contextual fear
                      conditioning test indicated a significantly reduced freezing
                      behavior in the PCE group compared to the vehicle exposed
                      group. Hippocampus based spatial memory test Morris water
                      maze showed that during the trial period, PCE animals
                      exhibit no preference for any particular quadrant while
                      control animals had an increased preference for the quadrant
                      where the hidden platform was present during the training
                      period. Electrophysiological experiments were performed on
                      the Schaffer collateral pathway of acute hippocampal slices
                      to measure synaptic plasticity. Impairment in both long term
                      potentiation (LTP) and long‐term depression (LTD), which
                      are important parameters of synaptic plasticity, were
                      observed. These impairments were associated with downstream
                      changes in the glutamatergic signaling. An increase in
                      cannabinoid receptor type 1(CB1) expression followed by
                      reduced neural cell adhesion molecule (NCAM) and its active
                      form polysialylated NCAM (PSA‐NCAM) expression have been
                      observed in the hippocampus of PCE animals. Interestingly,
                      restoration of PSA‐NCAM activity restored the LTP deficits
                      observed in PCE animals. Thus, based on the previous studies
                      and our current data, it can be postulated that, the
                      observed cognitive deficits in the PCE animals might be
                      partly due to an imbalance in glutamate receptors mediated
                      neurotransmission influenced by NCAM/PSA NCAM. Understanding
                      this specific NCAM/PSA‐NCAM interdependent signaling
                      cascade will lead to an identification of a specific
                      therapeutic target to improve gestational cannabinoid
                      exposure mediated memory deficits.},
      organization  = {Experimental Biology 2020 Meeting,},
      cin          = {AG Dityatev},
      ddc          = {570},
      cid          = {I:(DE-2719)1310007},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)1 / PUB:(DE-HGF)16},
      doi          = {10.1096/fasebj.2020.34.s1.03393},
      url          = {https://pub.dzne.de/record/154226},
}