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037 _ _ |a DZNE-2023-01065
041 _ _ |a English
082 _ _ |a 570
100 1 _ |a Pinky, Priyanka D
|b 0
245 _ _ |a Prenatal Cannabinoid Exposure Elicits Memory Deficits Associated with Reduced PSA-NCAM Expression, Altered Glutamatergic Signaling, and Adaptations in Hippocampal Synaptic Plasticity.
260 _ _ |a Basel
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520 _ _ |a 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.
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650 _ 7 |a adolescence
|2 Other
650 _ 7 |a behavior
|2 Other
650 _ 7 |a cannabinoid
|2 Other
650 _ 7 |a developmental
|2 Other
650 _ 7 |a glutamate
|2 Other
650 _ 7 |a marijuana
|2 Other
650 _ 7 |a memory
|2 Other
650 _ 7 |a prenatal
|2 Other
650 _ 7 |a synaptic plasticity
|2 Other
650 _ 7 |a polysialyl neural cell adhesion molecule
|2 NLM Chemicals
650 _ 7 |a Neural Cell Adhesion Molecules
|2 NLM Chemicals
650 _ 7 |a Cannabinoids
|2 NLM Chemicals
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Rats
|2 MeSH
650 _ 2 |a Female
|2 MeSH
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Pregnancy
|2 MeSH
650 _ 2 |a Adolescent
|2 MeSH
650 _ 2 |a Neural Cell Adhesion Molecules: metabolism
|2 MeSH
650 _ 2 |a Cannabinoids: pharmacology
|2 MeSH
650 _ 2 |a Cannabinoids: metabolism
|2 MeSH
650 _ 2 |a Neuronal Plasticity: physiology
|2 MeSH
650 _ 2 |a Hippocampus: metabolism
|2 MeSH
650 _ 2 |a Memory Disorders: metabolism
|2 MeSH
700 1 _ |a Bloemer, Jenna
|0 0000-0002-1090-0286
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700 1 _ |a Smith, Warren D
|b 2
700 1 _ |a Du, Yifeng
|b 3
700 1 _ |a Heslin, Ryan T
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700 1 _ |a Setti, Sharay E
|b 5
700 1 _ |a Pfitzer, Jeremiah C
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700 1 _ |a Chowdhury, Kawsar
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700 1 _ |a Hong, Hao
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700 1 _ |a Bhattacharya, Subhrajit
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700 1 _ |a Dhanasekaran, Muralikrishnan
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700 1 _ |a Dityatev, Alexander
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700 1 _ |a Reed, Miranda N
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700 1 _ |a Suppiramaniam, Vishnu
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770 _ _ |a Glutamatergic Transmission in Brain Development and Disease
773 _ _ |a 10.3390/cells12212525
|g Vol. 12, no. 21, p. 2525 -
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