Hippocampus-specific knockdown of Shati/Nat8l impairs cognitive function and electrophysiological response in mice

Author:

Izuo NaotakaORCID,Ikejima Daiki,Uno Kyosuke,Asano Takashi,Muramatsu Shin-IchiORCID,Nitta AtsumiORCID

Publisher

Elsevier BV

Reference33 articles.

1. A Novel molecule “Shati” is involved in methamphetamine-induced hyperlocomotion, sensitization, and conditioned place preference;Niwa;J. Neurosci.,2007

2. Methamphetamine-induced neuronal protein NAT8L is the NAA biosynthetic enzyme: implications for specialized acetyl coenzyme a metabolism in the CNS;Ariyannur;J. Neurosci.,2010

3. N-Acetylaspartate reductions in brain injury: impact on post-injury neuroenergetics, lipid synthesis, and protein acetylation;Moffett;Front Neuroenergy,2013

4. Deletion of SHATI/NAT8L increases dopamine D1 receptor on the cell surface in the nucleus accumbens, accelerating methamphetamine dependence;Toriumi;Int. J. Neuropsychopharmacol.,2014

5. Overexpression of Shati/Nat8l, an N-acetyltransferase, in the nucleus accumbens attenuates the response to methamphetamine via activation of group II mGluRs in mice;Miyamoto;Int. J. Neuropsychopharmacol.,2014

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