scholarly journals Do specific NMDA receptor subunits act as gateways for addictive behaviors?

2016 ◽  
Vol 16 (1) ◽  
pp. 118-138 ◽  
Author(s):  
F. W. Hopf

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Tiziana Imbriglio ◽  
Remy Verhaeghe ◽  
Nico Antenucci ◽  
Stefania Maccari ◽  
Giuseppe Battaglia ◽  
...  

AbstractmGlu5 metabotropic glutamate receptors are highly expressed and functional in the early postnatal life, and are known to positively modulate NMDA receptor function. Here, we examined the expression of NMDA receptor subunits and interneuron-related genes in the prefrontal cortex and hippocampus of mGlu5−/− mice and wild-type littermates at three developmental time points (PND9, − 21, and − 75). We were surprised to find that expression of all NMDA receptor subunits was greatly enhanced in mGlu5−/− mice at PND21. In contrast, at PND9, expression of the GluN2B subunit was enhanced, whereas expression of GluN2A and GluN2D subunits was reduced in both regions. These modifications were transient and disappeared in the adult life (PND75). Changes in the transcripts of interneuron-related genes (encoding parvalbumin, somatostatin, vasoactive intestinal peptide, reelin, and the two isoforms of glutamate decarboxylase) were also observed in mGlu5−/− mice across postnatal development. For example, the transcript encoding parvalbumin was up-regulated in the prefrontal cortex of mGlu5−/− mice at PND9 and PND21, whereas it was significantly reduced at PND75. These findings suggest that in mGlu5−/− mice a transient overexpression of NMDA receptor subunits may compensate for the lack of the NMDA receptor partner, mGlu5. Interestingly, in mGlu5−/− mice the behavioral response to the NMDA channel blocker, MK-801, was significantly increased at PND21, and largely reduced at PND75. The impact of adaptive changes in the expression of NMDA receptor subunits should be taken into account when mGlu5−/− mice are used for developmental studies.



2016 ◽  
Vol 138 (4) ◽  
pp. 546-556 ◽  
Author(s):  
Martina Kaniakova ◽  
Katarina Lichnerova ◽  
Kristyna Skrenkova ◽  
Ladislav Vyklicky ◽  
Martin Horak




2006 ◽  
Vol 27 (2) ◽  
pp. 169-175 ◽  
Author(s):  
Shang-Zhi Xu ◽  
Bettaiya Rajanna


1997 ◽  
Vol 28 ◽  
pp. S19
Author(s):  
Masahiko Watanabe ◽  
Kenji Sakimura ◽  
Masayoshi Mishina ◽  
Yoshiro Inoue


2012 ◽  
Vol 11 (3) ◽  
pp. 1891-1896 ◽  
Author(s):  
Maryam Ghafari ◽  
Harald Höger ◽  
Soheil Keihan Falsafi ◽  
Nina Russo-Schlaff ◽  
Arnold Pollak ◽  
...  


Author(s):  
Erica L. Fletcher ◽  
Iris Hack ◽  
Johann Helmut Brandst�tter ◽  
Heinz W�ssle


1995 ◽  
Vol 15 (3) ◽  
pp. 2338-2353 ◽  
Author(s):  
AS Niedzielski ◽  
RJ Wenthold


2019 ◽  
Vol 20 (13) ◽  
pp. 3273 ◽  
Author(s):  
Zdenka Kristofikova ◽  
Jana Sirova ◽  
Jan Klaschka ◽  
Saak V. Ovsepian

Aging and chronic sleep deprivation (SD) are well-recognized risk factors for Alzheimer’s disease (AD), with N-methyl-D-aspartate receptor (NMDA) and downstream nitric oxide (NO) signalling implicated in the process. Herein, we investigate the impact of the age- and acute or chronic SD-dependent changes on the expression of NMDA receptor subunits (NR1, NR2A, and NR2B) and on the activities of NO synthase (NOS) isoforms in the cortex of Wistar rats, with reference to cerebral lateralization. In young adult controls, somewhat lateralized seasonal variations in neuronal and endothelial NOS have been observed. In aged rats, overall decreases in NR1, NR2A, and NR2B expression and reduction in neuronal and endothelial NOS activities were found. The age-dependent changes in NR1 and NR2B significantly correlated with neuronal NOS in both hemispheres. Changes evoked by chronic SD (dysfunction of endothelial NOS and the increasing role of NR2A) differed from those evoked by acute SD (increase in inducible NOS in the right side). Collectively, these results demonstrate age-dependent regulation of the level of NMDA receptor subunits and downstream NOS isoforms throughout the rat brain, which could be partly mimicked by SD. As described herein, age and SD alterations in the prevalence of NMDA receptors and NOS could contribute towards cognitive decline in the elderly, as well as in the pathobiology of AD and the neurodegenerative process.



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