The effects of chronic administration of quetiapine on the methamphetamine-induced recognition memory impairment and dopaminergic terminal deficit in rats

2006 ◽  
Vol 172 (1) ◽  
pp. 39-45 ◽  
Author(s):  
Jue He ◽  
Yi Yang ◽  
Yingxin Yu ◽  
Xiaokun Li ◽  
Xin-Min Li
Neuroreport ◽  
2018 ◽  
Vol 29 (13) ◽  
pp. 1099-1103 ◽  
Author(s):  
Jue He ◽  
Fan Liu ◽  
Qian Zu ◽  
Zhizhong Xu ◽  
Huifei Zheng ◽  
...  

2009 ◽  
Vol 169 (1) ◽  
pp. 39-42 ◽  
Author(s):  
David Luck ◽  
Alonso Montoya ◽  
Matthew Menear ◽  
Amélie M. Achim ◽  
Samarthji Lal ◽  
...  

2021 ◽  
pp. 105832
Author(s):  
Masahito Sawahata ◽  
Hiroki Asano ◽  
Taku Nagai ◽  
Norimichi Ito ◽  
Takao Kohno ◽  
...  

2020 ◽  
Author(s):  
Sandra Martin Lorenzo ◽  
Valérie Nalesso ◽  
Claire Chevalier ◽  
Marie-Christine Birling ◽  
Yann Herault

ABSTRACTGene copy number variants (CNV) have an important role in the appearance of neurodevelopmental disorders. Particularly, the deletion of the 16p11.2 locus is associated with autism spectrum disorder, intellectual disability, and several other features. Earlier studies highlighted the implication of Kctd13 genetic imbalance in the 16p11.2 deletion through the regulation of the RHOA pathway. Here, we target the pathway and rescue the cognitive phenotypes of the 16p11.2 deletion mouse models. We used a chronic administration of fasudil (HA1077), an inhibitor of the Rho-associated protein kinase (ROCK), in mouse models carrying a heterozygous inactivation of Kctd13, or the deletion of the entire 16p11.2 BP4-BP5 region. We focused our attention on the most robust cognitive phenotypes seen in the 16p11.2 models and we showed that a chronic fasudil treatment can restore object recognition memory in both mouse models but does not change other behavioural traits. These findings confirm KCTD13 as one target gene causing cognitive deficits in 16p11.2 deletion patients, and the pertinence of the RHOA pathway as a therapeutic path and reinforce the contribution of other gene(s) involved in cognitive defects found in the 16p11.2 CNV models.HIGHLIGHTS- Kctd13 haploinsufficiency recapitulates most of the behaviour phenotypes found in the 16p11.2 Del/+ models- Fasudil treatment restores Kctd13 and 16p11.2 Del/+ mutant phenotypes in novel location and novel object recognition memory tests- Fasudil treatment restores the RhoA pathway in Kctd13+/- and 16p11.2 Del/+ models


Assessment ◽  
1994 ◽  
Vol 1 (4) ◽  
pp. 323-334 ◽  
Author(s):  
Grant L. Iverson ◽  
Michael D. Franzen

The purpose of this investigation was to examine the efficacy of using the Recognition Memory Test (RMT), Digit Span subtest (WAIS-R), and Knox Cube Test as markers for malingered memory deficits. Participants were 100 subjects from three general populations: university students, federal inmates, and patients with head injuries. Twenty students, 20 inmates, and 20 patients with head injuries resulting in memory impairment were instructed to try their best on the assessment procedures. The remaining 20 students and 20 inmates were instructed to malinger memory impairment on the procedures. The experimental-malingerers (i.e., students and inmates) performed more poorly than the patients with head injuries on nearly every score derived from the three tests. Discriminant function analyses using the age-corrected Digit Span scale score, the Knox Cube Test total score, and the RMT raw scores for words and faces as predictors of group membership resulted in an overall 98% correct classification rate and 100% correct on cross-validation. Simultaneously applying two empirically-derived RMT cutoff scores resulted in an overall correct classification rate of 100%. The extraordinarily high classification rates in this study were likely influenced by the experimental design and procedures.


PLoS ONE ◽  
2016 ◽  
Vol 11 (2) ◽  
pp. e0149574 ◽  
Author(s):  
Wenping Zhang ◽  
Fengjie Tian ◽  
Jinping Zheng ◽  
Senlin Li ◽  
Mei Qiang

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