scholarly journals Modeling human age-associated increase in Gadd45γ expression leads to spatial recognition memory impairments in young adult mice

2020 ◽  
Vol 94 ◽  
pp. 281-286
Author(s):  
David V.C. Brito ◽  
Kubra Gulmez Karaca ◽  
Janina Kupke ◽  
Franziska Mudlaff ◽  
Benjamin Zeuch ◽  
...  
2019 ◽  
Vol 40 (6) ◽  
pp. 1197-1210 ◽  
Author(s):  
David V.C. Brito ◽  
Janina Kupke ◽  
Kubra Gulmez Karaca ◽  
Benjamin Zeuch ◽  
Ana M.M. Oliveira

Molecules ◽  
2021 ◽  
Vol 26 (3) ◽  
pp. 528
Author(s):  
Nikolaos Pitsikas ◽  
Petros A. Tarantilis

Consistent experimental evidence suggests that anesthetic doses of the non-competitive N-methyl-d-aspartate (NMDA) receptor antagonist ketamine cause severe memory impairments in rodents. Crocins are among the various bioactive ingredients of the plant Crocus sativus L., and their implication in memory is well-documented. It has not yet been elucidated if crocins are able to attenuate the memory deficits produced by anesthetic ketamine. The present study was undertaken aiming to clarify this issue in the rat. For this aim, the object recognition, the object location and the habituation tests, reflecting non-spatial recognition memory, spatial recognition memory and associative memory, respectively, were utilized. A post-training challenge with crocins (15–30 mg/kg, intraperitoneally (i.p.), acutely) counteracted anesthetic ketamine (100 mg/kg, i.p.)-induced performance impairments in all the above-mentioned behavioral memory paradigms. The current findings suggest that crocins modulate anesthetic ketamine’s amnestic effects.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Sarah-Jane Leigh ◽  
Nadeem O. Kaakoush ◽  
R. Frederick Westbrook ◽  
Margaret J. Morris

2020 ◽  
Author(s):  
David V.C. Brito ◽  
Kubra Gulmez Karaca ◽  
Janina Kupke ◽  
Franziska Mudlaff ◽  
Benjamin Zeuch ◽  
...  

AbstractAging is associated with the progressive decay of cognitive function. Hippocampus-dependent processes, such as the formation of spatial memory, are particularly vulnerable to aging. Currently, the molecular mechanisms responsible for age-dependent cognitive decline are largely unknown. Here, we investigated the expression and function of the growth arrest DNA damage gamma (Gadd45γ) during aging and cognition. We report that Gadd45γ expression is increased in the hippocampus of aged humans and that Gadd45γ overexpression in the young adult mouse hippocampus compromises cognition. Moreover, Gadd45γ overexpression in hippocampal neurons disrupted CREB signaling and the expression of well-established activity-regulated genes. This work shows that Gadd45γ expression is tightly controlled in the hippocampus and its disruption may be a mechanism contributing to age-related cognitive impairments observed in humans.


1974 ◽  
Vol 13 (2) ◽  
pp. 216-229 ◽  
Author(s):  
Arjun D. Chanana ◽  
Juerg Schaedeli ◽  
Max W. Hess ◽  
Hans Cottier

1974 ◽  
Vol 63 (2) ◽  
pp. 665-674 ◽  
Author(s):  
V. Mareš ◽  
B. Schultze ◽  
W. Maurer

Neurons of the mouse were labeled with [3H]thymidine during their prenatal period of proliferation. The 3H activity of the Purkinje cell nuclei was then studied autoradiographically 8, 25, 55, and 90 days after birth. The measured grain number per nucleus decreased by about 14% between the 8th and 25th postnatal days and then remained constant up to 90 days. There was no significant decrease of the 3H activity of the Purkinje cell nuclei after correction of the measured grain number per nucleus for increasing nuclear volume of the growing Purkinje cells and for the influence of [3H]ß self-absorption in the material of the sections. Injection of a high dose of [3H]thymidine into young adult mice did not result in 3H labeling of either Purkinje or other neurons in other brain regions. The results agree with the concept of metabolic stability of nuclear DNA. "Metabolic" DNA could not be observed in these experiments.


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