GPCR-Mediated MAPK/ERK Cascade Activation in Mouse Striatal Slices

Author(s):  
Maricel Gómez-Soler ◽  
Víctor Fernández-Dueñas ◽  
Francisco Ciruela
Keyword(s):  
2000 ◽  
Vol 20 (24) ◽  
pp. 8980-8986 ◽  
Author(s):  
Antonella Meini ◽  
Alberto Benocci ◽  
Maria Frosini ◽  
Gianpietro Sgaragli ◽  
Gianpaolo Pessina ◽  
...  

2019 ◽  
Vol 20 (14) ◽  
pp. 3407 ◽  
Author(s):  
Paola Imbriani ◽  
Annalisa Tassone ◽  
Maria Meringolo ◽  
Giulia Ponterio ◽  
Graziella Madeo ◽  
...  

Caspases are a family of conserved cysteine proteases that play key roles in multiple cellular processes, including programmed cell death and inflammation. Recent evidence shows that caspases are also involved in crucial non-apoptotic functions, such as dendrite development, axon pruning, and synaptic plasticity mechanisms underlying learning and memory processes. The activated form of caspase-3, which is known to trigger widespread damage and degeneration, can also modulate synaptic function in the adult brain. Thus, in the present study, we tested the hypothesis that caspase-3 modulates synaptic plasticity at corticostriatal synapses in the phosphatase and tensin homolog (PTEN) induced kinase 1 (PINK1) mouse model of Parkinson’s disease (PD). Loss of PINK1 has been previously associated with an impairment of corticostriatal long-term depression (LTD), rescued by amphetamine-induced dopamine release. Here, we show that caspase-3 activity, measured after LTD induction, is significantly decreased in the PINK1 knockout model compared with wild-type mice. Accordingly, pretreatment of striatal slices with the caspase-3 activator α-(Trichloromethyl)-4-pyridineethanol (PETCM) rescues a physiological LTD in PINK1 knockout mice. Furthermore, the inhibition of caspase-3 prevents the amphetamine-induced rescue of LTD in the same model. Our data support a hormesis-based double role of caspase-3; when massively activated, it induces apoptosis, while at lower level of activation, it modulates physiological phenomena, like the expression of corticostriatal LTD. Exploring the non-apoptotic activation of caspase-3 may contribute to clarify the mechanisms involved in synaptic failure in PD, as well as in view of new potential pharmacological targets.


Neuropeptides ◽  
1984 ◽  
Vol 5 (1-3) ◽  
pp. 57-60
Author(s):  
K. Saito ◽  
N. Fujita ◽  
M. Nakahiro ◽  
R. Inoki

1985 ◽  
Vol 14 (5) ◽  
pp. 439-442 ◽  
Author(s):  
J.M. Murphy ◽  
S.D. Cunningham ◽  
W.J. McBride

1997 ◽  
Vol 73 (3) ◽  
pp. 243-246 ◽  
Author(s):  
Ikumi Arai ◽  
Takao Shimazoe ◽  
Shigenobu Shibata ◽  
Hirotaka Inoue ◽  
Akiko Yoshimatsu ◽  
...  

Pharmaceutics ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 135
Author(s):  
Angelica Jardim Costa ◽  
Adolfo Garcia Erustes ◽  
Rita Sinigaglia ◽  
Carlos Eduardo Neves Girardi ◽  
Gustavo José da Silva Pereira ◽  
...  

The pharmacological modulation of autophagy is considered a promising neuroprotective strategy. While it has been postulated that lithium regulates this cellular process, the age-related effects have not been fully elucidated. Here, we evaluated lithium-mediated neuroprotective effects in young and aged striatum. After determining the optimal experimental conditions for inducing autophagy in loco with lithium carbonate (Li2CO3), we measured cell viability, reactive oxygen species (ROS) generation and oxygen consumption with rat brain striatal slices from young and aged animals. In the young striatum, Li2CO3 increased tissue viability and decreased ROS generation. These positive effects were accompanied by enhanced levels of LC3-II, LAMP 1, Ambra 1 and Beclin-1 expression. In the aged striatum, Li2CO3 reduced the autophagic flux and increased the basal oxygen consumption rate. Ultrastructural changes in the striatum of aged rats that consumed Li2CO3 for 30 days included electrondense mitochondria with disarranged cristae and reduced normal mitochondria and lysosomes area. Our data show that the striatum from younger animals benefits from lithium-mediated neuroprotection, while the striatum of older rats does not. These findings should be considered when developing neuroprotective strategies involving the induction of autophagy in aging.


1997 ◽  
Vol 30 (5) ◽  
pp. 637-640 ◽  
Author(s):  
R. DeLucia ◽  
C.S. Planeta ◽  
M.P. Ferreira ◽  
M.L. Aizenstein ◽  
C. Scavone

1992 ◽  
Vol 213 (1) ◽  
pp. 17-24 ◽  
Author(s):  
Maurizio Raiteri ◽  
Mario Marchi ◽  
Giambattista Bonanno ◽  
Ernesto Fedele ◽  
Paola Versace

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