Role of the dopaminergic receptors D1 and D2 in the rapid-onset behavioural sensitisation to modafinil

2016 ◽  
Vol 26 ◽  
pp. S681-S682
Author(s):  
R. Wuo-Silva ◽  
D.F. Fukushiro ◽  
R. Santos-Baldaia ◽  
A.W. Hollais ◽  
E.M. Kawamoto ◽  
...  
Author(s):  
Domenico De Berardis ◽  
Tiziano Acciavatti ◽  
Daniela Campanella ◽  
Nicola Serroni ◽  
Luigi Olivieri ◽  
...  

1986 ◽  
Vol 149 (2) ◽  
pp. 191-201 ◽  
Author(s):  
Robert M. Post ◽  
David R. Rubinow ◽  
James C. Ballenger

Few biological theories of manic-depressive illness have focused on the longitudinal course of affective dysfunction and the mechanisms underlying its often recurrent and progressive course. The authors discuss two models for the development of progressive behavioural dysfunction—behavioural sensitisation and electrophysiological kindling—as they provide clues to important clinical and biological variables relevant to sensitisation in affective illness. The role of environmental context and conditioning in mediating behavioural and biochemical aspects of this sensitisation is emphasised. The sensitisation models provide a conceptual approach to previously inexplicable clinical phenomena in the longitudinal course of affective illness and may provide a bridge between psychoanalytic/psychosocial and neurobiological formulations of manic-depressive illness.


2021 ◽  
Vol 429 ◽  
pp. 118138
Author(s):  
Anna Lopatina ◽  
Tatiana Solodova ◽  
Anastasiya Sviridova ◽  
Mikhail Melnikov ◽  
Alexey Boyko

2019 ◽  
Vol 216 (8) ◽  
pp. 1874-1890 ◽  
Author(s):  
Nicolas Ricard ◽  
Rizaldy P. Scott ◽  
Carmen J. Booth ◽  
Heino Velazquez ◽  
Nicholas A. Cilfone ◽  
...  

To define the role of ERK1/2 signaling in the quiescent endothelium, we induced endothelial Erk2 knockout in adult Erk1−/− mice. This resulted in a rapid onset of hypertension, a decrease in eNOS expression, and an increase in endothelin-1 plasma levels, with all mice dying within 5 wk. Immunostaining and endothelial fate mapping showed a robust increase in TGFβ signaling leading to widespread endothelial-to-mesenchymal transition (EndMT). Fibrosis affecting the cardiac conduction system was responsible for the universal lethality in these mice. Other findings included renal endotheliosis, loss of fenestrated endothelia in endocrine organs, and hemorrhages. An ensemble computational intelligence strategy, comprising deep learning and probabilistic programing of RNA-seq data, causally linked the loss of ERK1/2 in HUVECs in vitro to activation of TGFβ signaling, EndMT, suppression of eNOS, and induction of endothelin-1 expression. All in silico predictions were verified in vitro and in vivo. In summary, these data establish the key role played by ERK1/2 signaling in the maintenance of vascular normalcy.


Nature ◽  
2011 ◽  
Vol 478 (7369) ◽  
pp. 374-377 ◽  
Author(s):  
Charles Wicks ◽  
Juan Carlos de la Llera ◽  
Luis E. Lara ◽  
Jacob Lowenstern
Keyword(s):  

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