Dopaminergic activity in the brain of a tropical wrasse in response to changes in light and hydrostatic pressure

2010 ◽  
Vol 166 (3) ◽  
pp. 513-519 ◽  
Author(s):  
Akihiro Takemura ◽  
Miyuki Uchimura ◽  
Yoriko Shibata
2021 ◽  
Vol 22 (13) ◽  
pp. 6974
Author(s):  
Omar Taleb ◽  
Mohammed Maammar ◽  
Christian Klein ◽  
Michel Maitre ◽  
Ayikoe Guy Mensah-Nyagan

Xanthurenic acid (XA) is a metabolite of the kynurenine pathway (KP) synthetized in the brain from dietary or microbial tryptophan that crosses the blood-brain barrier through carrier-mediated transport. XA and kynurenic acid (KYNA) are two structurally related compounds of KP occurring at micromolar concentrations in the CNS and suspected to modulate some pathophysiological mechanisms of neuropsychiatric and/or neurodegenerative diseases. Particularly, various data including XA cerebral distribution (from 1 µM in olfactory bulbs and cerebellum to 0.1–0.4 µM in A9 and A10), its release, and interactions with G protein-dependent XA-receptor, glutamate transporter and metabotropic receptors, strongly support a signaling and/or neuromodulatory role for XA. However, while the parent molecule KYNA is considered as potentially involved in neuropsychiatric disorders because of its inhibitory action on dopamine release in the striatum, the effect of XA on brain dopaminergic activity remains unknown. Here, we demonstrate that acute local/microdialysis-infusions of XA dose-dependently stimulate dopamine release in the rat prefrontal cortex (four-fold increase in the presence of 20 µM XA). This stimulatory effect is blocked by XA-receptor antagonist NCS-486. Interestingly, our results show that the peripheral/intraperitoneal administration of XA, which has been proven to enhance intra-cerebral XA concentrations (about 200% increase after 50 mg/kg XA i.p), also induces a dose-dependent increase of dopamine release in the cortex and striatum. Furthermore, our in vivo electrophysiological studies reveal that the repeated/daily administrations of XA reduce by 43% the number of spontaneously firing dopaminergic neurons in the ventral tegmental area. In the substantia nigra, XA treatment does not change the number of firing neurons. Altogether, our results suggest that XA may contribute together with KYNA to generate a KYNA/XA ratio that may crucially determine the brain normal dopaminergic activity. Imbalance of this ratio may result in dopaminergic dysfunctions related to several brain disorders, including psychotic diseases and drug dependence.


2006 ◽  
Vol 68 (4) ◽  
pp. 1300-1307 ◽  
Author(s):  
A. Damasceno-Oliveira ◽  
B. Fernandez-Duran ◽  
J. Goncalves ◽  
P. Serrao ◽  
P. Soares-Da-Silva ◽  
...  

2009 ◽  
Vol 13 (09) ◽  
pp. 1175-1191 ◽  
Author(s):  
Alexia Polissidis ◽  
Olga Chouliara ◽  
Andreas Galanopoulos ◽  
Georgia Rentesi ◽  
Maria Dosi ◽  
...  

2020 ◽  
Vol 97 (4) ◽  
pp. 1027-1038
Author(s):  
Shingo Udagawa ◽  
Sung‐Pyo Hur ◽  
Jun‐Hwan Byun ◽  
Hiroki Takekata ◽  
Yuki Takeuchi ◽  
...  

2019 ◽  
Vol 71 (4) ◽  
Author(s):  
Shaobao Liu ◽  
Ru Tao ◽  
Ming Wang ◽  
Jin Tian ◽  
Guy M. Genin ◽  
...  

Hydrostatic pressure (HP) regulates diverse cell behaviors including differentiation, migration, apoptosis, and proliferation. Abnormal HP is associated with pathologies including glaucoma and hypertensive fibrotic remodeling. In this review, recent advances in quantifying and predicting how cells respond to HP across several tissue systems are presented, including tissues of the brain, eye, vasculature and bladder, as well as articular cartilage. Finally, some promising directions on the study of cell behaviors regulated by HP are proposed.


2007 ◽  
Vol 153 (1-3) ◽  
pp. 385-389 ◽  
Author(s):  
Alfredo Damasceno-Oliveira ◽  
Begoña Fernández-Durán ◽  
José Gonçalves ◽  
Paula Serrão ◽  
Patrício Soares-da-Silva ◽  
...  

Endocrinology ◽  
2009 ◽  
Vol 150 (7) ◽  
pp. 3245-3251 ◽  
Author(s):  
Cleyde V. Helena ◽  
De'Nise T. McKee ◽  
Richard Bertram ◽  
Ameae M. Walker ◽  
Marc E. Freeman

Artificial copulomimetic cervical stimulation (CS) induces an immediate release of oxytocin (OT) and prolactin (PRL) followed by a daily PRL rhythm characterized by nocturnal and diurnal surges. Although we have shown that the initial release of PRL is induced by the immediate release of OT, we tested whether the PRL that is released in response to CS is responsible for the initiation and maintenance of the subsequent PRL surges. Thus, we injected OVX rats centrally or peripherally with ovine PRL (oPRL) at 2200 h. Central oPRL induced PRL surges in OVX rats that were similar in size and timing to those of CS rats, whereas peripheral oPRL induced surges that were of smaller amplitude and delayed. We then infused a PRL antagonist (S179D, 0.1 ng/h) centrally into OVX and OVX-CS rats and measured the release of endogenous PRL and the activity of neuroendocrine dopaminergic neurons. Central infusion of S179D did not influence basal PRL secretion in OVX rats but prevented the expression of the CS-induced PRL surges and the accompanying noontime increase of CS-induced dopaminergic activity when continued for 3 d. However, central infusion of S179D only on the day of CS did not prevent the daily rhythm of PRL surges. These results demonstrate that PRL acts centrally to induce the PRL rhythm and that PRL in the brain is essential for the maintenance but not for the initiation of the CS-induced rhythmic PRL surges.


1998 ◽  
Vol 10 (4) ◽  
pp. 84-86
Author(s):  
A.F.G. Leentjens ◽  
F.R.J. Verhey ◽  
F.W. Vreeling ◽  
H.M. van Praag

SummarySerotonin seems to play an important role in the regulation of dopaminergic and cholinergic neurotransmitter activities. In patients with Parkinsons' Disease, serotonergic activity is generally reduced, which is considered a compensating mechanism for the reduced dopaminergic activity. At the same time, reduction of serotonin activity may play a role in the expression of cognitive and affective symptoms. Functional intervention with serotonergic agents makes it possible to temporarily enhance or reduce the availability of serotonin in the brain. This will provide the opportunity to study motor, cognitive and affective symptoms in an integrated approach. This type of research has hardly been preformed in patients with Parkinson's Disease.


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