Behavioral effects of urotensin-II centrally administered in mice

Abstract

Urotensin-II (U-II) receptors are widely distributed in the central nervous system. Intracerebroventricular (i.c.v.) injection of U-II causes hypertension and bradycardia and stimulates prolactin and thyrotropin secretion. However, the behavioral effects of centrally administered U-II have received little attention. In the present study, we tested the effects of i.c.v. injections of U-II on behavioral, metabolic, and endocrine responses in mice. Administration of graded doses of U-II (1-10,000 ng/mouse) provoked: (1) a dose-dependent reduction in the number of head dips in the hole-board test; (2) a dose-dependent reduction in the number of entries in the white chamber in the black-and-white compartment test, and in the number of entries in the central platform and open arms in the plus-maze test; and (3) a dose-dependent increase in the duration of immobility in the forced-swimming test and tail suspension test. Intracerebroventricular injection of U-II also caused an increase in: food intake at doses of 100 and 1,000 ng/mouse, water intake at doses of 100-10,000 ng/mouse, and horizontal locomotion activity at a dose of 10,000 ng/mouse. Whatever was the dose, the central administration of U-II had no effect on body temperature, nociception, apomorphine-induced penile erection and climbing behavior, and stress-induced plasma corticosterone level. Taken together, the present study demonstrates that the central injection of U-II at doses of 1-10,000 ng/mouse induces anxiogenic- and depressant-like effects in mouse. These data suggest that U-II may be involved in some aspects of psychiatric disorders.

Chronic Administration of 13-Cis-Retinoic Acid Increases Depression-Related Behavior in Mice

“…The behavior of the animals in the tail suspension test was not assessed in these studies. However, increased immobility in both the forced swim and tail suspension tests does occur in mice and rats due to the pro-depressant effects of withdrawal from chronic amphetamine administration (Cryan et al, 2003), centrally administered urotensin-II (Do-Rego et al, 2005), and interleukin-1 and endotoxin injection (Dunn and Swiergiel, 2005). Interestingly, in the forced swim test, antidepressants that target the serotonergic system increase swimming behavior, thereby decreasing immobility (Detke et al, 1995).…”

MOLECULAR EVOLUTION OF GPCRS: Somatostatin/urotensin II receptors

“…Thus, i.c.v. administration of UII promotes anxiogenic and depressant-like effects in mice (Matsumoto et al 2004, Do Rego et al 2005 and enhances neural activity in rat periaqueductal gray matter (Gartlon et al 2004), a central region involved in anxiety control. In addition, targeted administration of UII into the pedunculopontine nucleus modulates paradoxical sleep through the direct activation of brainstem cholinergic neurons (Huitron-Resendiz et al 2005, de Lecea & Bourgin 2008.…”

“…A high density of UII-and URPbinding sites has been found in regions of the human and rat brains that are involved in motor control (Maguire et al 2000, Jegou et al 2006, Bucharles et al 2014, and i.c.v. administered UII and/or URP increases locomotion in mice, rats, and rainbow trout (Gartlon et al 2001, Lancien et al 2004, Do Rego et al 2005. The UII and URP mRNAs are abundantly expressed in the CNS, especially in the adult cranial and spinal motoneurons of many species…”

UII and UT in grouper: cloning and effects on the transcription of hormones related to growth control

“…In mammals, UII is well known for its smooth-musclestimulating activity and is considered the most potent mammalian vasoconstrictor (Ames et al 1999). Numerous studies have demonstrated that the UII/UT system is involved in the control of cardiovascular activity (Watson & May 2004, Vaudry et al 2010, locomotor activity, orexigenic and dipsogenic response (Do-Rego et al 2005), sleep (de Lecea & Bourgin 2008), and endocrine hormone secretion (Gartlon et al 2001). Moreover, some recent studies in mammals have shown that i) UII exerts mitogenic effects on some tumor cells, such as SW-13 cells (Takahashi et al 2003) and pheochromocytoma cells (Zeng et al 2006); ii) hUII is an autocrine/paracrine growth factor in porcine renal epithelial cells (Matsushita et al 2003) and involved in the pathogenesis of vascular remodeling (Zhang et al 2008); and iii) UII can stimulate the proliferation of human lung adenocarcinoma A549 cells, induce an increase in tumor volume and weight (Wu et al 2010), and promote the proliferation of rat bone marrow-derived endothelial progenitor cells (Xu et al 2012).…”