Central apelin-13 inhibits food intake via the CRF receptor in mice

Apelin, the novel identified peptide, is the endogenous ligand for the APJ. Previous studies have reported the effect of apelin on food intake, however the action of acute central injected apelin on food intake in mice remains unknown. The present study was designed to investigate the mechanism as well as the effect of central apelin-13 on food intake in mice. During the dark period, the cumulative food intake was significantly decreased at 4h after the intracerebroventricular (i.c.v.) injection of 1 and 3μg/mouse apelin-13 and the period food intake was significantly reduced during 2-4h after treatment. In the fasted mice, the cumulative food intake was significantly decreased at 2 and 4h after injection of 3μg/mouse apelin-13. The cumulative water intake was significantly reduced by apelin-13 (3μg/mouse) at 4h after injection in freely feeding and fasted mice. However, during light period, apelin-13 had no influence on food and water intake in freely feeding mice. The APJ receptor antagonist apelin-13(F13A) (6μg/mouse) and the corticotrophin-releasing factor (CRF) receptor antagonist α-helical CRF(9-41) (3μg/mouse) could reverse the inhibitory effect on cumulative food intake/0-4h induced by apelin-13 (3μg/mouse) in freely feeding mice during the dark period, whereas the anorexic effect could not be antagonized by the arginie vasopressin (AVP) receptor antagonist deamino(CH(2))(5)Tyr(Me)AVP (0.5μg/mouse). Taken together, these results suggest that central apelin-13 inhibits food intake in mice and it seems that APJ receptor and CRF receptor, but not AVP receptor, might be involved in this process.     

BiP mRNA expression is upregulated by dehydration in vasopressin neurons in the hypothalamus in mice

The immunoglobulin heavy chain binding protein (BiP) is an endoplasmic reticulum (ER) chaperone that facilitates the proper folding of newly synthesized secretory and transmembrane proteins. Here we report that BiP mRNA was expressed in the supraoptic nucleus (SON) and paraventricular nucleus (PVN) of the hypothalamus in wild-type mice under basal conditions. Dual in situ hybridization in the SON and PVN demonstrated that BiP mRNA was expressed in almost all the neurons of arginine vasopressin (AVP), an antidiuretic hormone. BiP mRNA expression levels were increased in proportion to AVP mRNA expression in the SON and PVN under dehydration. These data suggest that BiP is involved in the homeostasis of ER function in the AVP neurons in the SON and PVN.     

Co-expression of the Suaeda salsa SsNHX1 and Arabidopsis AVP1 confer greater salt tolerance to transgenic rice than the single SsNHX1

Transgenic rice plants co-expressing the Suaeda salsa SsNHX1 (vacuolar membrane Na⁺/H⁺ antiporter) and Arabidopsis AVP1 (vacuolar H⁺-PPase) showed enhanced salt tolerance during 3 d of 300 mM NaCl treatment under outdoor growth conditions. These transgenic rice seedlings also grew better on MS medium containing 150 mM NaCl compared to SsNHX1-transformed lines and non-transformed controls. Measurements on isolated vacuolar membrane vesicles derived from the salt stressed SsNHX1+AVP1-transgenic plants demonstrated that the vesicles had increased V-PPase hydrolytic activity in comparison with the Ss-transgenics and non-transgenics. Moreover the V-PPase activity was closely related to the development period of the SA-transgenic seedlings and markedly higher in 3-week-old seedlings than in 5-week-old seedlings. Statistic analysis indicated that the SA-transgenic rice plants contained relatively more ions with higher K⁺/Na⁺ ratio in their shoots compared to the SsNHX1-transformed lines upon salt treatment. Furthermore, these SA-transformants also exhibited relatively higher level of photosynthesis and root proton exportation capacity whereas reduced H₂O₂ generation in the same plants. In general, these results supported the hypothesis that simultaneous expression of the SsNHX1 and AVP1 conferred greater performance to the transgenic plants than that of the single SsNHX1.Feng-Yun Zhao and Xue-Jie Zhang contributed equally to this work     

The Role of OXT,OXTR, AVP,and AVPR1a Gene Expression in the Course of Schizophrenia

Schizophrenia is a serious and chronic mental illness, the symptoms of which usually appear for the first time in late adolescence or early adulthood. To date, much research has been conducted on the etiology of schizophrenia; however, it is still not fully understood. Oxytocin and vasopressin as neuromodulators that regulate social and emotional behavior are promising candidates for determining the vulnerability to schizophrenia. The aim of this study was to evaluate the expression of OXT, OXTR, AVP, and AVPR1a genes at the mRNA and protein levels in patients with schizophrenia. Due to the neurodegenerative nature of schizophrenia, the study group was divided into two subgroups, namely, G1 with a diagnosis that was made between 10 and 15 years after the onset of the illness, and G2 with a diagnosis made up to two years after the onset of the illness. Moreover, the relationship between the examined genes and the severity of schizophrenia symptoms, assessed using PANSS (Positive and Negative Syndrome Scale) and CDSS scales (Clinical Depression Scale for Schizophrenia) was evaluated. The analysis of the expression of the studied genes at the mRNA and protein levels showed statistically significant differences in the expression of all the investigated genes. OXT and AVPR1a gene expression at both the mRNA and protein levels were significantly lower in the schizophrenia group, and OXTR and AVP gene expression at both the mRNA and protein levels was higher in the schizophrenia subjects than in the controls. Furthermore, a significant correlation of OXT gene expression at the mRNA and protein levels with the severity of depressive symptoms in schizophrenia as assessed by CDSS was found.     

Mammalian FMRF-NH2-like peptide in rat pituitary: decrease by osmotic stimulus.

Previous studies with the Brattleboro rat suggested a possible interaction at the pituitary level between AVP and the neuropeptide, F-8-F-NH₂. In order to test this hypothesis, we studied the effect of various osmotic stimuli on neurohypophyseal F-8-F-NH₂. In rats drinking 2% NaCl solution for two days, neural lobe AVP and F-8-F-NH₂ levels were equally reduced by 87%. After maximal depletion, pituitary levels of F-8-F-NH₂ and AVP rebounded in parallel when normal drinking water was reintroduced. Pituitary stalk transection depleted neurohypophyseal F-8-F-NH₂. The results of this study suggest that neurohypophyseal F-8-F-NH₂ originates from the hypothalamus and, furthermore, is coreleased along with AVP in response to hyperosmotic stimuli.     

Altered alertness of vasopressin-secreting transgenic mice

We evaluated behavior and cognitive performance in a line of transgenic mice that overexpress the rat gene for vasopressin. Open field testing revealed greatest habituation in homozygous mice. Passive avoidance performance indicated equal learning and memory ability of transgenic compared to normal mice. Drinking behavior following exposure to 10% sucrose solution suggested diminished neophobia in homozygous mice. These observations are consistent with enhanced attention and alertness in the transgenic animals and support prior observations on the effects of vasopressin on behavior and cognitive function.     

Synthesis and renal effects of Ala-Gly-[Arg8]-vasopressin

A new neurohypophyseal hormone analogue, Ala-Gly-[Arg⁸]-vasopressin, was synthesized by the stepwise solution techniques and its effect on systemic blood pressure and renal function was examined in nondiuretic Sprague-Dawley rats. Clearance of inulin was used to study glomerular filtration rate. Intravenous administration of 50 pmole/100 g. b. wt. Ala-Gly-[Arg⁸]-vasopressin caused diuresis and natriuresis without significant change of mean arterial blood pressure. The fractional excretion of sodium was increased by 225% within 10 min after the analogue administration. The present study suggests that this analogue has a direct effect on renal tubular transport of electrolyte independent of affecting systemic circulation.