Vasoactive intestinal polypeptide precursor mRNA exhibits diurnal variation in the rat suprachiasmatic nuclei

1993 ◽  
Vol 20 (3) ◽  
pp. 259-262 ◽  
Author(s):  
Jing Yang ◽  
Felino Ramon A. Cagampang ◽  
Yasuhisa Nakayama ◽  
Shin-Ichi T. Inouye
1988 ◽  
Vol 116 (3) ◽  
pp. 335-341 ◽  
Author(s):  
G. Burns ◽  
B. L. Brown ◽  
P. R. M. Dobson

ABSTRACT We have previously reported a lack of effect of a depolarizing concentration of K+ on the release of vasoactive intestinal polypeptide (VIP) from the perifused rat hypothalamus, and suggested that this was due to the presence of an endogenous inhibitor of the release of VIP. In this study we report that the VIP response to K+ was restored if the hypothalami were obtained from animals killed during the dark phase of the light–dark cycle. Adrenaline blocked the K+-stimulated release of VIP when used at a concentration of 0·1 μmol/l; however, at a higher concentration (10 μmol/l) adrenaline stimulated the basal release of VIP. The use of specific receptor antagonists indicated that this dual effect of adrenaline was mediated through two distinct receptors, a stimulatory β-receptor and an inhibitory α2-receptor. The suggestion that adrenaline might be the endogenous inhibitor of the release of VIP, mediating the diurnal variation in the effect of K+, was supported by studies where 50 mmol K+/l was perifused concomitantly with an α2-antagonist, restoring the VIP response to K+ in light-phase hypothalami. In conclusion, adrenaline has a dual role in the control of VIP release and may function to inhibit the K+-stimulated release of VIP in our system. J. Endocr. (1988) 116, 335–341


2002 ◽  
Vol 14 (8) ◽  
pp. 639-646 ◽  
Author(s):  
H. E. Reed ◽  
D. J. Cutler ◽  
T. M. Brown ◽  
J. Brown ◽  
C. W. Coen ◽  
...  

2003 ◽  
Vol 177 (1) ◽  
pp. 7-15 ◽  
Author(s):  
HD Piggins ◽  
DJ Cutler

Biological oscillations with an endogenous period of near 24 h (circadian rhythms) are generated by the master circadian pacemaker or clock located in the suprachiasmatic nuclei (SCN) of the hypothalamus. This clock is synchronised to recurring environmental signals conveyed by selective neural pathways. One of the main chemical constituents of SCN neurones is vasoactive intestinal polypeptide (VIP). Such neurones are retinorecipient and activated by light. Exogenous application of VIP resets the SCN circadian clock in a light-like manner, both in vivo and in vitro. These resetting actions appear to be mediated through the VPAC2 receptor (a type of receptor for VIP). Unexpectedly, genetically ablating expression of the VPAC2 receptor renders the circadian clock arrhythmic at the molecular, neurophysiological and behavioural levels. These findings indicate that this intrinsic neuropeptide acting through the VPAC2 receptor participates in both resetting to light and maintenance of ongoing rhythmicity of the SCN.


Endocrinology ◽  
2008 ◽  
Vol 149 (6) ◽  
pp. 3130-3136 ◽  
Author(s):  
Catherine A. Christian ◽  
Suzanne M. Moenter

A surge of GnRH release signals the LH surge that triggers ovulation. The GnRH surge is dependent on a switch in estradiol feedback from negative to positive and, in rodents, a daily neural signal, likely from the suprachiasmatic nuclei. Vasoactive intestinal polypeptide (VIP) may be involved in suprachiasmatic nuclei-GnRH neuron communication. Here we assessed the effects of acute VIP (5 min treatment) on GnRH neuron function using targeted extracellular recordings of firing activity of GnRH neurons in brain slices. We examined the effect of VIP on firing rate at different times of day using an established ovariectomized, estradiol-treated (OVX+E) mouse model that exhibits daily LH surges timed to the late afternoon. Cells from OVX animals (no estradiol) did not respond to VIP, regardless of time of day. With estradiol, the effect of VIP on GnRH neurons was dependent on the time of recording. During negative feedback, OVX+E cells did not respond. VIP increased firing in cells recorded during surge onset, but this excitatory response was reduced at surge peak. Acute treatment of OVX+E cells during surge peak with a VIP receptor antagonist decreased GnRH neuron firing. This suggests endogenous VIP may both increase GnRH neuron firing during the surge and occlude response to exogenous VIP. These data provide functional evidence for VIP effects on GnRH neurons and indicate that both estradiol and time of day gate the GnRH neuron response to this peptide. VIP may provide an excitatory signal from the circadian clock that helps time the GnRH surge.


2007 ◽  
Vol 97 (3) ◽  
pp. 2553-2558 ◽  
Author(s):  
T. M. Brown ◽  
C. S. Colwell ◽  
J. A. Waschek ◽  
H. D. Piggins

Vasoactive intestinal polypeptide (VIP), acting via the VPAC2 receptor, is a key signaling pathway in the suprachiasmatic nuclei (SCN), the master clock controlling daily rhythms in mammals. Most mice lacking functional VPAC2 receptors are unable to sustain behavioral rhythms and lack detectable SCN electrical rhythms in vitro. Adult mice that do not produce VIP (VIP/PHI−/−) exhibit less severe alterations in wheel-running rhythms, but the effects of this deficiency on the amplitude, phasing, or periodicity of their SCN cellular rhythms are unknown. To investigate this, we used suction electrodes to extracellularly record multiple- and single-unit electrical activity in SCN brain slices from mice with varying degrees of VIP deficiency, ranging from wild-type (VIP/PHI+/+) to heterozygous (VIP/PHI+/−) and VIP/PHI−/− animals. We found decreasing proportions of rhythmic cells in SCN slices from VIP/PHI+/+ (∼91%, n = 23) through VIP/PHI-/+ (∼71%, n = 28) to VIP/PHI−/− mice (62%; n = 37) and a parallel trend toward decreasing amplitude in the remaining rhythmic cells. SCN neurons from VIP/PHI−/− mice exhibited a broad range in the period and phasing of electrical rhythms, concordant with the known alterations in their behavioral rhythms. Further, treatment of VIP/PHI−/− slices with a VPAC2 receptor antagonist significantly reduced the proportion of oscillating neurons, suggesting that VPAC2 receptors still become activated in the SCN of these mice. The results establish that VIP is important for appropriate periodicity and phasing of SCN neuronal rhythms and suggest that residual VPAC2 receptor signaling promotes rhythmicity in adult VIP/PHI−/− mice.


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