Arginine vasopressin (AVP) depletion in neurons of the suprachiasmatic nuclei affects the AVP content of the paraventricular neurons and stimulates adrenocorticotrophic hormone release

Gomez, Felipe; Chapleur, Michèle; Fernette, Brigitte; Burlet, C.; Nicolas, Jean‐Pierre; Burlet, Arlette

doi:10.1002/(sici)1097-4547(19971115)50:4<565::aid-jnr7>3.0.co;2-c

Cited by 27 publications

(17 citation statements)

References 36 publications

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“…Plasma VP (and oxytocin) levels, however, were not measured, and a physiological confirmation of the stimulatory effect of SCN-VP on the magnocellular system is ORDER REPRINTS thus lacking. In the meantime the inhibitory effect of VP on corticosterone release as just described has been reported by a number of other laboratories as well (Gomez et al, 1997;Wotjak et al, 1996), but still the effect is very surprising to many (endocrinologists) since the inhibitory action of VP is completely opposite to the previously described and better known stimulatory role of VP in the HPA stress response. The stimulatory action of VP on ACTH and corticosterone release was definitely established in the early 1980s (Gillies et al, 1982;Rivier and Vale, 1983;Rivier et al, 1984).…”

Section: Scn Output To Endocrine Neuronsmentioning

confidence: 73%

“…In contrast to the indirect connections to the hypophysiotropic neurons, the SCN seems to have a direct influence on magnocellular neurons of the PVN. Indeed, specific VP depletion in the SCN affects the VP content of magnocellular vs. parvocellular (i.e., hypophysiotropic neurons) PVN neurons in different ways (Gomez et al, 1997). VP content increases in magnocellular PVN neurons, whereas it decreases in parvocellular neurons, suggesting decreased release of VP in the general circulation, and an increased release of VP (and CRH) into the portal circulation.…”

Section: Scn Output To Endocrine Neuronsmentioning

confidence: 97%

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The Biological Clock: The Bodyguard of Temporal Homeostasis

Perreau-Lenz

Pévet²,

Buijs

et al. 2004

Chronobiology International

107

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In order for any organism to function properly, it is crucial that it be table to control the timing of its biological functions. An internal biological clock, located, in mammals, in the suprachiasmatic nucleus of the hypothalamus (SCN), therefore carefully guards this temporal homeostasis by delivering its message of time throughout the body. In view of the large variety of body functions (behavioral, physiological, and endocrine) as well as the large variety in their preferred time of main activity along the light:dark cycle, it seems logical to envision different means of time distribution by the SCN. In the present review, we propose that even though it presents a unimodal circadian rhythm of general electrical and metabolic activity, the SCN seems to use several sorts of output connections that are active at different times along the light:dark cycle to control the rhythmic expression of different body functions. Although the SCN is suggested to use diffusion of synchronizing factors in the rhythmic control of behavioral functions, it also needs neuronal connections for the control of endocrine functions. The distribution of the time-of-day message to neuroendocrine systems is either directly onto endocrine neurons or via intermediate neurons located in specific SCN targets. In addition, the SCN uses its connections with the autonomic nervous system for spreading its time-of-day message, either by setting the sensitivity of endocrine glands (i.e., thyroid, adrenal, ovary) or by directly controlling an endocrine output (i.e., melatonin synthesis). Moreover, the SCN seems to use different neurotransmitters released at different times along the light:dark cycle for each of the different connection types presented. Clearly, the temporal homeostasis of endocrine functions results from a diverse set of biological clock outputs.

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Section: Scn Output To Endocrine Neuronsmentioning

confidence: 73%

Section: Scn Output To Endocrine Neuronsmentioning

confidence: 97%

The Biological Clock: The Bodyguard of Temporal Homeostasis

Perreau-Lenz

Pévet²,

Buijs

et al. 2004

Chronobiology International

107

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“…The SCN regulates HPA axis activity through the PVN via AVP, which serves as a neurotransmitter in the SCN afferents to the hypothalamic PVN (Kalsbeek et al, 2010). The regulatory function of these afferents is confirmed by experiments with microinjections of AVP-cytotoxic monoclonal antibodies into the SCN, which produce a significant reduction of immunoreactive AVP and AVP mRNA expression there as well as in parvicellular neurons of the PVN (Gomez et al, 1997). Study of post-mortem human brains revealed a pronounced circadian variation in the activity of AVP-containing neurons in the SCN (Kalsbeek et al, 2010).…”

Section: Avp In Regulation Of Hpa Axis Stress Responsiveness During Amentioning

confidence: 92%

Stress Responsiveness of the Hypothalamic–Pituitary–Adrenal Axis: Age-Related Features of the Vasopressinergic Regulation

Goncharova¹

2013

Front. Endocrinol.

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The hypothalamic–pituitary–adrenal (HPA) axis plays a key role in adaptation to environmental stresses. Parvicellular neurons of the hypothalamic paraventricular nucleus secrete corticotrophin releasing hormone (CRH) and arginine vasopressin (AVP) into pituitary portal system; CRH and AVP stimulate adrenocorticotropic hormone (ACTH) release through specific G-protein-coupled membrane receptors on pituitary corticotrophs, CRHR1 for CRH and V1b for AVP; the adrenal gland cortex secretes glucocorticoids in response to ACTH. The glucocorticoids activate specific receptors in brain and peripheral tissues thereby triggering the necessary metabolic, immune, neuromodulatory, and behavioral changes to resist stress. While importance of CRH, as a key hypothalamic factor of HPA axis regulation in basal and stress conditions in most species, is generally recognized, role of AVP remains to be clarified. This review focuses on the role of AVP in the regulation of stress responsiveness of the HPA axis with emphasis on the effects of aging on vasopressinergic regulation of HPA axis stress responsiveness. Under most of the known stressors, AVP is necessary for acute ACTH secretion but in a context-specific manner. The current data on the AVP role in regulation of HPA responsiveness to chronic stress in adulthood are rather contradictory. The importance of the vasopressinergic regulation of the HPA stress responsiveness is greatest during fetal development, in neonatal period, and in the lactating adult. Aging associated with increased variability in several parameters of HPA function including basal state, responsiveness to stressors, and special testing. Reports on the possible role of the AVP/V1b receptor system in the increase of HPA axis hyperactivity with aging are contradictory and requires further research. Many contradictory results may be due to age and species differences in the HPA function of rodents and primates.

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“…Although how photic stimulation is transmitted to the ARC remains to be elucidated, there are several possible neural pathways from the suprachiasmatic nucleus, which receives photic information to integrate circadian rhythm [5], to the ARC, e.g. corticotropin-releasing hormone neurons via the periventricular nucleus [12,16], serotonergic and histaminergic neurons via the raphe and tuberomammillary nucleus [26,27,39]. To clarify the communication pathways for photic stimulation to the ARC could consolidate the present hypothesis.…”

Section: Discussionmentioning

confidence: 99%

Possible Involvement of Neuropeptide Y in Photo-Induced Suppression of Growth Hormone Pulses

Fujisawa

Matsuwaki

Yamanouchi

et al. 2013

The Journal of Veterinary Medical Science

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ABSTRACT. It is well established that growth hormone (GH) is secreted in a pulsatile manner. Although the GH pulse-generating mechanism is not fully understood, we have previously reported that neuropeptide Y (NPY) profiles in the cerebrospinal fluid were negatively correlated with serum GH pulses. In addition, it is known that photic stimulation suppresses GH pulses for a certain period of time. In the present study, to investigate the involvement of NPY in regulating GH pulse generation, NPY gene expression in the arcuate nucleus (ARC) of the hypothalamus in rats was analyzed at around the lights on. First, we confirmed that GH pulses did not occur for around 1.5 hr after the start of the light phase. Then, we analyzed the activity of neurons and expression of NPY mRNA 1 hr before and 0.5 and 2 hr after lights on. Both the activity of neurons, which was evaluated by immunohistochemical detection for phosphorylated-cAMP response element binding protein (pCREB), and NPY mRNA levels in the caudal ARC were higher at 0.5 hr after lights on than the other two time points, while pCREB-positive cell numbers in the rostral ARC remained unchanged throughout the experimental period. In addition, NPY immunoreactivity in the periventricular nucleus (PeVN) was also higher at 0.5 hr after lights on than the other time points. These results suggest that NPY neurons in the caudal ARC projecting to the PeVN play a role in inhibiting GH pulses at the commencement of the light phase. It is well known that the secretion pattern of growth hormone (GH) is described as a pulsatile manner in various mammalian species [11,17]. As well as other pituitaryderived hormones, GH secretion is thought to be under the control of several hypothalamic neuropeptides. From the results of passive immunization, antagonization and in vivo administration experiments, GH-releasing hormone (GHRH) and somatostatin (SRIF) have been recognized as major neuropeptides regulating GH pulses [4,19,22,34,36]. The general hypothesis is that GHRH, the stimulator of GH secretion, triggers the pulsatile secretion of GH, and SRIF, the inhibitor, keeps the baseline at low levels [35]. Furthermore, recent studies suggest that some other peptides, such as neuropeptide Y (NPY) and ghrelin, are also involved in the GH pulse-generating system [11,37].There are several factors known to modify the pulsatile secretion of GH. For example, stress is one of the GH-pulse inhibiting stimuli, and glucocorticoids, a major stressresponsive hormone, are thought to suppress GH secretion [31]. Other hormones such as thyroxin and insulin-like growth factor-I also have modifying effects on GH pulses [11]. Photic stimulation is known to be another GH pulse suppressive environmental factor [38]. Davies et al. [7] reported that nocturnal photic stimulation inhibited both spontaneous and induced GH secretion in rats and that a similar trough in GH was also observed during the first hour of the normal light phase. They also suggested that SRIF neurons located in the periventricular nucleus (Pe...

show abstract

Arginine vasopressin (AVP) depletion in neurons of the suprachiasmatic nuclei affects the AVP content of the paraventricular neurons and stimulates adrenocorticotrophic hormone release

Cited by 27 publications

References 36 publications

The Biological Clock: The Bodyguard of Temporal Homeostasis

The Biological Clock: The Bodyguard of Temporal Homeostasis

Stress Responsiveness of the Hypothalamic–Pituitary–Adrenal Axis: Age-Related Features of the Vasopressinergic Regulation

Possible Involvement of Neuropeptide Y in Photo-Induced Suppression of Growth Hormone Pulses

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