Characterization of the responses of oxytocin‐ and vasopressin‐secreting neurones in the supraoptic nucleus to osmotic stimulation

Brimble, M. J.; Dyball, R. E. J.

doi:10.1113/jphysiol.1977.sp011999

Cited by 272 publications

(209 citation statements)

References 21 publications

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“…Several studies have demonstrated that injection of hypertonic NaCl solution induces a rapid AVP release (32,33). In such an acute physiological situation, SDF-1 exerts an inhibitory effect on induced AVP secretion.…”

Section: Discussionmentioning

confidence: 99%

The chemokine SDF-1/CXCL12 modulates the firing pattern of vasopressin neurons and counteracts induced vasopressin release through CXCR4

Callewaere

Banisadr

Desarménien

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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Chemokines play a key role in inflammation. They are expressed not only in neuroinflammatory conditions, but also constitutively by different cell types, including neurons in the normal brain, suggesting that they may act as modulators of neuronal functions. Here, we investigated a possible neuroendocrine role of the chemokine stromal cell-derived factor 1 (SDF-1)͞CXCL12. We demonstrated the colocalization of SDF-1 and its receptor CXCR4 with arginine vasopressin (AVP) in the magnocellular neurons of the supraoptic nucleus (SON) and the paraventricular hypothalamic nucleus and on AVP projections to the neurohypophysis. Electrophysiological recordings of SON neurons demonstrated that SDF-1 affects the electrical activity of AVP neurons through CXCR4, resulting in changes in AVP release. We observed that SDF-1 can blunt the autoregulation of AVP release in vitro and counteract angiotensin II-induced plasma AVP release in vivo. Furthermore, a short-term physiological increase in AVP release induced by enhanced plasma osmolarity, which was produced by the administration of 1 M NaCl i.p., was similarly blocked by central injection of SDF-1 through CXCR4. A change in water balance by long-term salt loading induced a decrease in both SDF-1 and CXCR4 parallel to that of AVP immunostaining in SON. From these data, we demonstrate that chemokine actions in the brain are not restricted to inflammatory processes. We propose to add to the known autoregulation of AVP on its own neurons, a second autocrine system induced by SDF-1 able to modulate central AVP neuronal activity and release.dehydration ͉ hypothalamic magnocellular neurons ͉ neuroendocrine ͉ neuromodulation ͉ posterior pituitary A rginine vasopressin (AVP) and oxytocin (OT) are synthesized in the magnocellular neurosecretory neurons of the hypothalamic supraoptic nucleus (SON) and paraventricular nucleus (PVN) and then transported through the median eminence to the posterior lobe of the pituitary gland, where they are secreted into the general blood circulation. AVP is known to be primarily involved in water absorption in the distal nephron of the kidney, thus regulating drinking behavior, whereas the functions of OT during parturition to increase uterine contraction and during suckling have been well described (1).Chemokines are small, secreted molecules (7-14 kDa) with chemoattractant properties whose main accepted role is leukocyte recruitment in inflammatory sites (2, 3). Recent investigations into the possible involvement of chemokines in a number of neurological disorders associated with neuroinflammation have led to the possibility that many chemokines and their respective receptors can be expressed in the brain (4). However, recent data demonstrated that they not only are observed in neuroinflammatory conditions but also are constitutively expressed by different cell types, including neurons in the normal brain (5-7). These data suggest that chemokines may act as modulators of neuronal functions.Among chemokines and chemokine receptors with possible neuromo...

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Section: Discussionmentioning

confidence: 99%

The chemokine SDF-1/CXCL12 modulates the firing pattern of vasopressin neurons and counteracts induced vasopressin release through CXCR4

Callewaere

Banisadr

Desarménien

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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“…In dehydrated animals, both the hypertonicity and hypovolemia of body fluids provide stimuli that activate neurons in the SON and PVN, as well as sensor sites in the lamina terminalis projecting to these two nuclei (18). Electrophysiological investigations and studies of expression of c-fos in the SON and PVN show that both vasopressin-and oxytocin-containing neurons in these nuclei, as well as neurons in the lamina terminalis, are activated by hypertonicity and dehydration in the rat (17,(32)(33)(34). The vasopressin and oxytocin-containing neurons send efferent neural connections via the base of the hypothalamus and median eminence to the posterior pituitary gland, where oxytocin and vasopressin are secreted into the circulation (16).…”

Section: Discussionmentioning

confidence: 99%

Visualization of functionally activated circuitry in the brain

Wilson

Nag

Davern

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

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“…Phasic firing is a response by AVP cells to an increased physiological stress, such as hyperosmolality (Brimble and Dyball, 1977) or exsanguination (Poulain et al, 1977), and in vitro can be induced by an increase in the osmotic pressure of the perfusion media (Bourque and Renaud, 1984). The effects of osmotic stress, and also presumably those too of blood loss, are mediated in part by a net depolarization of the membrane potential that has several contributing factors (Bourque, 1998).…”

Section: Transient Activity During Increased Stressmentioning

confidence: 99%

“…Furthermore, in response to blood loss (Wakerley et al, 1975), progressive dehydration (Wakerley et al, 1978), or hypertonic saline injection (Brimble and Dyball, 1977), almost all AVP cells cease irregular firing and adopt the phasic pattern. This transition is maintained in vitro and hypothalamic explant preparations exhibit increased phasic activity when the osmotic pressure of the perfusion media is raised (Bourque and Renaud, 1984).…”

Section: Introductionmentioning

confidence: 99%

Burst Initiation and Termination in Phasic Vasopressin Cells of the Rat Supraoptic Nucleus: A Combined Mathematical, Electrical, and Calcium Fluorescence Study

Roper¹,

Callaway²,

Armstrong³

2004

J. Neurosci.

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Vasopressin secreting neurons of the rat hypothalamus discharge lengthy, repeating bursts of action potentials in response to physiological stress. Although many electrical currents and calcium-dependent processes have been isolated and analyzed in these cells, their interactions are less well fathomed. In particular, the mechanism of how each burst is triggered, sustained, and terminated is poorly understood. We present a mathematical model for the bursting mechanism, and we support our model with new simultaneous electrical recording and calcium imaging data. We show that bursts can be initiated by spike-dependent calcium influx, and we propose that the resulting elevation of bulk calcium inhibits a persistent potassium current. This inhibition depolarizes the cell above threshold and so triggers regenerative spiking and further calcium influx. We present imaging data to show that bulk calcium reaches a plateau within the first few seconds of the burst, and our model indicates that this plateau occurs when calcium influx is balanced by efflux and uptake into stores. We conjecture that the burst is terminated by a slow, progressive desensitization to calcium of the potassium leak current. Finally, we propose that the opioid dynorphin, which is known to be secreted from the somatodendritic region and has been shown previously to regulate burst length and phasic activity in these cells, is the autocrine messenger for this desensitization.

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Characterization of the responses of oxytocin‐ and vasopressin‐secreting neurones in the supraoptic nucleus to osmotic stimulation

Cited by 272 publications

References 21 publications

The chemokine SDF-1/CXCL12 modulates the firing pattern of vasopressin neurons and counteracts induced vasopressin release through CXCR4

The chemokine SDF-1/CXCL12 modulates the firing pattern of vasopressin neurons and counteracts induced vasopressin release through CXCR4

Visualization of functionally activated circuitry in the brain

Burst Initiation and Termination in Phasic Vasopressin Cells of the Rat Supraoptic Nucleus: A Combined Mathematical, Electrical, and Calcium Fluorescence Study

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