scholarly journals Phasic Spiking in Vasopressin Neurons: How and Why

2021 ◽  
Author(s):  
Duncan MacGregor
Keyword(s):  
Vasopressin Neurons

scholarly journals Circulating Secretin Activates Supraoptic Nucleus Oxytocin and Vasopressin Neurons via Noradrenergic Pathways in the Rat

Endocrinology ◽  
2010 ◽  
Vol 151 (6) ◽  
pp. 2681-2688 ◽  
Author(s):  
Sathya Velmurugan ◽  
Paula J. Brunton ◽  
Gareth Leng ◽  
John A. Russell
Keyword(s):  
Amino Acid ◽  
Firing Rate ◽  
Noradrenaline Release ◽  
Supraoptic Nucleus ◽  
Female Rats ◽  
Adrenoceptor Antagonist ◽  
Intracerebroventricular Infusion ◽  
Neuroendocrine Neurons ◽  
Vasopressin Neurons

Secretin is a 27-amino acid brain-gut peptide from duodenal S-cells. We tested the effects of systemic administration of secretin to simulate its postprandial release on neuroendocrine neurons of the supraoptic nucleus (SON) in urethane-anesthetized female rats. Secretin dose-dependently increased the firing rate of oxytocin neurons, more potently than cholecystokinin, and dose-dependently increased plasma oxytocin concentration. The effect of secretin on SON vasopressin neurons was also predominantly excitatory, in contrast to the inhibitory actions of cholecystokinin. To explore the involvement of noradrenergic inputs in secretin-induced excitation, benoxathian, an α1-adrenoceptor antagonist, was infused intracerebroventricularly. Benoxathian intracerebroventricular infusion blocked the excitation by secretin of both oxytocin and vasopressin neurons. To test the role of local noradrenaline release in the SON, benoxathian was microdialyzed onto the SON. The basal firing rate of oxytocin neurons was slightly reduced and the secretin-induced excitation was attenuated during benoxathian microdialysis. Hence, noradrenergic pathways mediate the excitation by systemic secretin of oxytocin neurons via α1-adrenoceptors in the SON. As both systemic secretin and oxytocin are involved in regulating gastrointestinal functions and natriuresis, systemically released secretin might act partly through oxytocin.

scholarly journals Glutamatergic Inputs Contribute to Phasic Activity in Vasopressin Neurons

2010 ◽  
Vol 30 (4) ◽  
pp. 1221-1232 ◽  
Author(s):  
J.-M. Israel ◽  
D. A. Poulain ◽  
S. H. R. Oliet
Keyword(s):  
Phasic Activity ◽  
Vasopressin Neurons

scholarly journals Activity-Dependent Modulation of Neurotransmitter Innervation to Vasopressin Neurons of the Supraoptic Nucleus

Endocrinology ◽  
2005 ◽  
Vol 146 (1) ◽  
pp. 348-354 ◽  
Author(s):  
Nancy K. Mueller ◽  
Shi Di ◽  
Charles M. Paden ◽  
James P. Herman
Keyword(s):  
Glutamic Acid ◽  
Glutamic Acid Decarboxylase ◽  
Supraoptic Nucleus ◽  
Glutamate Transporter ◽  
Acid Decarboxylase ◽  
Vesicular Glutamate Transporter ◽  
Salt Loading ◽  
Synaptic Boutons ◽  
Vasopressin Neurons ◽  
Activity Dependent

Confocal microscopy was used to assess activity-dependent neuroplasticity in neurotransmitter innervation of vasopressin immunoreactive magnocellular neurons in the supraoptic nucleus (SON). Vesicular glutamate transporter 2, glutamic acid decarboxylase, and dopamine β-hydroxylase (DBH) synaptic boutons were visualized in apposition to vasopressin neurons in the SON. A decrease in DBH synaptic boutons per cell was seen upon salt loading, indicating diminished noradrenergic/adrenergic innervation. Loss of DBH appositions to vasopressin neurons was associated with a general loss of DBH immunoreactivity in the SON. In contrast, the number of vesicular glutamate transporter 2 synaptic boutons per neuron increased with salt loading, consistent with increased glutamatergic drive of magnocellular SON neurons. Salt loading also caused an increase in the total number of glutamic acid decarboxylase synaptic boutons on vasopressinergic neurons, suggesting enhanced inhibitory innervation as well. These studies indicate that synaptic plasticity compensates for increased secretory demand and may indeed underlie increased secretion, perhaps via neurotransmitter-specific, activity-related changes in synaptic contacts on vasopressinergic magnocellular neurons in the SON.

scholarly journals Kainate Receptor-Induced Retrograde Inhibition of Glutamatergic Transmission in Vasopressin Neurons

2012 ◽  
Vol 32 (4) ◽  
pp. 1301-1310 ◽  
Author(s):  
V. D. J. Bonfardin ◽  
D. T. Theodosis ◽  
A. Konnerth ◽  
S. H. R. Oliet
Keyword(s):  
Kainate Receptor ◽  
Glutamatergic Transmission ◽  
Vasopressin Neurons

scholarly journals Transcriptomic Analysis Reveals that Atf3/c-Jun/Lgals3 axis is associated with Central Diabetes Insipidus after Hypothalamic Injury

2021 ◽  
Author(s):  
Mingfeng Zhou ◽  
Yichao Ou ◽  
Guangsen Wu ◽  
Kai Li ◽  
Junjie Peng ◽  
...  
Keyword(s):  
Diabetes Insipidus ◽  
Arginine Vasopressin ◽  
Body Fluid ◽  
Microglial Activation ◽  
The Body ◽  
Transcriptomic Analysis ◽  
Central Diabetes Insipidus ◽  
Electrolyte Imbalance ◽  
Hypothalamic Injury ◽  
Vasopressin Neurons

Background: Hypothalamic injury causes several complicated neuroendocrine-associated disorders, such as water-electrolyte imbalance, obesity, and hypopituitarism. Among these, central diabetes insipidus (CDI), characterized by polyuria, polydipsia, low urine specific gravity, and deficiency of arginine vasopressin contents, is a typical complication after hypothalamic injury. Methods: CDI was induced by hypothalamic pituitary stalk injury in male animals. Behavioral parameters and blood sample were collected to evaluate the characteristics of body fluid metabolism imbalance. The brains were harvested for high-throughput RNA sequencing and immunostaining to identify pathophysiological changes in corresponding hypothalamic nuclei. Results: Based on transcriptomic analysis, we demonstrated the upregulation of the Atf3/c-Jun axis and identified Lgals3, a microglial activation related gene, as the most significant target gene in response to the body fluid imbalance in CDI. Furthermore, we found that the microglia possessed elevated phagocytic ability, which could promote the elimination of arginine vasopressin neurons after hypothalamic injury. Conclusion: Our findings suggested that the Atf3/c-Jun/Lgals3 axis was associated with the microglial activation, and might participate in the loss of functional arginine vasopressin neurons in CDI after hypothalamic injury.

scholarly journals Formation of Endoplasmic Reticulum-Associated Compartment in Vasopressin Neurons: A Mechanism by Which Endoplasmic Reticulum Stress is Reduced

2015 ◽  
Vol 21 (3) ◽  
pp. 173-180
Author(s):  
Hiroshi ARIMA ◽  
Yoshinori AZUMA ◽  
Yoshiaki MORISHITA ◽  
Masayuki HAYASHI ◽  
Daisuke HAGIWARA
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Vasopressin Neurons

scholarly journals Paraventricular NUCB2/Nesfatin-1 Supports Oxytocin and Vasopressin Neurons to Control Feeding Behavior and Fluid Balance in Male Mice

Endocrinology ◽  
2016 ◽  
Vol 157 (6) ◽  
pp. 2322-2332 ◽  
Author(s):  
Masanori Nakata ◽  
Darambazar Gantulga ◽  
Putra Santoso ◽  
Boyang Zhang ◽  
Chiaki Masuda ◽  
...  
Keyword(s):  
Feeding Behavior ◽  
Fluid Balance ◽  
Male Mice ◽  
Vasopressin Neurons
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