Aquaporin 4 differentially modulates osmotic effects on vasopressin neurons in rat supraoptic nucleus

2021 ◽  
Author(s):  
Xiaoran Wang ◽  
Tong Li ◽  
Yang Liu ◽  
Shuwei Jia ◽  
Xiaoyu Liu ◽  
...  
Keyword(s):  
Supraoptic Nucleus ◽  
Aquaporin 4 ◽  
Vasopressin Neurons ◽  
Osmotic Effects

scholarly journals Alleviation of Cerebral Infarction of Rats With Middle Cerebral Artery Occlusion by Inhibition of Aquaporin 4 in the Supraoptic Nucleus

ASN NEURO ◽  
2020 ◽  
Vol 12 ◽  
pp. 175909142096055 ◽  
Author(s):  
Dan Cui ◽  
Shuwei Jia ◽  
Jiawei Yu ◽  
Dongyang Li ◽  
Tong Li ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Cerebral Infarction ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Supraoptic Nucleus ◽  
Artery Occlusion ◽  
Aquaporin 4 ◽  
Vasopressin Neurons ◽  
Cerebral Artery Occlusion

In ischemic stroke, vasopressin hypersecretion is a critical factor of cerebral swelling and brain injury. To clarify neural mechanisms underlying ischemic stroke-evoked vasopressin hypersecretion, we observed the effect of unilateral permanent middle cerebral artery occlusion (MCAO) in rats on astrocytic plasticity and vasopressin neuronal activity in the supraoptic nucleus (SON) as well as their associated cerebral injuries. MCAO for 8 hr caused cerebral infarction in the MCAO side where water contents also increased. Immunohistochemical examination revealed that the percentage of phosphorylated extracellular signal-regulated protein kinase 1/2 (pERK1/2)-positive vasopressin neurons in the SON of MCAO side was significantly higher than that in non-MCAO side and in sham group. In the cortex, pERK1/2 and aquaporin 4 expressions increased significantly in the infarction area, while glial fibrillary acidic protein (GFAP) reduced significantly compared with the noninfarction side in brain cortex. Microinjection of N-(1,3,4-Thiadiazolyl)nicotinamide-020 [TGN-020, a specific blocker of aquaporin 4] into the SON blocked MCAO-evoked increases in pERK1/2 in the SON as well as the reduction of GFAP and the increase in pERK1/2 and aquaporin 4 in the infarction area of the cortex. Finally, oxygen and glucose deprivation reduced GFAP expression and the colocalization and molecular association of GFAP with aquaporin 4 in the SON in brain slices. These effects were blocked by TGN-020 and/or phloretin, a blocker of astrocytic volume-regulated anion channels. These findings indicate that blocking aquaporin 4 in the SON may reduce the activation of vasopressin neurons and brain injuries elicited by vasopressin during ischemic stroke.

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 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.

Absence of a Difference in the Neurosecretory Activity of Supraoptic Nucleus Vasopressin Neurons of Neuroleptic-Treated Schizophrenic Patients

2005 ◽  
Vol 82 (2) ◽  
pp. 63-69 ◽  
Author(s):  
Yiannis I. Malidelis ◽  
Maria T. Panayotacopoulou ◽  
Joop J. van Heerikhuize ◽  
Unga A. Unmehopa ◽  
Dimitra P. Kontostavlaki ◽  
...  
Keyword(s):  
Supraoptic Nucleus ◽  
Schizophrenic Patients ◽  
Vasopressin Neurons

Calbindin D28k and calretinin in oxytocin and vasopressin neurons of the rat supraoptic nucleus

1999 ◽  
Vol 298 (1) ◽  
pp. 11-19 ◽  
Author(s):  
R. Arai ◽  
David M. Jacobowitz ◽  
Takehiko Hida
Keyword(s):  
Supraoptic Nucleus ◽  
Calbindin D28k ◽  
Vasopressin Neurons

Alleviation of brain injury by applying TGN-020 in the supraoptic nucleus via inhibiting vasopressin neurons in rats of focal ischemic stroke

Life Sciences ◽  
2021 ◽  
Vol 264 ◽  
pp. 118683 ◽  
Author(s):  
Dan Cui ◽  
Shuwei Jia ◽  
Tong Li ◽  
Dongyang Li ◽  
Xiaoran Wang ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Brain Injury ◽  
Supraoptic Nucleus ◽  
Vasopressin Neurons

Bicuculline blocks an inhibitory baroreflex input to supraoptic vasopressin neurons

1987 ◽  
Vol 252 (5) ◽  
pp. R947-R952 ◽  
Author(s):  
J. H. Jhamandas ◽  
L. P. Renaud
Keyword(s):  
Arterial Pressure ◽  
Supraoptic Nucleus ◽  
Neuronal Firing ◽  
Abrupt Increase ◽  
Long Evans ◽  
Peripheral Arterial ◽  
Vasopressin Neurons ◽  
Baroreceptor Activation ◽  
Alpha Agonist ◽  
Hypothalamic Supraoptic Nucleus

The excitability of vasopressin-secreting neurons in the hypothalamic supraoptic nucleus is transiently depressed by an abrupt increase in arterial pressure sufficient to activate peripheral arterial baroreceptors. The present experiments examined the ability of locally applied transmitter antagonists to alter this response. Extracellular data were obtained from 27 supraoptic vasopressin-secreting neurons in pentobarbital-anesthetized male Long-Evans rats. In seven of eight cells tested, bicuculline (100 microM) reversibly abolished or delayed the anticipated cessation in neuronal firing that accompanied a 40- to 60-mmHg increase in arterial pressure induced by a brief intravenous infusion of the alpha-agonist metaraminol. Similar tests applied to the remaining cells revealed that prazosin (10 microM), timolol (20 microM), or strychnine (100 microM) were ineffective. These findings suggest that gamma-aminobutyric acidA receptors mediate the depressant responses observed among supraoptic vasopressin-secreting neurons consequent to peripheral baroreceptor activation.

Osmotic stimulation of vasopressin mRNA content in the supraoptic nucleus requires synaptic activation

1995 ◽  
Vol 268 (4) ◽  
pp. R1034-R1039 ◽  
Author(s):  
C. D. Sladek ◽  
K. Y. Fisher ◽  
H. E. Sidorowicz ◽  
J. R. Mathiasen
Keyword(s):  
Synaptic Input ◽  
Supraoptic Nucleus ◽  
Kynurenic Acid ◽  
Excitatory Amino Acid ◽  
Vasopressin Release ◽  
Amino Acid Receptors ◽  
Mrna Content ◽  
Supraoptic Neurons ◽  
Vasopressin Neurons

The role of synaptic input to the vasopressin neurons in hypertonicity-induced increase in vasopressin mRNA content was evaluated. Synaptic connection with the anterior hypothalamus is required for hypertonicity to increase vasopressin release. However, the potential for other mechanisms to induce the increase in vasopressin mRNA content is suggested by the fact that hypertonicity induces depolarization of supraoptic neurons independently of synaptic input. Explants of the hypothalamoneurohypophysial system were used to study the effect of depolarization and hypertonicity in the presence and absence of nonspecific synaptic blockade by 15 mM MgSO4 or blockade of excitatory amino acid receptors with kynurenic acid. Vasopressin release and mRNA content were increased by depolarization with 40 mM KCl and by exposure to hypertonicity (P < 0.05). Basal and osmotically stimulated vasopressin release was decreased by MgSO4 and by kynurenic acid. Both agents prevented the hypertonicity-induced increase in vasopressin mRNA content. Thus either synaptic input or increased VP release is required for hypertonicity to increase vasopressin mRNA, and excitatory amino acids are implicated in this response.

scholarly journals Nesfatin-1 Neurons in Paraventricular and Supraoptic Nuclei of the Rat Hypothalamus Coexpress Oxytocin and Vasopressin and Are Activated by Refeeding

Endocrinology ◽  
2007 ◽  
Vol 149 (3) ◽  
pp. 1295-1301 ◽  
Author(s):  
Daisuke Kohno ◽  
Masanori Nakata ◽  
Yuko Maejima ◽  
Hiroyuki Shimizu ◽  
Udval Sedbazar ◽  
...  
Keyword(s):  
Feeding Behavior ◽  
Mrna Expression ◽  
Paraventricular Nucleus ◽  
Supraoptic Nucleus ◽  
Energy Homeostasis ◽  
Rat Hypothalamus ◽  
Hypothalamic Nuclei ◽  
Vasopressin Neurons ◽  
Fine Localization ◽  
Supraoptic Nuclei

Nesfatin-1, a newly discovered satiety molecule, is located in the hypothalamic nuclei, including the paraventricular nucleus (PVN) and supraoptic nucleus (SON). In this study, fine localization and regulation of nesfatin-1 neurons in the PVN and SON were investigated by immunohistochemistry of neuropeptides and c-Fos. In the PVN, 24% of nesfatin-1 neurons overlapped with oxytocin, 18% with vasopressin, 13% with CRH, and 12% with TRH neurons. In the SON, 35% of nesfatin-1 neurons overlapped with oxytocin and 28% with vasopressin. After a 48-h fast, refeeding for 2 h dramatically increased the number of nesfatin-1 neurons expressing c-Fos immunoreactivity by approximately 10 times in the PVN and 30 times in the SON, compared with the fasting controls. In the SON, refeeding also significantly increased the number of nesfatin-1-immunoreactive neurons and NUCB2 mRNA expression, compared with fasting. These results indicate that nesfatin-1 neurons in the PVN and SON highly overlap with oxytocin and vasopressin neurons and that they are activated markedly by refeeding. Feeding-activated nesfatin-1 neurons in the PVN and SON could play a role in the postprandial regulation of feeding behavior and energy homeostasis.

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