scholarly journals Dendritic membrane resistance modulates activity-induced Ca2+ influx in oxytocinergic magnocellular neurons of mouse PVN

2021 ◽  
Author(s):  
Wanhui Sheng ◽  
Scott W. Harden ◽  
Yalun Tan ◽  
Eric G. Krause ◽  
Charles J. Frazier
Keyword(s):  
Paraventricular Nucleus ◽  
Calcium Influx ◽  
Membrane Resistance ◽  
Optical Recording ◽  
Magnocellular Neurons ◽  
Axon Terminals ◽  
Dendritic Membrane ◽  
Oxytocin Release ◽  
Activity Dependent ◽  
Existing Data

ABSTRACTHypothalamic oxytocinergic magnocellular neurons have a fascinating ability to release peptide from both their axon terminals and from their dendrites. Existing data indicates there is a flexible relationship between somatic activity and dendritic release, but the mechanisms governing this relationship are not completely understood. Here we use a combination of electrical and optical recording techniques to quantify activity-dependent calcium influx in proximal vs. distal dendrites of oxytocinergic magnocellular neurons located in the paraventricular nucleus of the hypothalamus (OT-MCNs). Results reveal that the dendrites of OT-MCNs are weak conductors of somatic voltage changes, and yet activity-induced dendritic calcium influx can be robustly regulated by a diverse set of stimuli that open or close ionophores located along the dendritic membrane. Overall, this study reveals that dendritic membrane resistance is a dynamic and endogenously regulated feature of OT-MCNs that is likely to have substantial functional impact on central oxytocin release.IMPACT STATEMENTActivity-induced dendritic calcium influx in oxytocinergic magnocellular neurons can be robustly modulated by a highly diverse set of stimuli acting on distinct types of ionophores expressed along the dendritic membrane.

scholarly journals Dendritic osmosensors modulate activity-induced calcium influx in oxytocinergic magnocellular neurons of the mouse PVN

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Wanhui Sheng ◽  
Scott W Harden ◽  
Yalun Tan ◽  
Eric G Krause ◽  
Charles J Frazier
Keyword(s):  
Ion Channels ◽  
Paraventricular Nucleus ◽  
Calcium Influx ◽  
Optical Recording ◽  
Magnocellular Neurons ◽  
Axon Terminals ◽  
Dendritic Membrane ◽  
Oxytocin Release ◽  
The Relationship ◽  
Existing Data

Hypothalamic oxytocinergic magnocellular neurons have a fascinating ability to release peptide from both their axon terminals and from their dendrites. Existing data indicates that the relationship between somatic activity and dendritic release is not constant, but the mechanisms through which this relationship can be modulated are not completely understood. Here we use a combination of electrical and optical recording techniques to quantify activity-induced calcium influx in proximal vs. distal dendrites of oxytocinergic magnocellular neurons located in the paraventricular nucleus of the hypothalamus (OT-MCNs). Results reveal that the dendrites of OT-MCNs are weak conductors of somatic voltage changes, however activity-induced dendritic calcium influx can be robustly regulated by both osmosensitive and non-osmosensitive ion channels located along the dendritic membrane. Overall, this study reveals that dendritic conductivity is a dynamic and endogenously regulated feature of OT-MCNs that is likely to have substantial functional impact on central oxytocin release.

scholarly journals Increased oxytocin release precedes hyponatremia after pituitary surgery

Pituitary ◽  
2021 ◽  
Author(s):  
Paul Eugène Constanthin ◽  
Nathalie Isidor ◽  
Sophie de Seigneux ◽  
Shahan Momjian
Keyword(s):  
Transsphenoidal Surgery ◽  
Pituitary Surgery ◽  
Sodium Balance ◽  
Posterior Pituitary ◽  
Axon Terminals ◽  
Early Marker ◽  
Inappropriate Secretion ◽  
Oxytocin Release ◽  
Transsphenoidal Pituitary Surgery ◽  
First Time

Abstract Purpose The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is a well-known complication of transsphenoidal pituitary surgery, related to inappropriate secretion of arginine vasopressin (AVP). Its diagnosis is based on hyponatremia, with a peak of occurrence around day 7 after surgery and, to date, no early marker has been reported. In particular, copeptin levels are not predictive of hyponatremia in this case. Oxytocin (OXT) is secreted into the peripheral blood by axon terminals adjacent to those of AVP neurons in the posterior pituitary. Besides its role in childbirth and lactation, recent evidences suggested a role for OXT in sodium balance. The contribution of this hormone in the dysnatremias observed after pituitary surgery has however never been investigated. Methods We analyzed the urinary output of OXT in patients subjected to transsphenoidal pituitary surgery. Results While OXT excretion remained stable in patients who presented a normonatremic postoperative course, patients who were later diagnosed with SIADH-related hyponatremia presented with a significantly increased urinary secretion of OXT 4 days after surgery. Conclusion Taken together, these results show for the first time that urinary OXT output remains normally stable after transsphenoidal pituitary surgery. OXT excretion however becomes abnormally high on or around 4 days after surgery in patients later developing hyponatremia, suggesting that this abnormal dynamics of OXT secretion might serve as an early marker for transsphenoidal surgery-related hyponatremia attributed to SIADH.

Immunoglobulin E mediated membrane conductance changes in rat basophilic leukemia cells

1988 ◽  
Vol 66 (3) ◽  
pp. 328-331 ◽  
Author(s):  
Carlos Barajas-López ◽  
Jan D. Huizinga
Keyword(s):  
Immunoglobulin E ◽  
Calcium Influx ◽  
Membrane Conductance ◽  
Membrane Resistance ◽  
Leukemia Cells ◽  
Rat Basophilic Leukemia Cells ◽  
Conductance Changes ◽  
Electrophysiological Effects ◽  
Basophilic Leukemia ◽  
Stimulation Of

Electrophysiological effects of anaphylactic stimulation of rat basophilic leukemia cells (RBL-2H3) were studied using conventional microelectrodes. Stimulation of passively sensitized cells by anti-immunoglobulin E resulted in hyperpolarization followed by depolarization. These changes in membrane polarization were associated with a decrease in input membrane resistance. No effect of anaphylactic stimulation was seen in Ca2+-free solution or when Ca2+ influx was blocked by Co2+, but it was mimicked by the Ca2+ ionophore A-23187. This suggests that the changes in ionic conductances were associated with calcium influx. These results support the hypothesis that membrane conductance changes are involved in the stimulus-secretion process of the RBL-2H3 cells.

Vasopressin Increases GABAergic Inhibition of Rat Hypothalamic Paraventricular Nucleus Neurons In Vitro

2000 ◽  
Vol 83 (2) ◽  
pp. 705-711 ◽  
Author(s):  
M.L.H.J. Hermes ◽  
J. M. Ruijter ◽  
A. Klop ◽  
R. M. Buijs ◽  
L. P. Renaud
Keyword(s):  
Paraventricular Nucleus ◽  
Receptor Agonist ◽  
Hypothalamic Paraventricular Nucleus ◽  
Membrane Properties ◽  
Magnocellular Neurons ◽  
Membrane Hyperpolarization ◽  
Perforated Patch ◽  
Intrinsic Membrane Properties ◽  
Brain Slice Preparation

This investigation used an in vitro hypothalamic brain slice preparation and whole cell and perforated-patch recording to examine the response of magnocellular neurons in hypothalamic paraventricular nucleus (PVN) to bath applications of vasopressin (VP; 100–500 nM). In 22/38 cells, responses were characterized by an increase in the frequency of bicuculline-sensitive inhibitory postsynaptic potentials or currents with no detectable influence on excitatory postsynaptic events. Perforated-patch recordings confirmed that VP did not have an effect on intrinsic membrane properties of magnocellular PVN neurons ( n = 17). Analysis of intrinsic membrane properties obtained with perforated-patch recording ( n = 23) demonstrated that all of nine VP-sensitive neurons showed a rebound depolarization after transient membrane hyperpolarization from rest. By contrast, 12/14 nonresponding neurons displayed a delayed return to resting membrane potentials. Recordings of reversed inhibitory postsynaptic currents with chloride-loaded electrodes showed that responses to VP persisted in media containing glutamate receptor antagonists but were abolished in the presence of tetrodotoxin. In addition, responses were mimicked by vasotocin [Phe2, Orn8], a selective V1a receptor agonist, and blocked by [β-Mercapto-β,β-cyclopentamethylenepropionyl1,O-Me-Tyr2, Arg8]-VP (Manning compound), a V1a/OT receptor antagonist. Neither [deamino-Cys1,Val4,d-Arg8]-VP, a selective V2 receptor agonist, nor oxytocin were effective. Collectively, the results imply that VP acts at V1a receptors to excite GABAergic neurons that are presynaptic to a population of magnocellular PVN neurons the identity of which features a unique rebound depolarization. Endogenous sources of VP may be VP-synthesizing neurons in suprachiasmatic nucleus, known to project toward the perinuclear regions of PVN, and/or the magnocellular neurons within PVN.

ANG II-induced excitation of paraventricular nucleus magnocellular neurons: a role for glutamate interneurons

2004 ◽  
Vol 286 (5) ◽  
pp. R894-R902 ◽  
Author(s):  
K. J. Latchford ◽  
A. V. Ferguson
Keyword(s):  
Paraventricular Nucleus ◽  
Kynurenic Acid ◽  
Neuronal Excitability ◽  
Critical Role ◽  
Ang Ii ◽  
Magnocellular Neurons ◽  
Whole Cell Patch Clamp ◽  
Electrolyte Homeostasis ◽  
Hypothalamic Slices

The hypothalamic paraventricular nucleus (PVN) plays a critical role in cardiovascular and neuroendocrine regulation. ANG II (ANG) acts throughout the periphery in the maintenance of fluid-electrolyte homeostasis and has also been demonstrated to act as a neurotransmitter in PVN exerting considerable influence on neuronal excitability in this nucleus. The mechanisms underlying the ANG-mediated excitation of PVN magnocellular neurons have yet to be determined. We have used whole cell patch-clamp techniques in hypothalamic slices to examine the effects of ANG on magnocellular neurons. Application of ANG resulted in a depolarization of magnocellular neurons, a response that was abolished in TTX, suggesting an indirect mechanism of action. Interestingly, ANG also increased the frequency of excitatory postsynaptic potentials/currents in magnocellular neurons, an effect that was abolished after application of the glutamate antagonist kynurenic acid. ANG was without effect on the amplitude of excitatory postsynaptic currents, suggesting a presynaptic action on an excitatory interneuron within PVN. The ANG-induced depolarization was shown to be sensitive to kynurenic acid, revealing the requisite role of glutamate in mediating the ANG-induced excitation of magnocellular neurons. These observations indicate that the ANGergic excitation of magnocellular PVN neurons are dependent on an increase in glutamatergic input and thus highlight the importance of a glutamate interneuron in mediating the effects of this neurotransmitter.

ANG II blocks potassium currents in zona glomerulosa cells from rat, bovine, and human adrenals

1991 ◽  
Vol 260 (5) ◽  
pp. E772-E779 ◽  
Author(s):  
U. Brauneis ◽  
P. M. Vassilev ◽  
S. J. Quinn ◽  
G. H. Williams ◽  
D. L. Tillotson
Keyword(s):  
Single Channel ◽  
Calcium Influx ◽  
Membrane Resistance ◽  
Zona Glomerulosa ◽  
Ang Ii ◽  
K Channels ◽  
Channel Interaction ◽  
Whole Cell Patch Clamp ◽  
Outward Currents ◽  
K Currents

Angiotensin II (ANG II) is a principal secretagogue of adrenal zona glomerulosa (ZG) cells. The transduction process includes a depolarization of the plasma membrane and the activation of calcium influx. The ANG II-induced depolarization is associated with an increase in total membrane resistance. To directly address the mechanism underlying these observations, we examined the effect of ANG II on K+ currents of rat, bovine, and human ZG cells, using whole cell patch clamp. Although some differences were seen in the characteristics of K+ currents between species, ANG II consistently blocked outward currents in ZG cells [rat: 47.1 +/- 4.5% (SE), n = 17; bovine: 38.6 +/- 3.3%, n = 21; and human: 13-63%, n = 3]. With the use of the cell-attached mode, single-channel recordings in bovine ZG cells demonstrated K+ channels that were reversibly blocked when ANG II was added to the bath solution. This indicates that the block of K+ channels by ANG II involves a diffusible intracellular messenger rather than a direct receptor-channel interaction. The decreased conductance of K+ can account for the ANG II-induced membrane depolarization.

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