scholarly journals Synaptic control of rat supraoptic neurones during osmotic stimulation of the organum vasculosum lamina terminalis in vitro.

1995 ◽  
Vol 489 (2) ◽  
pp. 567-577 ◽  
Author(s):  
D Richard ◽  
C W Bourque
Keyword(s):  
Lamina Terminalis ◽  
Organum Vasculosum Lamina Terminalis ◽  
Osmotic Stimulation ◽  
Organum Vasculosum ◽  
Synaptic Control ◽  
Stimulation Of

Membrane properties of organum vasculosum lamina terminalis neurons recorded in vitro

1993 ◽  
Vol 264 (4) ◽  
pp. R811-R815 ◽  
Author(s):  
R. Nissen ◽  
C. W. Bourque ◽  
L. P. Renaud
Keyword(s):  
Supraoptic Nucleus ◽  
Lucifer Yellow ◽  
Membrane Properties ◽  
Lamina Terminalis ◽  
Spike Response ◽  
Axonal Projections ◽  
Organum Vasculosum Lamina Terminalis ◽  
Antidromic Responses ◽  
Organum Vasculosum

Intracellular recordings of organum vasculosum lamina terminalis (OVLT) neurons were obtained from superfused explants of rat hypothalamus. Most (32 of 34) OVLT neurons displayed a low threshold spike response during depolarizing pulses applied from holding membrane potentials negative to -70 mV. In 17 of 34 cells, electrical stimulation of the supraoptic nucleus area evoked antidromic responses. In 20 of the 34 cells, 8 of which were antidromically driven, identical stimuli also revealed either excitatory (n = 12) or inhibitory (n = 5) or mixed (n = 3) postsynaptic potentials. Axonal projections to the ipsilateral supraoptic nucleus were confirmed afterwards using reconstruction of Lucifer yellow-filled cells. A 10-40 mosmol/kgH2O increase in the osmolality of the superfusion media by addition of NaCl or mannitol prompted a membrane depolarization of 2-10 mV in each of nine OVLT neurons tested. These results indicate that OVLT neurons project to the supraoptic nucleus and possess intrinsic properties capable of influencing their excitability. Because neurons in OVLT depolarize consequent to elevations in media osmolality, the OVLT may provide a means by which hyperosmotic stimuli influence neuroendocrine function.

Abstract 072: Brain Epithelial Sodium Channels on Organum Vasculosum of the Lamina Terminalis Neurons Mediate Sympathoexcitatory Pressor Responses and Neuronal Excitation by Hypertonic NaCl

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Brian J Kinsman ◽  
Kirsteen N Browning ◽  
Sean D Stocker
Keyword(s):  
Sodium Channels ◽  
Salt Intake ◽  
Lamina Terminalis ◽  
Dietary Salt ◽  
Epithelial Sodium Channels ◽  
Adult Rats ◽  
Neuronal Excitation ◽  
Arterial Blood ◽  
Organum Vasculosum

High dietary salt intake raises cerebrospinal fluid (CSF) [Na + ] in salt sensitive subjects to elevate sympathetic nerve activity (SNA), and arterial blood pressure (ABP). This occurs through excitation of NaCl-sensitive sites in the brain, including the organum vasculosum of the lamina terminalis (OVLT). Intriguingly, intracerebroventricular (ICV) pretreatment with benzamil (a non-voltage gated Na + channel blocker) also attenuates those systemic responses to central NaCl. Thus, I hypothesized that benzamil acts on NaCl-sensitive OVLT neurons to attenuate neuronal excitation and elevated SNA and ABP in response to hypertonic NaCl. To evaluate this hypothesis, lumbar SNA and ABP were measured in anesthetized adult rats in response to ICV infusion of 0.15, 0.5, and 1.0 M NaCl with and without prior OVLT microinjection of benzamil (5nmol per 20nL). ICV infusion of NaCl produced concentration-dependent increases in lumbar SNA (0.15M: 101±3%, 0.5M: 118±3%, 1.0M: 130±9% n=4 per group, P<0.05) and mean ABP (0.15M: 1±1mmHg; 0.5M: 5±1mmHg, 1.0M: 12±2mmHg). OVLT microinjection of benzamil significantly attenuated the increase in lumbar SNA (0.15M: 100±2%, 0.5M: 108±2%, 1.0M: 115±3% n=4 per group, P<0.05) and mean ABP (0.15M: 1±0mmHg; 0.5M: 2±1mmHg, 1.0M: 6±2mmHg). In a parallel set of experiments, in vitro whole-cell recordings of OVLT neurons in slices were performed to assess whether blockade of epithelial sodium channels (ENaC) attenuated NaCl-induced excitation. Bath application of +7.5mM NaCl increase action potential (AP) discharge of OVLT neurons (n=11) from 0.46±0.16 Hz to 1.09±0.26 Hz (P<0.05). Subsequent addition of an ENaC selective concentration of benzamil (0.5μM) reversed AP discharge (0.75±0.24 Hz, P<0.05). Isotonic 0.5μM benzamil did not significantly change NaCl-sensitive OVLT neuron (n=13) AP discharge from baseline (0.54±0.14 Hz to 0.60±0.16 Hz, P>0.05). Collectively, this data indicates that elevations in CSF NaCl concentrations excite OVLT neurons via ENaC to elevate SNA and ABP.

scholarly journals Effect of exogenous glucocorticoid on osmotically stimulated antidiuretic hormone secretion and on water reabsorption in man

2006 ◽  
Vol 155 (6) ◽  
pp. 845-848 ◽  
Author(s):  
Volker Bähr ◽  
Norma Franzen ◽  
Wolfgang Oelkers ◽  
Andreas F H Pfeiffer ◽  
Sven Diederich
Keyword(s):  
Antidiuretic Hormone ◽  
Water Deprivation ◽  
Hormone Secretion ◽  
Water Reabsorption ◽  
Glucocorticoid Treatment ◽  
Osmotic Stimulation ◽  
Before And After ◽  
Stimulation Of

Objective: Glucocorticoids exert tonic suppression of antidiuretic hormone (ADH) secretion. Hypocortisolism in secondary adrenocortical insufficiency can result in a clinical picture similar to the syndrome of inappropriate ADH secretion. On the other hand, in vitro and in vivo results provide evidence for ADH suppression in states of hypercortisolism. To test the hypothesis that ADH suppression is of relevance during glucocorticoid therapy, we investigated the influence of prednisolone on the osmotic stimulation of ADH. Design and methods: Seven healthy men were subjected to water deprivation tests with the measurement of plasma ADH (pADH) and osmolality (posmol) before and after glucocorticoid treatment (5 days 30 mg prednisolone per day). Results: Before glucocorticoid treatment, the volunteers showed a normal test with an adequate increase of pADH (basal 0.54 ± 0.2 to 1.9 ± 0.72 pg/ml (mean ± S.D.)) in relation to posmol(basal 283.3 ± 8.5 to 293.7 ± 6 mosmol/kg). After prednisolone intake, pADH was attenuated (<0.4 pg/ml) in spite of an increase of posmol from 289.3 ± 3.6 to 297.0 ± 5.5 mosmol/kg. However, urine osmolar concentration increased normally during water deprivation after prednisolone. Urinary cAMP excretion increased during water deprivation without glucocorticoid treatment from 3.56 ± 0.55 to 6.07 ± 0.76 μmol/l, reflecting the increased pADH levels. The rise in cAMP excretion was completely blunted by prednisolone treatment. Conclusions: We speculate that there may be an ADH-independent stimulation of the formation or function of aquaporin-2 channels by prednisolone and/or a direct osmotic stimulation of water reabsorption independent of ADH and glucocorticoid control.

Sign in / Sign up

Export Citation Format

Share Document