Different electrophysiological effects of testosterone on medial preoptic/anterior hypothalamic neurons have similar time courses

1984 ◽  
Vol 298 (1) ◽  
pp. 135-137 ◽  
Author(s):  
K.M. Kendrick
1992 ◽  
Vol 99 (3) ◽  
pp. 317-338 ◽  
Author(s):  
L Reuss ◽  
B Simon ◽  
C U Cotton

The mechanisms of apparent streaming potentials elicited across Necturus gallbladder epithelium by addition or removal of sucrose from the apical bathing solution were studied by assessing the time courses of: (a) the change in transepithelial voltage (Vms). (b) the change in osmolality at the cell surface (estimated with a tetrabutylammonium [TBA+]-selective microelectrode, using TBA+ as a tracer for sucrose), and (c) the change in cell impermeant solute concentration ([TMA+]i, measured with an intracellular double-barrel TMA(+)-selective microelectrode after loading the cells with TMA+ by transient permeabilization with nystatin). For both sucrose addition and removal, the time courses of Vms were the same as the time courses of the voltage signals produced by [TMA+]i, while the time courses of the voltage signals produced by [TBA+]o were much faster. These results suggest that the apparent streaming potentials are caused by changes of [NaCl] in the lateral intercellular spaces, whose time course reflects the changes in cell water volume (and osmolality) elicited by the alterations in apical solution osmolality. Changes in cell osmolality are slow relative to those of the apical solution osmolality, whereas lateral space osmolality follows cell osmolality rapidly, due to the large surface area of lateral membranes and the small volume of the spaces. Analysis of a simple mathematical model of the epithelium yields an apical membrane Lp in good agreement with previous measurements and suggests that elevations of the apical solution osmolality elicit rapid reductions in junctional ionic selectivity, also in good agreement with experimental determinations. Elevations in apical solution [NaCl] cause biphasic transepithelial voltage changes: a rapid negative Vms change of similar time course to that of a Na+/TBA+ bi-ionic potential and a slow positive Vms change of similar time course to that of the sucrose-induced apparent streaming potential. We conclude that the Vms changes elicited by addition of impermeant solute to the apical bathing solution are pseudo-streaming potentials, i.e., junctional diffusion potentials caused by salt concentration changes in the lateral intercellular spaces secondary to osmotic water flow from the cells to the apical bathing solution and from the lateral intercellular spaces to the cells. Our results do not support the notion of junctional solute-solvent coupling during transepithelial osmotic water flow.


1977 ◽  
Vol 23 (5) ◽  
pp. 830-834 ◽  
Author(s):  
D E Freer ◽  
B E Statland

Abstract We report the intermediate-term effects of three consecutive evenings of moderate ethanol ingestion (0.75 g/kg body weight each evening) on activity values for alkaline phosphatase, gamma-glutamyltransferase, creatine kinase, aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase in sera of nine apparently healthy young adults. We define "intermediate-term" effects as those occurring between 10 h and 100 h after completion of the ethanol consumption schedule. The most pronounced changes in enzyme activity for the group of volunteers were: gamma-glutamyltransferase, +25% at 60 h after ethanol ingestion; alanine aminotransferase, +12% at 60 h after ethanol; and aspartate aminotransferase,--12% at 60 h after ethanol. All three enzymes exhibited similar time courses, i.e., mean peak activity changes were observed at 60 h, and all three mean enzyme activity values returned to near baseline by 100 h. The possible explanations for the observed changes and the clinical significance are discussed.


2000 ◽  
Vol 84 (6) ◽  
pp. 2777-2785 ◽  
Author(s):  
K. Hillsley ◽  
J. L. Kenyon ◽  
T. K. Smith

Myenteric afterhyperpolarizing (AH) neurons are primary afferent neurons within the gastrointestinal tract. Stimulation of the intestinal mucosa evokes action potentials (AP) that are followed by a slow afterhyperpolarization (AHPslow) in the soma. The role of intracellular Ca2+ ([Ca2+]i) and ryanodine-sensitive Ca2+ stores in modulating the electrical activity of myenteric AH neurons was investigated by recording membrane potential and bis-fura-2 fluorescence from 34 AH neurons. Mean resting [Ca2+]i was ∼200 nM. Depolarizing current pulses that elicited APs evoked AHPslow and an increase in [Ca2+]i, with similar time courses. The amplitudes and durations of AHPslow and the Ca2+ transient were proportional to the number of evoked APs, with each AP increasing [Ca2+]i by ∼50 nM. Ryanodine (10 μM) significantly reduced both the amplitude and duration (by 60%) of the evoked Ca2+ transient and AHPslow over the range of APs tested (1–15). Calcium-induced calcium release (CICR) was graded and proportional to the number of APs, with each AP triggering a rise in [Ca2+]i of ∼30 nM Ca2+ via CICR. This indicates that CICR amplifies Ca2+ influx. Similar changes in [Ca2+]i and AHPslow were evoked by two APs in control and six APs in ryanodine. Thus, the magnitude of the change in bulk [Ca2+]i and not the source of the Ca2+ is the determinant of the magnitude of AHPslow. Furthermore, lowering of free [Ca2+]i, either by reducing extracellular Ca2+ or injecting high concentrations of Ca2+buffer, induced depolarization, increased excitability, and abolition of AHPslow. In addition, activation of synaptic input to AH neurons elicited a slow excitatory postsynaptic potential (sEPSP) that was completely blocked in ryanodine. These results demonstrate the importance of [Ca2+]i and CICR in sensory processing in AH neurons. Activity-dependent CICR may be a mechanism to grade the output of AH neurons according to the intensity of sensory input.


1988 ◽  
Vol 137 (1) ◽  
pp. 589-596
Author(s):  
L. Barr

As is common for amphibians, the sphincter pupillae of the axolotl contracts in vitro in response to illumination with visible light. 1. In a comparison of photomechanical responses of albino and normally pigmented axolotls, similar time courses and maxima of force development were found. 2. The dependence of isometric active force development on the length of the sphincter pupillae is similar to that of other smooth muscles. 3. The action spectrum of the axolotl is similar to the absorption spectrum of frog rhodopsin. 4. At low stimulus strengths, the increase of normalized, isometric, active force with increasing stimulus strength is approximately seven times as great in albino axolotls as in normally pigmented ones. 5. Melanin appears to decrease the light sensitivity of the irises of normally pigmented animals by acting as a simple light shield.


1985 ◽  
Vol 58 (3) ◽  
pp. 892-898 ◽  
Author(s):  
G. A. Patterson ◽  
P. Rock ◽  
W. A. Mitzner ◽  
N. F. Adkinson ◽  
J. T. Sylvester

We determined the effects of extracorporeal perfusion with a constant flow (75 ml . min-1 . kg-1) of autologous blood on hemodynamics and fluid balance in sheep lungs isolated in situ. After 5 min, perfusate leukocyte and platelet counts fell by two-thirds. Pulmonary arterial pressure (Ppa) increased to a maximum of 32.0 +/- 3.4 Torr at 30 min and thereafter fell. Lung lymph flow (QL), measured from the superior thoracic duct, and perfusate thromboxane B2 (TXB2) concentrations followed similar time courses but lagged behind Ppa, reaching maxima of 4.1 +/- 1.2 ml/h and 2.22 +/- 0.02 ng/ml at 60 min. Lung weight gain, measured as the opposite of the weight change of the extracorporeal reservoir, and perfusate 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) concentration increased rapidly during the first 60 min and then more gradually. After 210 min, weight gain was 224 +/- 40 g and 6-keto-PGF1 alpha concentration, 4.99 +/- 0.01 ng/ml. The ratio of lymph to plasma oncotic pressure (pi L/pi P) at 30 min was 0.61 +/- 0.06 and did not change significantly. Imidazole (5 mM) reduced the changes in TXB2, Ppa, QL, and weight and platelet count but did not alter 6-keto-PGF1 alpha, pi L/pi P, or leukocyte count. Indomethacin (0.056 mM) reduced TXB2, 6-keto-PGF1 alpha, and the early increases in weight, Ppa, and QL but did not alter the time courses of leukocyte or platelet counts. Late in perfusion, however, Ppa and QL were greater than in either untreated or imidazole-treated lungs.


1996 ◽  
Vol 270 (6) ◽  
pp. H2029-H2037 ◽  
Author(s):  
R. Dumaine ◽  
H. A. Hartmann

We used a fast inactivation-deficient mutant (QQQ) of the human heart Na+ channel alpha-subunit (hH1a) to assess the influence of the inactivation gate on tetrodotoxin (TTX) use-dependent block (UDB) and postrepolarization block (PRB). PRB had similar time courses in both channels, suggesting no direct interaction of the inactivation gate with the TTX binding site. The UDB saturated with high concentrations of TTX in hH1a but not in QQQ, revealing the modulatory action of fast inactivation on UDB. TTX did not stabilize the inactivated states of QQQ, and the extra block developing during long depolarizations suggests a higher-affinity site involved in the gating of the channel. These results cannot be solely explained by a slow recovery from the block in the inactivated states. They suggest a common use-dependent block mechanism for hH1a and QQQ involving a high-affinity site. We propose that an activated state is primarily responsible for UDB during short depolarization in the range of the action potential plateau and that fast inactivation modulates the accessibility of the toxin to this site.


1997 ◽  
Vol 200 (7) ◽  
pp. 1061-1071 ◽  
Author(s):  
N A Curtin ◽  
M J Kushmerick ◽  
R W Wiseman ◽  
R C Woledge

Recovery after contraction of white muscle fibres of dogfish was investigated using 31P-NMR and measurements of heat production. The muscle fibres were stimulated to perform either a single isometric tetanus or a series of brief isometric tetani; the NMR measurements showed that approximately half of the phosphocreatine (PCr) was used. The period of activity was followed by a recovery period without stimulation. Both NMR and heat measurements agreed in showing that recovery was very slow, requiring at least 60 min for PCr resynthesis and for the production of recovery heat. The NMR results showed that changes in intracellular pH and in the concentrations of PCr and intracellular phosphate (Pi) had very similar time courses. Intracellular pH moved in the alkaline direction during the period of activity and then returned monotonically during recovery. The non-phosphate buffer power was 13.0 +/- 3.1 mmol l-1 intracellular water per pH unit (N = 4, mean +/- S.E.M.). The results are consistent with the view that oxidative processes resynthesize PCr during recovery, which is slow because of the low mitochondrial content of these muscle fibres.


1986 ◽  
Vol 239 (2) ◽  
pp. 269-274 ◽  
Author(s):  
T Page ◽  
N J Kuhn

Arteriovenous glucose difference across the mammary gland of the lactating rat was used as an ‘instantaneous’ monitor of mammary glucose uptake. Plasma [glucose] and arteriovenous glucose difference varied according to whether Halothane, diethyl ether or sodium pentobarbitone anaesthesia was used. In pentobarbitone-treated rats a 60% glucose extraction in the fed state decreased to 5% after 18 h starvation, and recovered to 40% and 59% after 15 min and 60 min re-feeding respectively. The increase and decrease in plasma [fatty acids] and the depletion and restoration of hepatic glycogen mostly followed similar time courses. Re-feeding was accompanied by a brief surge of plasma [insulin]. Starved lactating rats showed a markedly greater capacity than age-matched virgin rats in the oral and intraperitoneal glucose tolerance tests. Mammary glucose uptake in the starved rat was significantly restored by oral or intraperitoneal glucose or by insulin, but not by acetoacetate or by heparin-induced elevation of plasma [fatty acids]. The role of insulin and of possible changes in mammary sensitivity to insulin in the return of mammary glucose uptake on re-feeding is discussed.


1959 ◽  
Vol 42 (3) ◽  
pp. 655-664 ◽  
Author(s):  
W. J. Adelman ◽  
J. Adams

The effects of external calcium deprivation on certain characteristics of the action potential of the lobster motor axon have been studied. Upon exposure to calcium-free solution the spike amplitude is rapidly decreased within a few minutes and is followed by a slow linear decline. The rates of spike rise and fall are proportionally reduced more than the spike but follow similar time courses during calcium lack. Associated with these phenomena are the loss in the normal slow spike repolarization process, the development of a large and lengthy undershoot, and the appearance of a high degree of refractoriness. The mean increase in the refractory period is 525 per cent upon 10 minutes' exposure to calcium-free solution. These effects are completely reversible upon returning the axons to normal solution. These results are compared to similar effects of calcium deprivation on frog myelinated axons and squid and lobster giant axons recently observed by other workers.


2008 ◽  
Vol 295 (2) ◽  
pp. H667-H676 ◽  
Author(s):  
Victor A. Maltsev ◽  
John W. Kyle ◽  
Sudhish Mishra ◽  
Abertas Undrovinas

Late Na+ current ( INaL) is a major component of the action potential plateau in human and canine myocardium. Since INaL is increased in heart failure and ischemia, it represents a novel potential target for cardioprotection. However, the molecular identity of INaL remains unclear. We tested the hypothesis that the cardiac Na+ channel isoform (Nav1.5) is a major contributor to INaL in adult dog ventricular cardiomyocytes (VCs). Cultured VCs were exposed to an antisense morpholino-based oligonucleotide (Nav1.5 asOligo) targeting the region around the start codon of Nav1.5 mRNA or a control nonsense oligonucleotide (nsOligo). Densities of both transient Na+ current ( INaT) and INaL (both in pA/pF) were monitored by whole cell patch clamp. In HEK293 cells expressing Nav1.5 or Nav1.2, Nav1.5 asOligo specifically silenced functional expression of Nav1.5 (up to 60% of the initial INaT) but not Nav1.2. In both nsOligo-treated controls and untreated VCs, INaT and INaL remained unchanged for up to 5 days. However, both INaT and INaL decreased exponentially with similar time courses (τ = 46 and 56 h, respectively) after VCs were treated with Nav1.5 asOligo without changes in 1) decay kinetics, 2) steady-state activation and inactivation, and 3) the ratio of INaL to INaT. Four days after exposure to Nav1.5 asOligo, INaT and INaL amounted to 68 ± 6% (mean ± SE; n = 20, P < 0.01) and 60 ± 7% ( n = 11, P < 0.018) of those in VCs treated by nsOligo, respectively. We conclude that in adult dog heart Nav1.5 sodium channels have a “functional half-life” of ∼35 h (0.69τ) and make a major contribution to INaL.


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