scholarly journals Kinetics of light-dependent Ca fluxes across the plasma membrane of rod outer segments. A dynamic model of the regulation of the cytoplasmic Ca concentration.

1987 ◽  
Vol 90 (3) ◽  
pp. 397-425 ◽  
Author(s):  
D L Miller ◽  
J I Korenbrot
Keyword(s):  
Plasma Membrane ◽  
Outer Segment ◽  
Time Course ◽  
Small Volume ◽  
Dynamic Balance ◽  
Light Sensitivity ◽  
Ca Ions ◽  
Concentration Changes ◽  
The Difference ◽  
Kinetics Of

We measured simultaneously in single toad rods the membrane photocurrent and the Ca concentration in a small volume surrounding the outer segment. Illumination causes a rise in the extracellular Ca concentration. Photocurrents and Ca concentration changes occur over the same range of light intensities. Analysis of the time course of the Ca concentration changes suggests that these concentration changes arise from the difference in the transport rates of light-activated Ca influx and efflux across the outer segment plasma membrane. The Ca influx occurs through the light-sensitive channels of the outer segment membrane and the efflux through Na/Ca exchangers. In 0.1 mM external Ca, approximately 1-2% of the dark current is carried by Ca ions. The Ca efflux in the dark is identical to the influx, approximately 2 X 10(6) ions/s. Upon illumination, the Ca influx decreases with a time course and light sensitivity identical to those of the photocurrent. The Ca efflux, on the other hand, has very different kinetics from those of the photocurrent. Upon illumination, the Ca efflux decreases with a time course and light sensitivity determined by the change in membrane voltage and in the free cytoplasmic Ca concentration near the plasma membrane. In response to bright stimuli, which saturate the photocurrent for prolonged periods of time, the Ca efflux decays with an exponential time course from its value in darkness. The average time constant of this decay is 2.5 s. From the kinetics of the light-activated Ca fluxes, it is possible to predict that illumination causes a decrease in the cytoplasmic Ca concentration. We present a model of the regulation of the cytoplasmic Ca concentration by the dynamic balance of the Ca influx and efflux from the rod outer segment. The model accounts for our experimental observations and allows us to predict the time course and extent of the light-dependent decrease in the free cytoplasmic concentration.

scholarly journals Effects of cyclic GMP on the kinetics of the photocurrent in rods and in detached rod outer segments.

1987 ◽  
Vol 90 (4) ◽  
pp. 527-551 ◽  
Author(s):  
S Hestrin ◽  
J I Korenbrot
Keyword(s):  
Cyclic Gmp ◽  
Outer Segment ◽  
Time Course ◽  
Intact Cell ◽  
Light Sensitivity ◽  
Biochemical Properties ◽  
Intact Cells ◽  
Outer Segments ◽  
High Concentrations ◽  
Kinetics Of

We investigated the effects of high concentrations of cytoplasmic cyclic GMP on the photocurrent kinetics and light sensitivity of the tiger salamander rod both in intact cells and in detached outer segments. Photoreceptors were internally perfused with cGMP by applying patch pipettes containing cGMP to the inner or outer segment. Large increases in the concentration of cGMP in the outer segment cytoplasm were achieved only when the patch pipette was applied directly to the outer segment. The dark-current amplitude increased with increasing cGMP concentrations up to approximately 1,400 pA. Internal perfusion with 5.0 mM cGMP introduced a delay of 1-3 s in the photocurrent. The magnitude of the delay was inversely proportional to the light intensity. In addition, the photocurrent time course was slowed down and the light sensitivity, measured 1 s after the flash, was decreased approximately 100-fold when compared with that of the intact cell. The observed effects of cGMP were compared with those predicted by a model that assumes that the initial photocurrent time course is determined by the kinetics of the light-activated phosphodiesterase (PDE) and the cGMP dependence of the light-sensitive channels. At high concentrations of cGMP, the experimental data were similar to those predicted by the model and based on the known biochemical properties of the light-activated PDE and cGMP-activated channels.

scholarly journals Delays in inactivation development and activation kinetics in myxicola giant axons.

1982 ◽  
Vol 80 (1) ◽  
pp. 83-102 ◽  
Author(s):  
L Goldman ◽  
J L Kenyon
Keyword(s):  
Time Constant ◽  
Time Course ◽  
Series Resistance ◽  
Activation Kinetics ◽  
Time To Peak ◽  
Exponential Decline ◽  
Na Inactivation ◽  
The Difference ◽  
True Property ◽  
Kinetics Of

Na inactivation was studied in Myxicola (two-pulse procedure, 6-ms gap between conditioning and test pulses). Inactivation developed with an initial delay (range 130-817 microseconds) followed by a simple exponential decline (time constant tau c). Delays (deviations from a simple exponential) are seen only for brief conditioning pulses were gNa is slightly activated. Hodgkin-Huxley kinetics with series resistance, Rs, predict deviations from a simple exponential only for conditioning pulses that substantially activate gNa. Reducing INa fivefold (Tris substitution) had no effect on either tau c or delay. Delay in not generated by Rs or by contamination from activation development. The slowest time constant in Na tails is approximately 1 ms (Goldman and Hahin, 1978) and the gap was 6 ms. Shortening the gap to 2 ms had no effect on either tau c or delay. Delay is a true property of the channel. Delay decreased with more positive conditioning potentials, and also decreased approximately proportionally with time to peak gNa during the conditioning pulse, as expected for sequentially coupled activation and inactivation. In a few cases the difference between Na current values for brief conditioning pulses and the tau c exponential could be measured. Difference values decayed exponentially with time constant tau m. The inactivation time course is described by a model that assumes a process with the kinetics of gNa activation as a precursor to inactivation.

scholarly journals Rhodopsin kinetics in the cat retina.

1981 ◽  
Vol 77 (3) ◽  
pp. 317-334 ◽  
Author(s):  
H Ripps ◽  
L Mehaffey ◽  
I M Siegel
Keyword(s):  
Time Course ◽  
Continuous Light ◽  
Regenerative Process ◽  
Full Time ◽  
Difference Spectra ◽  
Cat Retina ◽  
Simple Exponential Function ◽  
Fundus Reflectometry ◽  
The Difference ◽  
Kinetics Of

The bleaching and regeneration of rhodopsin in the living cat retina was studied by means of fundus reflectometry. Bleaching was effected by continuous light exposures of 1 min or 20 min, and the changes in retinal absorbance were measured at 29 wavelengths. For all of the conditions studied (fractional bleaches of from 65 to 100%), the regeneration of rhodopsin to its prebleach levels required greater than 60 min in darkness. After the 1-min exposures, the difference spectra recorded during the first 10 min of dark adaptation were dominated by photoproduct absorption, and rhodopsin regeneration kinetics were obscured by these intermediate processes. Extending the bleaching duration to 20 min gave the products of photolysis an opportunity to dissipate, and it was possible to follow the regenerative process over its full time-course. It was not possible, however, to fit these data with the simple exponential function predicted by first-order reaction kinetics. Other possible mechanisms were considered and are presented in the text. Nevertheless, the kinetics of regeneration compared favorably with the temporal changes in log sensitivity determined electrophysiologically by other investigators. Based on the bleaching curve for cat rhodopsin, the photosensitivity was determined and found to approximate closely the value obtained for human rhodopsin; i.e., the energy Ec required to bleach 1-e-1 of the available rhodopsin was 7.09 log scotopic troland-seconds (corrected for the optics of the cat eye), as compared with approximately 7.0 in man.

scholarly journals Biosynthesis and vectorial transport of opsin on vesicles in retinal rod photoreceptors.

1986 ◽  
Vol 34 (1) ◽  
pp. 5-16 ◽  
Author(s):  
D S Papermaster ◽  
B G Schneider ◽  
D DeFoe ◽  
J C Besharse
Keyword(s):  
Plasma Membrane ◽  
Outer Segment ◽  
Photoreceptor Cells ◽  
Disk Surface ◽  
Light Sensitivity ◽  
Apical Plasma Membrane ◽  
Rod Photoreceptor ◽  
Electron Microscopic ◽  
Retinal Rod ◽  
Membrane Bound

Retinal rod photoreceptor cells absorb light at one end and establish synaptic contacts on the other. Light sensitivity is conferred by a set of membrane and cytosol proteins that are gathered at one end of the cell to form a specialized organelle, the rod outer segment (ROS). The ROS is composed of rhodopsin-laden, flattened disk-shaped membranes enveloped by the cell's plasma membrane. Rhodopsin is synthesized on elements of the rough endoplasmic reticulum and Golgi apparatus near the nucleus in the inner segment. From this synthetic site, the membrane-bound apoprotein, opsin, is released from the Golgi in the membranes of small vesicles. These vesicles are transported through the cytoplasm of the inner segment until they reach its apical plasma membrane. At that site, opsin-laden vesicles appear to fuse near the base of the connecting cilium that joins the inner and outer segments. This fusion inserts opsin into the plasma membrane of the photoreceptor. Opsin becomes incorporated into the disk membrane by a process of membrane expansion and fusion to form the flattened disks of the outer segment. Within the disks, opsin is highly mobile, and rapidly rotates and traverses the disk surface. Despite its mobility in the outer segment, quantitative electron microscopic, immunocytochemical, and autoradiographic studies of opsin distribution demonstrate that little opsin is detectable in the inner segment plasma membrane, although its bilayer is in continuity with the plasma membrane of the outer segment. The photoreceptor successfully establishes the polarized distribution of its membrane proteins by restricting the redistribution of opsin after vectorially transporting it to one end of the cell on post-Golgi vesicles.

scholarly journals PO 8542 CLINICAL ILLNESS AND OUTCOMES IN NIGERIAN CHILDREN WITH PERSISTENT EARLY-APPEARING ANAEMIA FOLLOWING ARTEMISININ-BASED COMBINATION TREATMENTS OF UNCOMPLICATED PLASMODIUM FALCIPARUM MALARIA

2019 ◽  
Vol 4 (Suppl 3) ◽  
pp. A51.2-A51
Author(s):  
Kazeem Akano ◽  
Bayo Fatunmbi ◽  
Godwin Ntadom ◽  
Omobolaji T Alebiosu ◽  
Odafe Akpoborie ◽  
...  
Keyword(s):  
Time Course ◽  
Treatment Initiation ◽  
Plasmodium Falciparum Malaria ◽  
Compartment Model ◽  
Sub Saharan Africa ◽  
Combination Treatments ◽  
The Difference ◽  
Sub Saharan ◽  
Pre Treatment ◽  
Kinetics Of

BackgroundEarly-appearing anaemia (EAA) is not uncommon in malarious children following artemisinin-based combination treatments (ACTs) of uncomplicated infections and it may become persistent (PEAA). There is little evaluation of the factors contributing to and the kinetics of the resolution of haemoglobin deficit characteristic of ACT-related PEAA.MethodsPEAA was defined as haemoglobin concen„tration <10 g/dL for at least 1 week after treatment initiation with artemether-lumefantrine (AL), artesunate-amodiaquine (ASAQ) or dihydroartemisinin-piperaquine (DP) in malarious children with haemoglobin ≥10 g/dL pre-treatment. Drug-attributable fall in haemoglobin (DAFHb) was defined as the difference between pre-treatment and the lowest recorded haemoglobin value in the first week after treatment initiation. Stepwise multiple logistic regression model was used to evaluate independent predictors of PEAA. Time course of deficits in haemoglobin from baseline was used to estimate the disposition kinetics of haemoglobin deficits using a one compartment model.ResultsAsymptomatic PEAA occurred in 46 of 540 children. A duration of illness ≤3 days before presentation, haemoglobin <11.7 g/dL pre-treatment and 8.3 g/dL 1 day after treatment initiation. DAFHb ≥2 g/dL and treatment with DP independently predicted PEAA. Time to 90% reduction in haemoglobin deficit was significantly longer in AL-treated children compared with other treatments. Declines in haemoglobin deficits were monoexponential with the following overall estimated parameters: Cmax 2.6 g/dL (95% CI 2.3–2.9), Tmax 3.2 days (95% CI 2.2–4.1), AUC 31.9 g.dL-1.day (95% CI 25–38.8), Kel0.3 day-1 (95% CI 0.3–0,4), t1/23.9 days (95% CI 2.6–5.1), CLp 0.6L.day-1 (95% CI 0.5–0.7), and Vd 2.4L (95% CI 1.7–3). Overall, mean anaemia recovery time of 17.9 days (95% CI 15.5–20.2, n=39) was equivalent to 5 multiples of half-time of haemoglobin deficit on Bland-Altman analysis. Eight children, after recovery from PEAA progressed to asymptomatic late-appearing anaemia (LAA).ConclusionAsymptomatic PEAA, which may progress to LAA, is not uncommon in young children following ACTs. Its occurrence, and progression to LAA, may have implications for case management and control efforts for ACT-related anaemia in sub-Saharan Africa.

scholarly journals GLUT4 trafficking in insulin-stimulated rat adipose cells: evidence that heterotrimeric GTP-binding proteins regulate the fusion of docked GLUT4-containing vesicles

1999 ◽  
Vol 343 (3) ◽  
pp. 571-577 ◽  
Author(s):  
Cynthia M. FERRARA ◽  
Samuel W. CUSHMAN
Keyword(s):  
Plasma Membrane ◽  
Cell Surface ◽  
Adenosine Deaminase ◽  
Glucose Transport ◽  
Time Course ◽  
Transport Activity ◽  
Experimental Conditions ◽  
Distinct Sequence ◽  
Kinetics Of ◽  
Adipose Cells

Agents that activate the G-protein Gi (e.g. adenosine) increase, and agents that activate Gs [e.g. isoprenaline (isoproterenol)] decrease, steady-state insulin-stimulated glucose transport activity and cell-surface GLUT4 in isolated rat adipose cells without changing plasma membrane GLUT4 content. Here we have further examined the effects of RsGs and RiGi ligands (in which Rs and Ri are Gs- and Gi-coupled receptors respectively) on insulin-stimulated cell-surface GLUT4 and the kinetics of GLUT4 trafficking in these same cells. Rat adipose cells were preincubated for 2 min with or without isoprenaline (200 nM) and adenosine deaminase (1 unit/ml), to stimulate Gs and decrease the stimulation of Gi respectively, followed by 0-20 min with insulin (670 nM). Treatment with isoprenaline and adenosine deaminase decreased insulin-stimulated glucose transport activity by 58%. Treatment with isoprenaline and adenosine deaminase also resulted in similar decreases in insulin-stimulated cell-surface GLUT4 as assessed by both bis-mannose photolabelling of the substrate-binding site and biotinylation of the extracellular carbohydrate moiety when evaluated under similar experimental conditions. After stimulation with insulin in the absence of Gs and the presence of Gi agents, a distinct sequence of plasma membrane events took place, starting with an increase in immunodetectable GLUT4, then an increase in the accessibility of GLUT4 to bis-mannose photolabel, and finally an increase in glucose transport activity. Pretreatment with isoprenaline and adenosine deaminase before stimulation with insulin did not affect the time course of the increase in immunodetectable GLUT4 in the plasma membrane, but did delay both the increase in accessibility of GLUT4 to photolabel and the increase in glucose transport activity. These results suggest that RsGs and RiGi modulate insulin-stimulated glucose transport by influencing the extent to which GLUT4 is associated with occluded vesicles attached to the plasma membrane during exocytosis, perhaps by regulating the fusion process through which the GLUT4 in docked vesicles becomes exposed on the cell surface.

A comparison of spontaneous EPSCs in layer II and layer IV-V neurons of the rat entorhinal cortex in vitro

1996 ◽  
Vol 76 (2) ◽  
pp. 1089-1100 ◽  
Author(s):  
N. Berretta ◽  
R. S. Jones
Keyword(s):  
Entorhinal Cortex ◽  
Time Course ◽  
Cell Voltage ◽  
Amplitude Distribution ◽  
Mean Amplitude ◽  
Decay Phase ◽  
Similar Extent ◽  
The Difference ◽  
Kinetics Of

1. We have compared the characteristics of spontaneous excitatory postsynaptic currents (sEPSCs) in neurons of layer IV-V and layer II of the rat entorhinal cortex (EC) using whole cell voltage-clamp recordings in a slice preparation. 2. The frequency of sEPSCs was similar in the two layers, but the events in layer IV-V had a larger mean amplitude, faster rise time, and were faster to decay. The difference in amplitude could be attributed to the presence of a population of larger events in the layer IV-V neurons that were not present in layer II. 3. Electrotonic length was greater in layer II neurons, suggesting that the difference in kinetics of the sEPSCs may be explained partly by electrotonic attenuation. 4. The frequency of sEPSCs in both layers was reduced by tetrodotoxin (TTX) to a similar extent (15-20%). However, the amplitude distribution was unchanged in layer II, whereas in layer IV-V TTX abolished most of the larger amplitude sEPSCs. 5. 6-cyano-7-nitroquinoxaline-2,3-dione or 6-nitro-7-sulphamoylbenzo (f)-quinoxaline-2,3-dione, abolished most of the sEPSCs in neurons of both layers. However, even at negative holding potentials, a population of slower time-course sEPSCs remained in the presence of these antagonists. 6. The slow sEPSCs were more frequent in layer IV-V but had similar characteristics in both layers, being increased in amplitude at more positive holding potentials or in Mg2+-free medium, and blocked by 2-amino-5-phosphonovalerate (AP5). 7. AP5 alone (i.e., without addition of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid antagonists) reduced the peak amplitude and decay phase of sEPSCs in layer IV-V neurons but appeared to have little effect on amplitude and only a weak effect on decay phase in layer II. 8. Thus both layer IV-V and layer II neurons of the EC suffer continuous spontaneous excitation. However, layer IV-V neurons exhibit larger amplitude sEPSCs, probably mediated by release of multiple quanta of neurotransmitter. In addition, although both types of neurons display spontaneous excitation mediated by N-methyl-D-aspartate receptors, this component appears more pronounced in the deeper layers.

scholarly journals Excitation-Contraction Coupling in a Barnacle Muscle Fiber As Examined with Voltage Clamp Technique

1968 ◽  
Vol 51 (2) ◽  
pp. 157-175 ◽  
Author(s):  
S. Hagiwara ◽  
K. Takahashi ◽  
D. Junge
Keyword(s):  
Membrane Potential ◽  
Voltage Clamp ◽  
Time Course ◽  
External Medium ◽  
Transition Metal Ions ◽  
Membrane Potential Change ◽  
Final Level ◽  
Ca Ions ◽  
The Difference ◽  
Barnacle Muscle Fiber

Relations between the membrane potential and the tension associated with changes in membrane potential were analyzed in barnacle giant muscle fibers by using voltage clamp techniques. With a step change in membrane potential the tension reaches its final level with a time course which is expressed by the difference of two exponential functions. The time constants τ1 (0.2–0.4 sec at 23°C) and τ2 (0.07–0.12 sec at 23°C) are independent of the new membrane potential at least for a relatively small membrane potential change while the final level of tension is a function of the potential. Decreasing the temperature increases both τ1 and τ2 (Q10 = -2 to -3) and the increase of the tonicity of the external medium increases τ1 but not τ2. The final level of tension is related by an S-shaped curve to the membrane potential. The slope of the final tension-membrane potential curve increases with increasing external Ca concentration and is reduced when a small amount of transition metal ions is added to the medium. This suggests that the influx of Ca ions through the membrane is an important factor in the development of tension.

Destruction of Actin Filaments by Osmium Tetroxide

1977 ◽  
Vol 35 ◽  
pp. 466-467
Author(s):  
P. Maupin-Szamier ◽  
T. D. Pollard
Keyword(s):  
Actin Filaments ◽  
Time Course ◽  
Osmium Tetroxide ◽  
Rabbit Muscle ◽  
Muscle Actin ◽  
Sodium Phosphate Buffer ◽  
Transmission Electron ◽  
The Difference ◽  
Rates Of Decay ◽  
Short Time

We have studied the destruction of rabbit muscle actin filaments by osmium tetroxide (OSO4) to develop methods which will preserve the structure of actin filaments during preparation for transmission electron microscopy.Negatively stained F-actin, which appears as smooth, gently curved filaments in control samples (Fig. 1a), acquire an angular, distorted profile and break into progressively shorter pieces after exposure to OSO4 (Fig. 1b,c). We followed the time course of the reaction with viscometry since it is a simple, quantitative method to assess filament integrity. The difference in rates of decay in viscosity of polymerized actin solutions after the addition of four concentrations of OSO4 is illustrated in Fig. 2. Viscometry indicated that the rate of actin filament destruction is also dependent upon temperature, buffer type, buffer concentration, and pH, and requires the continued presence of OSO4. The conditions most favorable to filament preservation are fixation in a low concentration of OSO4 for a short time at 0°C in 100mM sodium phosphate buffer, pH 6.0.

Influence of Radioiodine Therapy on Urinary Iodine Excretion

1998 ◽  
Vol 37 (03) ◽  
pp. 107-112 ◽  
Author(s):  
I. Lauer ◽  
M. Bähre ◽  
E. Richter ◽  
B. Melier
Keyword(s):  
Time Course ◽  
Radioiodine Therapy ◽  
Urinary Iodine ◽  
Target Volume ◽  
Urinary Iodine Excretion ◽  
Urinary Creatinine ◽  
Iodine Excretion ◽  
Kinetics Of ◽  
Persistent Elevation ◽  
Benign Thyroid

Summary Aim: In 214 patients with benign thyroid diseases the time-course of urinary iodine excretion (UIE) was investigated in order to identify changes after radioiodine therapy (RITh). Method: UIE was measured photometrically (cerium-arsenite method) and related to urinary creatinine on the first and last day of the radioiodine test and then three days, seven days, four weeks, and six months after 1311 administration. Results: As compared with the level found immediately before radioiodine therapy, median UIE had almost doubled four weeks after therapy and was still significantly elevated six months after therapy. This increase correlated significantly with the target volume as measured by scintigraphy and sonography. Conclusions: The persistent elevation of UIE for months after RITh is a measure of treatment-induced damage to thyrocytes. Therefore, in view of the unfavourable kinetics of iodine that follow it, RITh should if possible be given via a single-dose regime.

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