Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Furaptra (Raju, B., E. Murphy, L. A. Levy, R. D. Hall, and R. E. London. 1989. Am. J. Physiol. 256:C540-C548) is a "tri-carboxylate" fluorescent indicator with a chromophore group similar to that of fura-2 (Grynkiewicz, G., M. Poenie, and R. Y. Tsien. 1985. J. Biol. Chem. 260:3440-3450). In vitro calibrations indicate that furaptra reacts with Ca2+ and Mg2+ with 1:1 stoichiometry, with dissociation constants of 44 microM and 5.3 mM, respectively (16-17 degrees C; ionic strength, 0.15 M; pH, 7.0). Thus, in a frog skeletal muscle fiber stimulated electrically, the indicator is expected to respond to the change in myoplasmic free [Ca2+] (delta[Ca2+]) with little interference from changes in myoplasmic free [Mg2+]. The apparent longitudinal diffusion constant of furaptra in myoplasm was found to be 0.68 (+/- 0.02, SEM) x 10(-6) cm2 s-1 (16-16.5 degrees C), a value which suggests that about half of the indicator was bound to myoplasmic constituents of large molecular weight. Muscle membranes (surface and/or transverse-tubular) appear to have some permeability to furaptra, as the total quantity of indicator contained within a fiber decreased after injection; the average time constant of the loss was 302 (+/- 145, SEM) min. In fibers containing less than 0.5 mM furaptra and stimulated by a single action potential, the calibrated peak value of delta[Ca2+] averaged 5.1 (+/- 0.3, SEM) microM. This value is about half that reported in the preceding paper (9.4 microM; Konishi, M., and S. M. Baylor. 1991. J. Gen. Physiol. 97:245-270) for fibers injected with purpurate-diacetic acid (PDAA). The latter difference may be explained, at least in part, by the likelihood that the effective dissociation constant of furaptra for Ca2+ is larger in vivo than in vitro, owing to the binding of the indicator to myoplasmic constituents. The time course of furaptra's delta[Ca2+], with average values (+/- SEM) for time to peak and half-width of 6.3 (+/- 0.1) and 9.5 (+/- 0.4) ms, respectively, is very similar to that of delta[Ca2+] recorded with PDAA. Since furaptra's delta[Ca2+] can be recorded at a single excitation wavelength (e.g., 420 nm) with little interference from fiber intrinsic changes, movement artifacts, or delta[Mg2+], furaptra represents a useful myoplasmic Ca2+ indicator, with properties complementary to those of other available indicators.
J Gen Physiol 1991 Feb
PMID:Myoplasmic calcium transients in intact frog skeletal muscle fibers monitored with the fluorescent indicator furaptra. 201 81

Juvenile coho salmon (Oncorhynchus kisutch) were placed on five dietary regimes: fed 1 week, fasted 1 week, fed 3 weeks, fasted 3 weeks, and fasted 1 week/refed 2 weeks. Plasma levels of glucose, fatty acids, insulin, glucagon, and glucagon-like peptide (GLP) and the activities of key metabolic enzymes were determined. Plasma glucose levels in the fed control groups were 98.4 +/- 3.4 (SEM) and 104.8 +/- 4.7 mg/dl at 1 and 3 weeks, respectively. Plasma glucose in the fasted 1 week group was significantly elevated to 128.8 +/- 9.2 mg/dl. Animals fasted 3 weeks or fasted 1 week/refed 2 weeks displayed plasma glucose levels similar to those of fed animals. Fasted groups possessed significantly less liver glycogen than fed or fasted/refed groups. Plasma fatty acids were elevated only after 3 weeks of fasting (from 0.39 +/- 0.04 microEq/ml to 0.61 +/- 0.06 microEq/ml). This response was reflected in elevated liver lipase activity (from 6.02 +/- 0.44 nmol fatty acid released/hr/mg protein to 14.22 +/- 0.90 units). No significant alterations in liver lipogenesis, assessed by glucose-6-phosphate dehydrogenase activity and by 3H2O incorporation into fatty acids, were observed. Gluconeogenic flux, determined indirectly through kinetic parameters of pyruvate kinase, was enhanced in animals fasted 3 weeks and in animals recovering from a 1-week fast. Plasma insulin levels were highest in fed groups (7.7 +/- 2.3 and 5.9 +/- 1.4 ng/ml at 1 week and 3 weeks, respectively) and were significantly depressed in fasted groups. Plasma levels of glucagon and GLP were also depressed in fasted groups. These results indicate that plasma glucose levels are maintained in salmon during fasting and that fasting-induced hyperlipidemia is mediated by lipolytic enzyme activity. Insulin, glucagon, and GLP may interact with these enzyme systems to coordinate nutritional metabolism of fish.
Gen Comp Endocrinol 1991 Mar
PMID:Effects of nutritional state on in vivo lipid and carbohydrate metabolism of coho salmon, Oncorhynchus kisutch. 205 44

Gap junctional conductance (gj) between cardiac ventricular myocyte pairs is rapidly, substantially, and reversibly reduced by sarcoplasmic acidification with CO2 when extracellular calcium activity is near physiological levels (1.0 mM CaCl2 added; 470 microM Ca++). Intracellular calcium concentration (Cai), measured by fura-2 fluorescence in cell suspensions, was 148 +/- 39 nM (+/- SEM, n = 6) and intracellular pH (pHi), measured with intracellular ion-selective microelectrodes, was 7.05 +/- 0.02 (n = 5) in cell pair preparations bathed in medium equilibrated with air. Cai increased to 515 +/- 12 nM (n = 6) and pHi decreased to 5.9-6.0 in medium equilibrated with 100% CO2. In air-equilibrated low-calcium medium (no added CaCl2; 2-5 microM Ca++), Cai was 61 +/- 9 nM (n = 13) at pHi 7.1. Cai increased to only 243 +/- 42 nM (n = 9) at pHi 6.0 in CO2-equilibrated low-calcium medium. Junctional conductance, in most cell pairs, was not substantially reduced by acidification to pHi 5.9-6.0 in low-calcium medium. Cell pairs could still be electrically uncoupled reversibly by the addition of 100 microM octanol, an agent which does not significantly affect Cai. In low-calcium low-sodium medium (choline substitution for all but 13 mM sodium), acidification with CO2 increased Cai to 425 +/- 35 nM (n = 11) at pHi 5.9-6.0 and gj was reduced to near zero. Junctional conductance could also be reduced to near zero at pHi 6.0 in low-calcium medium containing the calcium ionophore, A23187. The addition of the calcium ionophore did not uncouple cell pairs in the absence of acidification. In contrast, acidification did not substantially reduce gj when intracellular calcium was low. Increasing intracellular calcium did not appreciably reduce gj at pHi 7.0. These results suggest that, although other factors may play a role, H+ and Ca++ act synergistically to decrease gj.
J Gen Physiol 1990 Jun
PMID:Gap junctional conductance between pairs of ventricular myocytes is modulated synergistically by H+ and Ca++. 211 74

The plasma concentration of alpha 1-acid glycoprotein, a putative endogenous inhibitor of the site labeled by tritiated imipramine, was measured by a radial immunodiffusion assay in 36 normal human volunteers and 51 drug-free patients who fulfilled DSM-III criteria for major depression. The depressed patients exhibited a significant elevation in the plasma concentration (+/- SEM) of alpha 1-acid glycoprotein (79.6 +/- 4 mg/dL) when compared with the age- and sex-matched controls (61.7 +/- 3 mg/dL). Fourteen of the 51 patients with major depression had plasma alpha 1-acid glycoprotein concentrations that were higher than the highest values of the normal controls. There was no relationship between plasma alpha 1-acid glycoprotein concentrations and sex or affinity of platelet tritiated imipramine binding of either the normal volunteers or the depressed patients. In the depressed patients, there was a significant positive correlation between plasma concentrations of alpha 1-acid glycoprotein and postdexamethasone plasma cortisol concentrations, and two measures of depression severity, the Montgomery-Asberg Rating Scale for Depression and the Center for Epidemiologic Studies-Depression Scale, and a significant negative correlation with age. These data provide the first evidence of alterations of an endogenous inhibitor of the tritiated imipramine binding site/serotonin transporter in depressed patients.
Arch Gen Psychiatry 1990 Apr
PMID:Elevated plasma concentrations of alpha 1-acid glycoprotein, a putative endogenous inhibitor of the tritiated imipramine binding site, in depressed patients. 215 80

Intramembranous charge movement was measured in cut twitch fibers mounted in a double Vaseline-gap chamber with either a tetraethylammonium chloride (TEA.Cl) or a TEA2.SO4 solution (13-14 degrees C) in the central pool. Charge vs. voltage data were fitted by a single two-state Boltzmann distribution function. The average values of V (the voltage at which steady-state charge is equally distributed between the two Boltzmann states), k (the voltage dependence factor), and qmax/cm (the maximum charge divided by the linear capacitance, both per unit length of fiber) were V = -53.3 mV (SEM, 1.1 mV), k = 6.3 mV (SEM, 0.3 mV), qmax/cm = 18.0 nC/microF (SEM, 1.1 nC/microF) in the TEA.Cl solution; and V = -35.1 mV (SEM, 1.8 mV), k = 10.5 mV (SEM, 0.9 mV), qmax/cm = 36.3 nC/microF (SEM, 3.2 nC/microF) in the TEA2.SO4 solution. These values of k are smaller than those previously reported for cut twitch fibers and are as small as those reported for intact fibers. If a correction is made for the contributions of currents from under the Vaseline seals, V = -51.2 mV (SEM, 1.1 mV), k = 7.2 mV (SEM, 0.4 mV), qmax/cm = 22.9 nC/microF (SEM, 1.4 nC/microF) in the TEA.Cl solution; and V = -34.0 mV (SEM, 1.9 mV), k = 10.1 mV (SEM, 1.1 mV), qmax/cm = 38.8 nC/microF (SEM, 3.2 nC/microF) in the TEA2.SO4 solution. With this correction, however, the fit of the theoretical curve to the data is poor. A good fit with this correction can be obtained with a sum of two Boltzmann distribution functions. The first has average values V = -33.0 mV (SEM, 2.8 mV), k = 11.0 mV (SEM, 0.5 mV), qmax/cm = 10.6 nC/microF (SEM, 1.0 nC/microF) in the TEA.Cl solution; and V = -20.0 mV (SEM, 3.3 mV), k = 17.0 mV (SEM, 2.0 mV), qmax/cm = 36.4 nC/microF (SEM, 2.3 nC/microF) in the TEA2.SO4 solution. The second has average values V = -56.5 mV (SEM, 1.3 mV), k = 2.9 mV (SEM, 0.4 mV), qmax/cm = 13.2 nC/microF (SEM, 1.0 nC/microF) in the TEA.Cl solution; and V = -41.6 mV (SEM, 1.4 mV), k = 2.5 mV (SEM, 0.8 mV), qmax/cm = 11.8 nC/microF (SEM, 1.7 nC/microF) in the TEA2.SO4 solution. When a fiber is depolarized to near V of the second Boltzmann function, a slowly developing "hump" appears in the ON-segment of the current record.(ABSTRACT TRUNCATED AT 400 WORDS)
J Gen Physiol 1990 Aug
PMID:Intramembranous charge movement in frog cut twitch fibers mounted in a double vaseline-gap chamber. 221 83

We examined whether pentobarbital (PB) inhibited the acute extracellular release of dopamine that occurs in the striatum following the onset of ischemic injury in the gerbil model of stroke. The cerebral dialysis technique was employed to monitor striatal extracellular dopamine concentrations before and after carotid artery occlusion while perfusing either a control solution of artificial cerebrospinal fluid (CSF) or a 1 mM solution of pentobarbital in CSF (PB/CSF). During perfusion with CSF, extracellular dopamine increased from a baseline concentration of 0.40 +/- 0.09 (SEM) pmoles/10 minute collection interval to 30.0 +/- 9.0 pmoles/10 minutes after carotid artery occlusion. In contrast, during perfusion with PB/CSF, dopamine levels increased from a baseline of 1.37 +/- 0.3 pmoles/10 minutes to 8.30 +/- 2.6 pmoles/10 minutes; this increase was significantly less than the increase in controls. In animals with established ischemia, repeatedly alternating the perfusion fluid between CSF and PB/CSF demonstrated that dopamine concentrations were significantly increased with CSF alone and decreased with PB/CSF. These findings demonstrate that pentobarbital perfusion either before or following the onset of ischemia inhibits extracellular release of dopamine in the striatum. Inhibition of neurotransmitter release may, in part, be responsible for the protective effect of pentobarbital in ischemic brain injury.
J Neural Transm Gen Sect 1990
PMID:Pentobarbital inhibits extracellular release of dopamine in the ischemic striatum. 222 89

Intact single twitch fibers from frog muscle were stretched to long sarcomere length, micro-injected with the pH indicator dye phenol red, and activated by action potential stimulation. Indicator-related absorbance changes (denoted by delta A0 and delta A90) were measured with 0 degree and 90 degrees polarized light (oriented, respectively, parallel and perpendicular to the fiber axis). Two components of delta A were detected that had generally similar time courses. The "isotropic" component, calculated as the weighted average (delta A0 + 2 delta A90)/3, had the wavelength dependence expected for a change in myoplasmic pH. If calibrated in pH units, this signal's peak amplitude, which occurred 15-20 ms after stimulation, corresponded to a myoplasmic alkalization of average value 0.0025 +/- 0.0002 (+/- SEM; n = 9). The time course of this change, as judged from a comparison with that of the fibers' intrinsic birefringence signal, was delayed slightly with respect to that of the myoplasmic free [Ca2+] transient. On average, the times to half-peak and peak of the phenol red isotropic signal lagged those of the birefringence signal by 2.4 +/- 0.2 ms (+/- SEM; n = 8) and 8.4 +/- 0.5 ms (+/- SEM; n = 4), respectively. The other component of the phenol red signal was "dichroic," i.e., detected as a difference (delta A0-delta A90 greater than 0) between the two polarized absorbance changes. The wavelength dependence of this signal was similar to that of the phenol red resting dichroic signal (Baylor and Hollingworth. 1990. J. Gen. Physiol. 96:449-471). Because of the presence of the active dichroic signal, and because approximately 80% of the phenol red molecules appear to be bound in the resting state to either soluble or structural sites, the possibility exists that myoplasmic events other than a change in pH underlie the phenol red isotropic signal.
J Gen Physiol 1990 Sep
PMID:Changes in phenol red absorbance in response to electrical stimulation of frog skeletal muscle fibers. 223 Jul 9

Previous experiments using systemic and preoptic area (POA) hormone treatments have shown that aromatization of testosterone (T) to estrogen (E) is essential for activation of male-typical copulatory behavior in castrated male Japanese quail (Coturnix japonica). Two experiments were conducted to determine whether circulating estrogen levels characteristic of normal intact males are high enough to activate male-typical or female-typical copulatory behavior. In Experiment 1, blood samples were drawn every 4 hr from groups of sexually active male quail housed under a 16L:8D light-dark cycle, and assayed for estradiol (E2) concentration. The mean +/- SEM serum E2 was 54.2 +/- 3.6 pg/ml, and no daily cycle in serum E2 was seen. The males were then tested for sexual behavior; 88% mounted females, and 23% crouched when mounted by males. In Experiment 2, 51 males were castrated and implanted with Silastic tubes containing estradiol benzoate (EB) and/or cholesterol designed to produce five different levels of serum E2, then tested for male- and female-typical copulatory behavior and bled. The serum E2 in EB-implanted quail which mounted (253 +/- 30 pg/ml) was significantly higher than that of intact quail in Experiment 1, and only 10.2% of intact males had serum E2 as high as the minimum associated with mounting in EB-implanted males. These results show that serum E2 levels in intact males are not high enough to support male-typical copulation, and that aromatization in the POA to produce locally high E2 levels may be required. In addition, it was found that the threshold serum E2 to elevate receptivity significantly was 3.6 times the intact male level, and only slightly higher than serum E2 reported for intact females. Thus the lack of receptivity in intact males is probably due to insufficient circulating E2, and the male is not defeminized with respect to sensitivity to E2 for activation of receptivity.
Gen Comp Endocrinol 1990 Feb
PMID:Circulating estradiol and the activation of male and female copulatory behavior in Japanese quail (Coturnix japonica). 230 45

It has previously been observed that spontaneous contractions start in a region of damage of isolated right ventricular trabeculae of rat, propagate along the muscle, and induce triggered arrhythmias (Mulder, B.J.M., P.P. de Tombe, and H.E.D.J. ter Keurs. 1989. J. Gen. Physiol. 93:943-961). The present study was designed to analyze the mechanisms that lead to triggered propagated contractions (TPCs). TPCs were elicited in 29 trabeculae by stimulation with trains (2 Hz; 15-s intervals) at varied number of stimuli (n), lowered temperature (19-21 degrees C), and varied [Ca++]o (1.5-4 mM) in the superfusate. Length (SL) and shortening of sarcomeres in the muscle were measured at two sites using laser diffraction techniques; twitch force (Ft) was measured with a silicon strain gauge. Time between the last stimulus in the train and the onset of sarcomere shortening due to a TPC at a site close to the damaged end region (latency) and propagation velocity of the contraction (Vprop) were correlated with Ft. For 10 trabeculae, TPCs were calculated to start in the end region itself 586 +/- 28 ms (mean +/- 1 SEM) after the last stimulus of a train (n = 15; [Ca++]o: 1.5 mM), i.e., at the end of or after the rapid release of the damaged end during twitch relaxation. When Ft was increased by increasing either SL prior to stimulation or the afterload during twitches, methods that do not affect intracellular calcium levels, latency decreased, but Vprop remained constant. No TPC occurred when Ft was less than 20% of maximal Ft. Both increasing [Ca++]o and n increased Ft to a maximum, increased Vprop progressively (maximum Vprop, 17 mm/s), but decreased latency. These observations suggest that initiation of TPCs depends on the force developed by the preceding twitch, and therefore on the degree of stretch and subsequent rapid release of damaged areas in the myocardium, while Vprop along the trabeculae is determined by intracellular calcium concentration.
J Gen Physiol 1990 Jun
PMID:Spontaneous contractions in rat cardiac trabeculae. Trigger mechanism and propagation velocity. 237 99

Currents generated by depolarizing voltage pulses were recorded in neurons from the pyramidal cell layer of the CA1 region of rat or guinea pig hippocampus with single electrode voltage-clamp or tight-seal whole-cell voltage-clamp techniques. In neurons in situ in slices, and in dissociated neurons, subtraction of currents generated by identical depolarizing voltage pulses before and after exposure to tetrodotoxin revealed a small, persistent current after the transient current. These currents could also be recorded directly in dissociated neurons in which other ionic currents were effectively suppressed. It was concluded that the persistent current was carried by sodium ions because it was blocked by TTX, decreased in amplitude when extracellular sodium concentration was reduced, and was not blocked by cadmium. The amplitude of the persistent sodium current varied with clamp potential, being detectable at potentials as negative as -70 mV and reaching a maximum at approximately -40 mV. The maximum amplitude at -40 mV in 21 cells in slices was -0.34 +/- 0.05 nA (mean +/- 1 SEM) and -0.21 +/- 0.05 nA in 10 dissociated neurons. Persistent sodium conductance increased sigmoidally with a potential between -70 and -30 mV and could be fitted with the Boltzmann equation, g = gmax/(1 + exp[(V' - V)/k)]). The average gmax was 7.8 +/- 1.1 nS in the 21 neurons in slices and 4.4 +/- 1.6 nS in the 10 dissociated cells that had lost their processes indicating that the channels responsible are probably most densely aggregated on or close to the soma. The half-maximum conductance occurred close to -50 mV, both in neurons in slices and in dissociated neurons, and the slope factor (k) was 5-9 mV. The persistent sodium current was much more resistant to inactivation by depolarization than the transient current and could be recorded at greater than 50% of its normal amplitude when the transient current was completely inactivated. Because the persistent sodium current activates at potentials close to the resting membrane potential and is very resistant to inactivation, it probably plays an important role in the repetitive firing of action potentials caused by prolonged depolarizations such as those that occur during barrages of synaptic inputs into these cells.
J Gen Physiol 1990 Jun
PMID:A voltage-dependent persistent sodium current in mammalian hippocampal neurons. 237


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