Rapid Changes in Light-Scattering in the Prism ofTorpedoElectric Organ Slice Associated with the Production of Postsynaptic Potentials

1996 ◽  
Vol 218 (1) ◽  
pp. 298-301 ◽  
Author(s):  
I. Tasaki
2021 ◽  
Vol 13 (5) ◽  
pp. 935
Author(s):  
Matthew Varnam ◽  
Mike Burton ◽  
Ben Esse ◽  
Giuseppe Salerno ◽  
Ryunosuke Kazahaya ◽  
...  

SO2 cameras are able to measure rapid changes in volcanic emission rate but require accurate calibrations and corrections to convert optical depth images into slant column densities. We conducted a test at Masaya volcano of two SO2 camera calibration approaches, calibration cells and co-located spectrometer, and corrected both calibrations for light dilution, a process caused by light scattering between the plume and camera. We demonstrate an advancement on the image-based correction that allows the retrieval of the scattering efficiency across a 2D area of an SO2 camera image. When appropriately corrected for the dilution, we show that our two calibration approaches produce final calculated emission rates that agree with simultaneously measured traverse flux data and each other but highlight that the observed distribution of gas within the image is different. We demonstrate that traverses and SO2 camera techniques, when used together, generate better plume speed estimates for traverses and improved knowledge of wind direction for the camera, producing more reliable emission rates. We suggest combining traverses and the SO2 camera should be adopted where possible.


2003 ◽  
Vol 447 (1) ◽  
pp. 97-108 ◽  
Author(s):  
S. P. Srinivas ◽  
Joseph A. Bonanno ◽  
Els Larivi�re ◽  
Danny Jans ◽  
Willy Van Driessche

1985 ◽  
Vol 86 (3) ◽  
pp. 395-411 ◽  
Author(s):  
B M Salzberg ◽  
A L Obaid ◽  
H Gainer

Large changes in the opacity of the unstained mouse neurohypophysis follow membrane potential changes known to trigger the release of peptide hormones. These intrinsic optical signals, arising in neurosecretory terminals, reflect variations in light scattering and depend upon both the frequency of stimulation and [Ca2+]o. Their magnitude is decreased in the presence of Ca2+ antagonists and by the replacement of H2O in the medium by D2O. These observations suggest a correspondence between the intrinsic optical changes and secretory activity in these nerve terminals.


1988 ◽  
Vol 139 (1) ◽  
pp. 195-231
Author(s):  
B. M. Salzberg ◽  
A. L. Obaid

Potentiometric probes are small (300–500 Mr) amphipatic molecules that bind to, but do not cross, cell membranes and behave as fast linear transducers of membrane voltage. Their optical properties, particularly absorbance and fluorescence, respond to changes in potential in less than 2 microseconds, and they may be used to follow electrical events in membranes which are inaccessible to microelectrodes. We have used these dyes to study the properties of the action potential in the neurosecretory terminals of vertebrate neurohypophyses and, in particular, to investigate the behaviour of the local population of calcium channels. These channels are sensitive to the peptide toxin omega-conotoxin GVIA, derived from the venom of the marine snail Conus geographicus, but insensitive to dihydropyridine channel modulators. In the neurohypophysis of the mouse, it is possible to demonstrate that the calcium channels that are blocked by omega-conotoxin are those that are required for secretion of peptide hormones. In the terminals of the neurohypophysis, excitation is coupled to secretion, and the secretory event is accompanied by large and rapid changes in light scattering. These intrinsic optical signals provide a millisecond time-resolved monitor of events in the terminal that follow the entry of calcium, and may precede the release of hormones. We will consider how the changes in light scattering can be related to secretion, and how the extrinsic (absorption) and intrinsic optical signals may provide complementary information about excitation-secretion coupling.


1989 ◽  
Vol 93 (4) ◽  
pp. 715-729 ◽  
Author(s):  
A L Obaid ◽  
R Flores ◽  
B M Salzberg

Extrinsic absorption changes exhibited by potentiometric dyes have established the ionic basis of the action potential in synchronously activated populations of nerve terminals in the intact neurohypophyses of amphibia and mammals (Salzberg et al., 1983; Obaid et al., 1983, 1985b). Also, large and rapid changes in light scattering, measured as transparency, have been shown to follow membrane depolarization and to be intimately associated with the release of neuropeptides from the nerve terminals of the mouse neurohypophysis (Salzberg et al., 1985; Gainer et al., 1986). We report some experiments that help to define the pharmacological profile of the calcium channels present in intact neurosecretory terminals of vertebrates. For these, we used the peptide toxin omega-conotoxin GVIA (1-5 microM) and the dihydropyridine compounds Bay-K 8644 and nifedipine (2-5 microM), together with the after-hyperpolarization of the nerve terminal action potential. This undershoot depends upon the activation of a calcium-mediated potassium channel, as suggested by its sensitivity to [Ca++]o and charybdotoxin. omega-conotoxin GVIA substantially reduced the after-hyperpolarization in neurosecretory terminals of Xenopus, while neither of the dihydropyridine compounds had any effect under conditions that mimic natural stimulation. The effects of these calcium channel modifiers on the action potential recorded optically from the terminals of the Xenopus neurohypophysis were faithfully reflected in the behavior of the light-scattering changes observed in the neurohypophysis of the CD-1 mouse. omega-conotoxin GVIA (5 microM) reduced the size of the intrinsic optical signal associated with secretion by 50%, while the dihydropyridines had little effect. These observations suggest that the type of calcium channel that dominates the secretory behavior of intact vertebrate nerve terminals is at least partially blocked by omega-conotoxin GVIA and is insensitive, under normal conditions, to dihydropyridines.


1996 ◽  
Vol 88 (3) ◽  
pp. 683-691 ◽  
Author(s):  
P. KAATZ ◽  
D.P. SHELTON

Sign in / Sign up

Export Citation Format

Share Document