Electroretinogram of the parietal eye of lizards: Photoreceptor, glial, and lens cell contributions

1999 ◽  
Vol 16 (5) ◽  
pp. 895-907 ◽  
Author(s):  
EDUARDO SOLESSIO ◽  
GUSTAV A. ENGBRETSON

Local electroretinograms (ERGs) were recorded in the parietal eye of Xantusia vigilis. The responses to monochromatic light under dark- and light-adapted conditions were studied. We found that two antagonistic chromatic mechanisms dominate the overall response. With the electrode tip in the lumen of the eye, light stimulation under dark-adapted conditions evoked responses of negative polarity with maximum sensitivity to green light. Intense green background illumination saturated the green-sensitive mechanism, and superposition of a blue stimulus then elicited responses of opposite polarity, driving the potentials back toward the dark resting level. The spectral sensitivities of the two chromatic mechanisms were determined using chromatic adaptation. The lower threshold, green-sensitive mechanism has a maximum sensitivity at 495 nm while the antagonistic mechanism, with its maximal spectral sensitivity at 430 nm, is at least 2 log units less sensitive. The polarity of the ERG recording inverts as the electrode traverses the photoreceptor layer, suggesting that the photoreceptors are the major source of the ERG. This result was confirmed with intracellular recordings from photoreceptors, glial, and lens cells. The glial and lens cells of the parietal eye respond to local changes in [K+]o. Intracellular recordings of the responses of these cells to light stimuli follow time courses similar to changes in extracellular potassium concentrations measured with K+-specific electrodes. These results suggest that the glial and lens cell membranes are highly permeable to potassium and, therefore, the electrical responses of these cells are evoked by changes in [K+]o elicited by light stimulation of the photoreceptors. Nevertheless, the major component of the parietal eye ERG is the photoreceptor signal. A circuit model of the ERG sources is presented.

1976 ◽  
Vol 39 (5) ◽  
pp. 1117-1133 ◽  
Author(s):  
B. Oakley ◽  
D. G. Green

1. Double-barrel, potassium-specific microelectrodes have been used to measure light-induced transient changes in [K+]o in the frog eye cup preparation. These changes in [K+]o have been termed the potassioretinogram (KRG). 2. The KRG consists of two components: a rapid increase in [K+]o in the proximal retina and a slow decrease in [K+]o in the distal retina. 3. The KRG decrease has the rhodopsin action spectrum, is maximal in the photoreceptor layer, persists after aspartate treatment, and has an increment threshold curve which saturates at moderate background intensities. The rhodopsin rods are, therefore, most likely the only neurons which generate this ionic change, although the Muller (glial) cells may also be involved in this process. 4. The KRG decrease has the same time course as the c-wave of the electroretinogram for all variations in the stimulus parameters, including intensity, duration, and chromaticity. 5. It is suggested that the c-wave may be produced by the pigment epithelial cells as they hyperpolarize in response to the decrease in [K+]o around the photoreceptors.


1991 ◽  
Vol 66 (1) ◽  
pp. 103-111 ◽  
Author(s):  
C. Jiang ◽  
G. G. Haddad

1. A brain slice preparation was used to study the hypoglossal (XII) neuronal response to anoxia. Both intra- and extracellular potassium activities (K+i,K+o) were measured by the use of ion-selective microelectrodes, and K+ flux was assessed by the use of pharmacologic blockers. 2. Extracellular recordings showed that a short period of anoxia (4 min) induced an increase in K+o of 26.4 +/- 7.5 mM (mean +/- SD, n = 20) in the XII nucleus of adult rats. 3. Intracellular recordings (n = 31) in XII neurons showed a substantial decrease in K+i during anoxia. Fourteen neurons were analyzed in detail and these showed that XII neurons depolarized to -25.3 +/- 7.7 mV, whereas K+i dropped from 93.6 +/- 14.9 to 32 +/- 9.0 mM. These results strongly suggested that K+ is lost from XII neurons during anoxia. 4. Although the extracellular space (ECS) shrank by approximately 50% during anoxia, the possibility that the increase in K+o and decrease in K+i were mainly caused by shrinkage of the ECS and swelling of intraneuronal space was excluded to a great degree because the changes in K+i and K+o during anoxia were relatively very large. 5. To study the mechanisms by which K+ is lost from XII neurons, we used several pharmacologic blockers. High concentration of ouabain (10 mM) and strophanthidin (80 microM) increased K+o from baseline (3-4 mM) to 40.9 +/- 2.5 mM (n = 6) but did not abolish an additional anoxia-induced increase in K+o, suggesting that mechanisms other than Na(+)-K(+)-adenosine triphosphatase inhibition were also responsible for the anoxia-induced K+ leakage.(ABSTRACT TRUNCATED AT 250 WORDS)


1971 ◽  
Vol 57 (3) ◽  
pp. 363-384 ◽  
Author(s):  
A. M. Granda ◽  
S. Yazulla

Responses to diffuse monochromatic light were recorded from single units in the diencephalon of pigeon. Units were both excited and inhibited by light stimulation. Intensity-response functions based on latency measures to the first spike after stimulation were used to generate action spectra. One class of spectral sensitivity functions presumably from rods, showed peak sensitivities near 500 nm: these functions were unaffected by changing criterion values used to generate the functions. A second class of cone functions showed multiple peak sensitivities at 540 nm and 600–620 nm. These units shifted their peak sensitivities with a change in criterion values. Unit response types tended to be localized differentially in the nucleus rotundus. Excitatory units were located in the dorsal half of the nucleus, while inhibitory units were located in the ventral half, with a few exceptions. An attempt was made to integrate the present findings with previous behavioral, electrophysiological, photochemical, and anatomical data in the pigeon.


1991 ◽  
Vol 11 (3) ◽  
pp. 1531-1537 ◽  
Author(s):  
Q R Liu ◽  
M Tini ◽  
L C Tsui ◽  
M L Breitman

The elements regulating lens-specific expression of the mouse gamma F-crystallin gene were examined. Here we show that mouse gamma F-crystallin sequences -67 to +45 contain a low basal level of lens-specific promoter activity and that sequences -67 to -25, which are highly conserved among different gamma-crystallin genes, are able to function as a strong transcriptional activator when duplicated and placed upstream of the TATA box. We also show that nuclear factors from lens and nonlens cells are able to form different complexes with sequences centered at -46 to -36 and demonstrate that binding of the factor from lens cells correlates with lens-specific promoter activity of the mouse gamma F-crystallin gene.


1930 ◽  
Vol 2 (4) ◽  
pp. 249-263 ◽  
Author(s):  
A. H. Hutchinson ◽  
Dorothy Newton

An isolated strain of Yeast, derived from Fleischman's preparation, when exposed to monochromatic light responds quite differently to light of different wave-lengths. Slight retardation in growth by red and orange light, stimulation by yellow and green, and increasingly marked retardation in the blue and violet, characterize the effects of the mercury lines of the visible spectrum. There is a sudden transition to stimulation in the near ultra-violet. (λ 3984 Å). Stimulation continues at λ 3650 Å and characterises the region λ 2894 Å to λ 2700 Å, but otherwise the lines employed in this investigation retard growth.Generally the effect either of stimulation or retardation is greater when the control is one of rapid growth rate, but the reverse is the case at the red end of the visible spectrum.


1979 ◽  
Vol 11 (5-6) ◽  
pp. 283-287 ◽  
Author(s):  
F.C.S. Ramaekers ◽  
M.W.A.C Hukkelhoven ◽  
A. Groeneveld ◽  
H. Bloemendal

2000 ◽  
Vol 83 (1) ◽  
pp. 406-417 ◽  
Author(s):  
Daryl W. Hochman ◽  
Philip A. Schwartzkroin

Antagonism of the chloride-cotransport system in hippocampal slices has been shown to block spontaneous epileptiform (i.e., hypersynchronized) discharges without diminishing excitatory synaptic transmission. Here we test the hypotheses that chloride-cotransport blockade, with furosemide or low-chloride (low-[Cl−]o) medium, desynchronizes the firing activity of neuronal populations and that this desynchronization is mediated through nonsynaptic mechanisms. Spontaneous epileptiform discharges were recorded from the CA1 and CA3 cell body layers of hippocampal slices. Treatment with low-[Cl−]o medium led to cessation of spontaneous synchronized bursting in CA1 ≥5–10 min before its disappearance from CA3. During the time that CA3 continued to burst spontaneously but CA1 was silent, electrical stimulation of the Schaffer collaterals showed that hyperexcited CA1 synaptic responses were maintained. Paired intracellular recordings from CA1 pyramidal cells showed that during low-[Cl−]otreatment, the timing of action potential discharges became desynchronized; desynchronization was identified with phase lags in firing times of action potentials between pairs of neurons as well as a with a broadening and diminution of the CA1 field amplitude. Continued exposure to low-[Cl−]o medium increased the degree of the firing-time phase shifts between pairs of CA1 pyramidal cells until the epileptiform CA1 field potential was abolished completely. Intracellular recordings during 4-aminopyridine (4-AP) treatment showed that prolonged low-[Cl−]oexposure did not diminish the frequency or amplitude of spontaneous postsynaptic potentials. CA3 antidromic responses to Schaffer collateral stimulation were not significantly affected by prolonged low-[Cl−]o exposure. In contrast to CA1, paired intracellular recordings from CA3 pyramidal cells showed that chloride-cotransport blockade did not cause a significant desynchronization of action potential firing times in the CA3 subregion at the time that CA1 synchronous discharge was blocked but did reduce the number of action potentials associated with CA3 burst discharges. These data support our hypothesis that the anti-epileptic effects of chloride-cotransport antagonism in CA1 are mediated through the desynchronization of population activity. We hypothesize that interference with Na+,K+,2Cl−cotransport results in an increase in extracellular potassium ([K+]o) that reduces the number of action potentials that are able to invade axonal arborizations and varicosities in all hippocampal subregions. This reduced efficacy of presynaptic action potential propagation ultimately leads to a reduction of synaptic drive and a desynchronization of the firing of CA1 pyramidal cells.


1976 ◽  
Vol 68 (5) ◽  
pp. 487-501 ◽  
Author(s):  
J E Lisman ◽  
Y Sheline

The early receptor potential (ERP) was recorded intracellularly from Limulus ventral photoreceptors. The ERP in cells dissected under red light was altered by exhaustive illumination. No recovery to the original wafeform was observed, even after 1 h in the dark. The ERP waveform could be further altered by chromatic adaptation or by changes in pH. The results indicate that at pH 7.8 there are two interconvertible pigment states with only slightly different lambdamax, whereas at pH 9.6 there are two interconvertible states with very different lambdamax. Under all conditions studied the ERPs were almost identical with those previously obtained in squid retinas. This strongly suggests that light converts Limulus rhodopsin to a stable photoequilibrium mixture of rhodopsin to a stable photoequilibrium mixture of rhodopsin and metarhodopsin and that, as in squid, the lambdamax of metarhodopsin depends on pH. This conversion at pH 7.8 is associated with a small (0.7 log unit) decrease in the maximum sensitivity of the late receptor potential. Thus the component of adaptation linked to changes in rhodopsin concentration is unimportant in comparison to the "neural" component.


1979 ◽  
Vol 74 (6) ◽  
pp. 713-737 ◽  
Author(s):  
B Oakley ◽  
D G Flaming ◽  
K T Brown

It has been hypothesized that the light-evoked rod hyperpolarization (the receptor potential) initiates the light-evoked decrease in extracellular potassium ion concentration, [K+]o, in the distal retina. The hypothesis was tested using the isolated, superfused retina of the toad, Bufo marinus; the receptor potential was recorded intracellularly from red rods, and [K+]o was measured in the photoreceptor layer with K+-specific microelectrodes. In support of the hypothesis, variations in stimulus irradiance or duration, or in retinal temperature, produced qualitatively similar effects on both the receptor potential and the decrease in [K+]o. A mechanism for the relationship between the receptor potential and the decrease in [K+]o was suggested by Matsuura et al. (1978. Vision Res. 18:767-775). In the dark, the passive efflux of K+ out of the rod is balanced by an equal influx of K+ fromthe Na+/K+ pump. The light-evoked rod hyperpolarization is assumed to reduce the passive efflux, with little effect on the pump. Thus, the influx will exceed the efflux, and [K+]o will decrease. Consistent with this mechanism, the largest and most rapid decrease in [K+]o was measured adjacent to the rod inner segments, where the Na+/K+ pump is most likely located; in addition, inhibition of the pump with ouabain abolished the decrease in [K]o more rapidly than the rod hyperpolarization. Based upon this mechanism, Matsuura et al. (1978) developed a mathematical model: over a wide range of stimulus irradiance, this model successfully predicts the time-course of the decrease in [K+]o, given only the time-course of the rod hyperpolarization.


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