scholarly journals Oxygen distribution and consumption in the cat retina during normoxia and hypoxemia.

1992 ◽  
Vol 99 (2) ◽  
pp. 177-197 ◽  
Author(s):  
R A Linsenmeier ◽  
R D Braun
Keyword(s):  
Oxygen Consumption ◽  
Dark Adaptation ◽  
Light Adaptation ◽  
Metabolic Effects ◽  
Extracellular Potassium ◽  
Oxygen Distribution ◽  
Simple Diffusion ◽  
Extracellular Potassium Concentration ◽  
Proximal Half ◽  
Cat Retina

Oxygen tension (PO2) was measured with microelectrodes within the retina of anesthetized cats during normoxia and hypoxemia (i.e., systemic hypoxia), and photoreceptor oxygen consumption was determined by fitting PO2 measurements to a model of steady-state oxygen diffusion and consumption. Choroidal PO2 fell linearly during hypoxemia, about 0.64 mmHg/mmHg decrease in arterial PO2 (PaO2). The choroidal circulation provided approximately 91% of the photoreceptors' oxygen supply under dark-adapted conditions during both normoxia and hypoxemia. In light adaptation the choroid supplied all of the oxygen during normoxia, but at PaO2's less than 60 mmHg the retinal circulation supplied approximately 10% of the oxygen. In the dark-adapted retina the decrease in choroidal PO2 caused a large decrease in photoreceptor oxygen consumption, from approximately 5.1 ml O2/100 g.min during normoxia to 2.6 ml O2/100 g.min at a PaO2 of 50 mmHg. When the retina was adapted to a rod saturating background, normoxic oxygen consumption was approximately 33% of the dark-adapted value, and hypoxemia caused almost no change in oxygen consumption. This difference in metabolic effects of hypoxemia in light and dark explains why the standing potential of the eye and retinal extracellular potassium concentration were previously found to be more affected by hypoxemia in darkness. Frequency histograms of intraretinal PO2 were used to characterize the oxygenation of the vascularized inner half of the retina, where the oxygen distribution is heterogeneous and simple diffusion models cannot be used. Inner retinal PO2 during normoxia was relatively low: 18 +/- 12 mmHg (mean and SD; n = 8,328 values from 36 profiles) in dark adaptation, and significantly lower, 13 +/- 6 mmHg (n = 4,349 values from 19 profiles) in light adaptation. Even in the dark-adapted retina, 30% of the values were less than 10 mmHg. The mean PO2 in the inner (i.e., proximal) half of the retina was well regulated during hypoxemia. In dark adaptation it was significantly reduced only at PaO2's less than 45 mmHg, and it was reduced less at these PaO2's in light adaptation.

scholarly journals Effects of light and darkness on oxygen distribution and consumption in the cat retina.

1986 ◽  
Vol 88 (4) ◽  
pp. 521-542 ◽  
Author(s):  
R A Linsenmeier
Keyword(s):  
Light Adaptation ◽  
Outer Nuclear Layer ◽  
Oxygen Distribution ◽  
Half Time ◽  
Outer Retina ◽  
Dimensional Model ◽  
One Dimensional ◽  
Cat Retina ◽  
Electrode Penetration ◽  
Outer Half

These experiments were done to investigate the effects of light and darkness on the oxygenation of the retina in anesthetized cats. Measurements were made with double-barreled oxygen microelectrodes capable of recording both oxygen tension (PO2) and local voltages. Diffuse white illumination presented to a dark-adapted retina led to an increase in PO2 of up to 30 mmHg in the outer half of the retina. Changes were maximal at approximately 75% depth, corresponding to the outer nuclear layer. No change or decrease in PO2 was observed in the inner retina. Light-evoked increases in outer retinal PO2 were graded with the duration and strength of illumination, and were maximal in response to 60 s of illumination at rod saturation. For these stimuli, the increase at the onset of illumination was slower (average half-time, 12.2 s) than the recovery at the end of illumination (average half-time, 5.9 s), but for stimuli above rod saturation, PO2 recovered much more slowly. The profile of PO2 was measured during electrode penetration and withdrawal and during light and dark adaptation. Dark-adapted profiles were characterized by a minimum PO2 of nearly 0 mmHg at depths of 65-85%, and a steep gradient from the minimum to the choroid. During light adaptation at rod saturation, PO2 was elevated in the outer half of the retina and the minimum was eliminated. Fits of the profiles to a one-dimensional model of oxygen diffusion indicated that light reduced the oxygen consumption of the outer retina to approximately 50% of its dark-adapted value.

Effects of adaptation level and hypoglycemia on function of the cat retina during hypoxemia

1997 ◽  
Vol 14 (2) ◽  
pp. 339-350 ◽  
Author(s):  
M. A. McRipley ◽  
J. Ahmed ◽  
E. P. -C. Chen ◽  
R. A. Linsenmeier
Keyword(s):  
Oxygen Consumption ◽  
Ganglion Cell ◽  
Action Potentials ◽  
Light Adaptation ◽  
Ganglion Cells ◽  
Adaptation Level ◽  
Atp Production ◽  
Threshold Response ◽  
Cell Responses ◽  
Cat Retina

AbstractAcute hypoxemia (low PaO2) leads to changes in oxygen consumption and electrical responses of the outer retina of cats, but inner retinal ERG components and ganglion cell responses have been shown to be quite resistant to hypoxemia. The purpose of this study was to determine whether the resistance of the inner retina depends on (1) the stimulus conditions, specifically the degree of light adaptation; and (2) the ability of the photoreceptors to increase glycolysis during hypoxemia. To address these issues, recordings of single ganglion cell action potentials and of the b-wave and scotopic threshold response (STR) of the electroretinogram (ERG) were made from the eyes of anesthetized cats during hypoxemia alone and hypoxemia plus hypoglycemia. Ganglion cells appeared to be equally resistant to hypoxemia at high and low backgrounds (3.3 to 9.7 log equivalent quanta(555 nm)-deg-2-s-1), and the STR, recorded with dim stimuli during dark adaptation, when photoreceptor oxygen consumption is most susceptible to hypoxemia, was unchanged until PaO2 was below 30 mm Hg. The amplitude of the b-wave was similarly resistant to hypoxemia when the animal was normoglycemic. During hypoglycemia, however, both the b-wave and the STR became more sensitive to hypoxemia, beginning to change at PaO2s as high as 50 mm Hg when blood glucose was 40–50 mg/dl. It is argued that hypoglycemia limits or prevents the increased glycolytic ATP production that would ordinarily occur when the photoreceptor oxygen supply decreases, and that increased photoreceptor glycolysis is essential in the protection of the retina against mild hypoxemia.

Alpha ganglion cells of the rabbit retina lose antagonistic surround responses under dark adaptation

1997 ◽  
Vol 14 (2) ◽  
pp. 395-401 ◽  
Author(s):  
Jay F. Muller ◽  
Ramon F. Dacheux
Keyword(s):  
Dark Adaptation ◽  
Light Adaptation ◽  
Ganglion Cells ◽  
Rabbit Retina ◽  
Evoked Responses ◽  
Full Field ◽  
Cat Retina ◽  
Dendritic Arbors ◽  
Field Organization ◽  
Receptive Field Organization

AbstractAlpha ganglion cells from the midperiphery of the rabbit retina were recorded intracellularly under visual control, in a superfused everted eyecup, and labeled with HRP. Their physiology and large somata with broad dendritic arbors identified them as uniform populations of ON- and OFF-center alpha ganglion cells, which typically displayed transient/sustained light-evoked responses. When dark adapted, the light-evoked responses from both ON- and OFF-center alpha ganglion cells were more sustained than those generally seen under light-adapted conditions. During dark-adapted (scotopic) conditions, stimulation with dim full-field illumination and small spots, either positioned over the soma or displaced 450 μm from the soma, all elicited pure center responses. After light adaptation (photopic conditions), the displaced small spots that previously evoked center responses elicited antagonistic surround responses from both ON- and OFF-center cells. Thus, as originally described in cat retina (Barlow et al., 1957), the receptive-field organization of ganglion cells changed between dark and light adaptation, and an absence or presence of surround antagonism was indicative of scotopic versus photopic states.

Oxygen distribution and consumption in the macaque retina

2007 ◽  
Vol 293 (3) ◽  
pp. H1696-H1704 ◽  
Author(s):  
Gülnur Birol ◽  
Shufan Wang ◽  
Ewa Budzynski ◽  
Norbert D. Wangsa-Wirawan ◽  
Robert A. Linsenmeier
Keyword(s):  
Oxygen Consumption ◽  
Dark Adaptation ◽  
Human Retina ◽  
Oxygen Distribution ◽  
Outer Retina ◽  
Choroidal Circulation ◽  
Physiological Conditions ◽  
State Diffusion ◽  
Clinical Conditions ◽  
Steady State Diffusion

The oxygen distribution in the retina of six anesthetized macaques was investigated as a model for retinal oxygenation in the human retina in and adjacent to the fovea. Po2 was measured as a function of retinal depth under normal physiological conditions in light and dark adaptation with O2 microelectrodes. Oxygen consumption (Qo2) of the photoreceptors was extracted by fitting a steady-state diffusion model to Po2 measurements. In the perifovea, the Po2 was 48 ± 13 mmHg (mean and SD) at the choroid and fell to a minimum of 3.8 ± 1.9 mmHg around the photoreceptor inner segments in dark adaptation, rising again toward the inner retina. The Po2 in the inner half of the retina in darkness was 17.9 ± 7.8 mmHg. When averaged over the outer retina, photoreceptor Qo2 (called Qav) was 4.6 ± 2.3 ml O2·100 g−1·min−1 under dark-adapted conditions. Illumination sufficient to saturate the rods reduced Qav to 72 ± 11% of the dark-adapted value. Both perifoveal and foveal photoreceptors received most of their O2 from the choroidal circulation. While foveal photoreceptors have more mitochondria, the Qo2 of photoreceptors in the fovea was 68% of that in the perifovea. Oxygenation in macaque retina was similar to that previously found in cats and other mammals, reinforcing the relevance of nonprimate animal models for the study of retinal oxygenation, but there was a smaller reduction in Qo2 with light than observed in cats, which may have implications for understanding the influence of light under some clinical conditions.

Extracellular potassium concentration in chronic alumina cream foci of cats

1984 ◽  
Vol 52 (3) ◽  
pp. 421-434 ◽  
Author(s):  
U. Heinemann ◽  
I. Dietzel
Keyword(s):  
Border Zone ◽  
Constant Current ◽  
Extracellular Potassium ◽  
Local Concentration ◽  
Base Line ◽  
Extracellular Potassium Concentration ◽  
Concentration Changes ◽  
K Concentration ◽  
Repetitive Electrical Stimulation ◽  
Normal Cortex

Changes in extracellular K+ concentration [( K+]o) were measured with ion-selective microelectrodes in chronic epileptic foci induced by topical application of A1(OH)3 cream on the sensorimotor cortex of cats. The foci were morphologically characterized by a scar surrounded by an area of marked gliosis. Base-line levels of [K+]o in gliotic tissue and its immediate border zone were comparable to those in normal cortical tissue. Peak levels of [K+]o obtained during repetitive electrical stimulation of the cortical surface and thalamic ventrobasal complex were only slightly enhanced with 11.6 mM in chronic foci and 10.8 mM in normal cortex. Iontophoretic K+ application into gliotic tissue was accompanied by slow negative potential shifts comparable to those observed in normal cortex. Passage of constant current through gliotic tissue caused local [K+]o changes in the vicinity of the current-passing electrode. Since these [K+]o changes were similar to those observed in normal tissue, it was concluded that the amount of transcellularly transported K ions was comparable in both tissues. Changes in the size of extracellular space (ES) were investigated by measuring local concentration changes of iontophoretically injected tetramethylammonium and choline ions. During stimulus-induced seizure activity, the ES shrank outside the gliotic area at sites of maximal [K+]o elevation, while it increased at sites within the gliotic tissue where [K+]o rises were smaller. The results suggest that the spatial buffer capacity of gliotic tissue for K+ is not severely impaired. Since the relationship between rises in [K+]o and subsequent undershoots at sites immediately bordering the gliotic tissue is comparable to that in normal cortex, the ability of this epileptic tissue for active K+ uptake appears to be unaffected. This conclusion is further supported by the observation that iontophoretically induced rises in [K+]o during undershoots are reduced to a similar extent as in normal cortex.

Effect of elevated potassium on the ion content of mouse astrocytes and neurons

1992 ◽  
Vol 70 (S1) ◽  
pp. S263-S268 ◽  
Author(s):  
H. Steve White ◽  
Sien Yao Chow ◽  
Y. C. Yen-Chow ◽  
Dixon M. Woodbury
Keyword(s):  
Cortical Neurons ◽  
Cell Types ◽  
Mouse Cell ◽  
Ion Concentration ◽  
Cellular Heterogeneity ◽  
Resting Membrane Potential ◽  
Extracellular Potassium ◽  
Individual Response ◽  
Extracellular Potassium Concentration ◽  
The Brain

Potassium is tightly regulated within the extracellular compartment of the brain. Nonetheless, it can increase 3- to 4-fold during periods of intense seizure activity and 10- to 20-fold under certain pathological conditions such as spreading depression. Within the central nervous system, neurons and astrocytes are both affected by shifts in the extracellular concentration of potassium. Elevated potassium can lead to a redistribution of other ions (e.g., calcium, sodium, chloride, hydrogen, etc.) within the cellular compartment of the brain. Small shifts in the extracellular potassium concentration can markedly affect acid–base homeostasis, energy metabolism, and volume regulation of these two brain cells. Since normal neuronal function is tightly coupled to the ability of the surrounding glial cells to regulate ionic shifts within the brain and since both cell types can be affected by shifts in the extracellular potassium, it is important to characterize their individual response to an elevation of this ion. This review describes the results of side-by-side studies conducted on cortical neurons and astrocytes, which assessed the effect of elevated potassium on their resting membrane potential, intracellular volume, and their intracellular concentration of potassium, sodium, and chloride. The results obtained from these studies suggest that there exists a marked cellular heterogeneity between neurons and astrocytes in their response to an elevation in the extracellular potassium concentration.Key words: astrocytes, neurons, ion concentration, neuronal–glial interactions, mouse, cell culture.

The Cockroach DCMD Neurone: I. Lateral Inhibition and the Effects of Light- and Dark-adaptation

1982 ◽  
Vol 99 (1) ◽  
pp. 61-90 ◽  
Author(s):  
DONALD H. EDWARDS
Keyword(s):  
Lateral Inhibition ◽  
Dark Adaptation ◽  
Light Adaptation ◽  
Absolute Intensity ◽  
Recurrent Network ◽  
Light Spot ◽  
Movement Detector ◽  
Threshold Response ◽  
Inhibitory Network ◽  
Local Background

1. The responses of the cockroach descending contralateral movement detector (DCMD) neurone to moving light stimuli were studied under both light- and dark-adapted conditions. 2. With light-adaptation the response of the DCMD to two moving 2° (diam.) spots of white light is less than the response to a single spot when the two spots are separated by less than 10° (Fig. 2). 3. With light-adaptation the response of the DCMD to a single moving light spot is a sigmoidally shaped function of the logarithm of the light intensity (Fig. 3a). With dark-adaptation the response of a DCMD to a single moving light spot is a bell-shaped function of the logarithm of the stimulus intensity (Fig. 3b). The absolute intensity that evokes a threshold response is about one-and-a-half log units less in the dark-adapted eye than in the light-adapted eye. 4. The decrease in the DCMD's response that occurs when two stimuli are closer than 10°, and when a single bright stimulus is made brighter, indicates that lateral inhibition operates among the afferents to the DCMD. 5. It is shown that this inhibition cannot be produced by a recurrent lateral inhibitory network. A model of the afferent path that contains a non-recurrent lateral inhibitory network can account for the response/intensity plots of the DCMD recorded under both light-adapted and dark-adapted conditions. 6. The threshold intensity of the DCMD is increased if a stationary pattern of light is present near the path of the moving spot stimulus. This is shown to be due to a peripheral tonic lateral inhibition that is distinct from the non-recurrent lateral inhibition described earlier. 7. It is suggested that the peripheral lateral inhibition acts to adjust the threshold of afferents to local background light levels, while the proximal non-recurrent network acts to enhance the acuity of the eye to small objects in the visual field, and to filter out whole-field stimuli.

GABA-Receptor–Independent Dorsal Root Afferents Depolarization in the Neonatal Rat Spinal Cord

1998 ◽  
Vol 79 (5) ◽  
pp. 2581-2592 ◽  
Author(s):  
E. Kremer ◽  
A. Lev-Tov
Keyword(s):  
Spinal Cord ◽  
Dorsal Root ◽  
Gaba Receptor ◽  
Neonatal Rat ◽  
Extracellular Potassium ◽  
Rat Spinal Cord ◽  
Extracellular Potassium Concentration ◽  
Dorsal Roots ◽  
Intact Brain ◽  
Dorsal Root Afferents

Kremer, E. and A. Lev-Tov. GABA-receptor–independent dorsal root afferents depolarization in the neonatal rat spinal cord. J. Neurophysiol. 79: 2581–2592, 1998. Dorsal root afferent depolarization and antidromic firing were studied in isolated spinal cords of neonatal rats. Spontaneous firing accompanied by occasional bursts could be recorded from most dorsal roots in the majority of the cords. The afferent bursts were enhanced after elevation of the extracellular potassium concentration ([K+]e) by 1–2 mM. More substantial afferent bursts were produced when the cords were isolated with intact brain stems. Rhythmic afferent bursts could be recorded from dorsal roots in some of the cords during motor rhythm induced by bath-applied serotonin and N-methyl-d-aspartate (NMDA). Bilaterally synchronous afferent bursts were produced in pairs of dorsal roots after replacing the NaCl in the perfusate with sodium-2-hydroxyethansulfonate or after application of the γ-aminobutyric acid-A (GABAA) receptor antagonist bicuculline with or without serotonin (5-HT) and NMDA. Antidromic afferent bursts also could be elicited under these conditions by stimulation of adjacent dorsal roots, ventrolateral funiculus axons, or ventral white commissural (VWC) fibers. The antidromic bursts were superimposed on prolonged dorsal root potentials (DRPs) and accompanied by a prolonged increase in intraspinal afferent excitability. Surgical manipulations of the cord revealed that afferent firing in the presence of bicuculline persisted in the hemicords after hemisection and still was observed after removal of their ventral horns. Cutting the VWC throughout its length did not perturb the bilateral synchronicity of the discharge. These findings suggest that the activity of dorsal horn neurons is sufficient to produce the discharge and that the bilateral synchronicity can be maintained by cross connectivity that is relayed from side to side dorsal to the VWC. Antagonists of GABAB, 5-HT2/5-HT1C, or glutamate metabotropic group II and III receptors could not abolish afferent depolarization in the presence of bicuculline. Depolarization comparable in amplitude to DRPs, could be produced in tetrodotoxin-treated cords by elevation of [K+]e to the levels reported to develop in the neonatal rat spinal cord in response to dorsal root stimulation. A mechanism involving potassium transients produced by neuronal activity therefore is suggested to be the major cause of the GABA-independent afferent depolarization reported in our study. Possible implications of potassium transients in the developing and the adult mammalian spinal cord are discussed.

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