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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

On the grounds of clinico-physiologic investigations the author revises the existing dual theory of photoreception. The paper describes complex clinical investigations of visual functions in patients with alimentary and essential hemeralopias and shows that rods and cones do not function in conditions of scotopic illumination without the presence of rhodopsin. On the grounds of investigations of the phenomenon of inversion and depression in the short-wave part of the visible spectrum in normal persons after dark adaptation in conditions of scotopic illumination, the author comes to a conclusion that there is a so-called "rhodopsin filter" just the presence of which in the process of dark adaptation creates conditions for appearance of this phenomenon. The author believes that there exist two kinds of photoreception: a direct disc two-component and a mediated rhodopsin one-component, as well as the third, transitory, that corresponds to those conditions of illumination in which the Purkinje's phenomenon appears.
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PMID:[Additions to the theory of the dual nature of photoreception]. 228 Sep 34

The effects of local anesthetics and a divalent cation, Ca2+, on the function of rhodopsin were estimated from the measurements of light-induced proton uptake. The light-induced proton uptake by rhodopsin in the rod outer segment disk membrane was enhanced at lower pH (4) but depressed at higher pHs (6 to 8) by the tertiary amine local anesthetics lidocaine, bupivacaine, tetracaine, and dibucaine. The order of local anesthetic-induced depression of the proton uptake followed that of their clinical anesthetic potencies. The depression of the proton uptake versus the concentration of the uncharged form of local anesthetic nearly describes the same curve for small and large dose of added anesthetic. Furthermore, a neutral local anesthetic, benzocaine, depressed the proton uptake at all pHs between 4 and 7. These results indicate that the depression of the proton uptake is due to the effect of only the uncharged form. It is hypothesized that the uncharged form of local anesthetics interacts hydrophobically with the rhodopsin in the disk membrane. The dual effect of local anesthetics on the proton uptake, on the other hand, suggests that the activation of the function of rhodopsin may be caused by the charged form. There was no significant change in the light-induced proton uptake by rhodopsin when 1 mM of Ca2+ was introduced into the disk membrane at varying pHs in the absence or presence of local anesthetics. This fact indicates that Ca2+ ion does not influence the diprotonating process of metarhodopsin; neither does it interfere with the local anesthetic-induced changes in the rhodopsin molecule.
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PMID:Dual effect of local anesthetics on the function of excitable rod outer segment disk membrane. 300 96

Patients with acute and chronic central serous retinopathy (CSR) were studied by psychophysical and photochemical means to establish the extent of visual depression and to investigate the basis of rod dysfunction in this disorder. In acute disease with serous detachment of the retina, the loss of sensitivity attains 3 log units and parallels the height of retinal elevation as does its recovery with resolution of the episode. Immediately after resolution, there is a residual 0.5 log unit threshold elevation. In chronic disease, marked loss of function exists over areas of abnormal retinal pigment epithelium in the absence of clinically detectable serous detachment. Although rhodopsin levels are low in both acute and chronic CSR, this relative lack of visual pigment does not totally account for the functional deficits in either situation.
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PMID:Retinal dysfunction in central serous retinopathy. 355 51

In the preceding article, we investigated the spatial properties of the induction of the prolonged depolarizing afterpotential (PDA) by shifting visual pigment from the rhodopsin (R) to the metarhodopsin (M) state in the barnacle photoreceptor. In this work, we have studied the ranges within the cell of the antagonistic effects on the PDA of M-to-R transfer. When this transfer occurs during a PDA, it depresses the PDA; when it precedes PDA induction, it impedes that induction ("anti-PDA"). These ranges were previously shown (by a statistical technique) to be at least a few tens of nanometers within a half-second (D greater than 10(-13) cm2 s-1). We now demonstrate, with local illumination techniques in which a PDA was induced in one side of the cell and PDA depression or anti-PDA was induced in the other side, that both ranges are much smaller than the cell diameter (approximately 100 microns) within 30 s (D less than 10(-6)). We further show, using a less direct but shorter-range technique involving colored polarized light, that the interaction of the PDA with the anti-PDA is restricted to less than approximately 6 microns (D less than 6 X 10(-9)). This figure is quite low and suggests that the interaction may be confined to the pigment molecules, possibly in a complex of the type suggested in the preceding article.
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PMID:Spatial properties of the prolonged depolarizing afterpotential in barnacle photoreceptors. II. Antagonistic interactions. 395 93

The effects of volatile anesthetics upon the function of bovine rhodopsin were estimated from the measurements of light-induced proton uptake. The light-induced pH changes were measured at both 20 degrees C and 37 degrees C with suspensions to which volatile anesthetics were added in the liquid form. Each anesthetic depressed the light-induced proton uptake concentration-dependently. The anesthetic-induced depression was greater at 37 degrees C than at 20 degrees C. For each anesthetic the concentration needed to depress the proton uptake by 10% was roughly identical to that used clinically. Anesthetics also were added to the suspensions in the gaseous form with air. The light-induced proton uptake was decreased in proportion to the partial pressure of the anesthetic. The partial pressures of halothane and methoxyflurane that depressed the proton uptake by 10% at 37 degrees C were 2.0 x 10(-7) and 1.1 x 10(-2) atm., respectively. From these facts it is suggested that volatile anesthetics affect the light-induced conformational changes of rhodopsin molecule during the metarhodopsin I to metarhodopsin II transition and cause inhibition of the light-induced proton uptake of rhodopsin in the rod outer segment disk membrane.
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PMID:Effects of volatile anesthetics on light-induced proton uptake of rhodopsin in bovine rod outer segment disk membrane. 609 4

Fundus reflectometry of the cat retina showed that under certain circumstances a rapid increase in density may follow intense bleaching exposures. The spectral characteristics of the density changes indicated that neither rhodopsin nor its bleach products could be responsible for this effect. The poor condition of the animals in which the phenomenon was observed and its conspicuous absence in the majority of the experimental runs suggested that the effect was associated with a process other than the resynthesis of rhodopsin. It was shown that an extrareceptoral event, spreading depression (SD) of the retina, is the most likely source of the rapid spectral change. The well-known tissue alterations associated with SD were induced in the retina independently of pigment density change. The resultant difference spectra resembled those produced when the rapid density increase occurred spontaneously. It seems likely that the abnormal physiological condition of those cats in which the phenomenon is more frequently observed primes the retina for the light-induced generation of spreading depression.
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PMID:"Rapid regeneration" in the cat retina: a case for spreading depression. 725 78

The study of signaling pathways has begun to uncover the mechanism by which cells respond and adapt to extracellular stimuli. It has become increasingly clear that the signaling pathways interact with one another to form a complex network through which regulation occurs. Here, we focus on three mechanisms by which signaling pathways interact and the physiological consequences of these interactions. Coincident signaling in long-term depression of synaptic responses in the cerebellum, protein kinase A gating of Ras to mitogen-activated protein kinase signal flow in proliferative responses, and a modified gating mechanism by phosducin resulting in feedback regulation of signal flow from rhodopsin to the cGMP phosphodiesterase in retinal light adaptation are analyzed as examples of different types of interactions between signaling pathways. These interactions allow the cell to spatially and temporally integrate complex information and respond in an appropriate and defined manner.
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PMID:Modes of interactions between signaling pathways. 1007 24

In 1991 a new type of G-protein-coupled receptor (GPCR) was cloned, the type 1a metabotropic glutamate (mGlu) receptor, which, despite possessing the defining seven-transmembrane topology of the GPCR superfamily, bore little resemblance to the growing number of other cloned GPCRs. Subsequent studies have shown that there are eight mammalian mGlu receptors that, together with the calcium-sensing receptor, the GABA(B) receptor (where GABA is gamma-aminobutyric acid) and a subset of pheromone, olfactory and taste receptors, make up GPCR family C. Currently available data suggest that family C GPCRs share a number of structural, biochemical and regulatory characteristics, which differ markedly from those of the other GPCR families, most notably the rhodopsin/family A GPCRs that have been most widely studied to date. This review will focus on the group I mGlu receptors (mGlu1 and mGlu5). This subgroup of receptors is widely and differentially expressed in neuronal and glial cells within the brain, and receptor activation has been implicated in the control of an array of key signalling events, including roles in the adaptative changes needed for long-term depression or potentiation of neuronal synaptic connectivity. In addition to playing critical physiological roles within the brain, the mGlu receptors are also currently the focus of considerable attention because of their potential as drug targets for the treatment of a variety of neurological and psychiatric disorders.
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PMID:Structural, signalling and regulatory properties of the group I metabotropic glutamate receptors: prototypic family C G-protein-coupled receptors. 1167 21

Retinal dystrophies, known in man, dog, mouse, and rat, involve progressive loss of photoreceptor cells with onset during or soon after the developmental period. Functional (electroretinogram), chemical (rhodopsin analyses) and morphological (light and electron microscopy) data obtained in the rat indicated two main processes: (a) overproduction of rhodopsin and an associated abnormal lamellar tissue component, (b) progressive loss of photoreceptor cells. The first abnormality recognized was the appearance of swirling sheets or bundles of extracellular lamellae between normally developing retinal rods and pigment epithelium; membrane thickness and spacing resembled that in normal outer segments. Rhodopsin content reached twice normal values, was present in both rods and extracellular lamellae, and was qualitatively normal, judged by absorption maximum and products of bleaching. Photoreceptors attained virtually adult form and ERG function. Then rod inner segments and nuclei began degenerating; the ERG lost sensitivity and showed selective depression of the a-wave at high luminances. Outer segments and lamellae gradually degenerated and rhodopsin content decreased. No phagocytosis was seen, though pigment cells partially dedifferentiated and many migrated through the outer segment-debris zone toward the retina. Eventually photoreceptor cells and the b-wave of the ERG entirely disappeared. Rats kept in darkness retained electrical activity, rhodopsin content, rod structure, and extracellular lamellae longer than litter mates in light.
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PMID:Inherited retinal dystrophy in the rat. 1388 27

"Bleaching desensitization" in rod photoreceptors refers to the prolonged depression of phototransduction sensitivity exhibited by rods after their exposure to bright light, i.e., after photolysis (bleaching) of a substantial fraction of rhodopsin in the outer segments. Rod recovery from bleaching desensitization depends critically on operation of the retinoid visual cycle: in particular, on the removal of all-trans retinal bleaching product from opsin and on the delivery of 11-cis retinal to opsin's chromophore binding site. The present paper summarizes representative findings that address the mechanism of bleaching desensitization.
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PMID:Bleaching desensitization: background and current challenges. 1461 37


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