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Biomedical subjects

M Piccolino

Publications and source records attributed to M Piccolino.

At least 19 recordsLinked to original sources
PubMed1992

Binding of the benzodiazepine ligand [3H]-RO 15-1788 to membrane preparations of the rabbit and turtle retina.

1. We have studied the binding of [3H]-RO 15-1788 to membrane preparations of the retina of rabbit (Lepus cunicula) and turtle (Pseudemys scripta elegans). 2. In both species, [3H]-RO 15-1788 binding was maximal at 0 degrees C and decreased with increasing temperature. It was saturable, protein concentration-dependent and specific. Flunitrazepam, unlabelled RO 15-1788 and ethyl-beta-carboline were the most effective displacers, whereas RO 5,4864 was ineffective. 3. In both turtle and rabbit retina, Scatchard analysis indicated the presence of a single binding site for [3H]-RO 15-1788. The KD was 0.75 nM in both turtle and rabbit, while the Bmax were 520 and 250 fmol/mg protein in turtle and rabbit respectively. A study of the association rate of [3H]-RO 15-1788 binding revealed faster kinetics in turtle, as compared to rabbit.

Animals↗
PubMed1989

Binding of [3H] muscimol to the retina of rabbit and turtle.

1. We studied the binding of [3H]muscimol to membrane preparations of the retina of rabbit (Lepus cuniculus) and turtle (Pseudemys scripta elegans). 2. In both species, [3H]muscimol binding was maximal at 0 degrees C and decreased with increasing temperature, it was saturable, protein concentration dependent and specific. Muscimol, GABA and bicuculline were the most effective displacers, whereas baclofen and diaminobutyric acid were ineffective. 3. In the turtle retina, Scatchard analysis indicated the presence of a single site with a KD of 20.81 nM, and a Bmax of 3.620 pmol/mg prot. 4. In the rabbit, a single site could be identified in the nanomolar concentration range (KD of 12.8 nM, Bmax of 1.327). A study of the association rate of [3H]muscimol binding revealed a faster kinetics in turtle, as compared to rabbit.

Animals↗
PubMed1987

Morphological changes induced in turtle retinal neurons by exposure to 6-hydroxydopamine and 5,6-dihydroxytryptamine.

Following intraocular injection of the dopamine neurotoxin 6-hydroxydopamine (10-50 micrograms on two successive days in a Ringer vehicle containing ascorbate and pargyline) and an incubation period of 1 to 18 days, degeneration was noted in presumptive amacrine cells in the retina of the turtle, Pseudemys scripta elegans. Injection of vehicle alone produced no effect. Affected perikarya initially showed swollen mitochondria, lysosomes and distended cisternae. At later stages the cells took on a darkened appearance. In contrast, affected amacrine processes in the inner plexiform layer became markedly distended and lost their cytoplasmic contents, resulting in empty, very swollen profiles. No degeneration was noted distal to the affected cell bodies, i.e. the affected cells were not interplexiform neurons. Cells lesioned by 6-hydroxydopamine were shown to accumulate [3H]dopamine. Intraocular administration of 5,6-dihydroxytryptamine (a single dose of 10-40 micrograms in the same vehicle) followed by 4-6 days incubation resulted in a marked darkening of certain bipolar cell axon terminals, cell bodies and Landolt's clubs. The toxic effects of 5,6-dihydroxytryptamine were blocked by zimelidine, a serotonin uptake blocker. Thus, these two neurotoxins have different targets in the turtle retina. At the highest dose tested, however, 6-hydroxydopamine did produce degenerative changes in the presumed serotonergic bipolar cell.

5,6-Dihydroxytryptamine↗
PubMed1987

Dopaminergic mechanisms underlying the reduction of electrical coupling between horizontal cells of the turtle retina induced by d-amphetamine, bicuculline, and veratridine.

Previous studies have shown that dopamine, bicuculline, or d-amphetamine reduce the electrical and dye-coupling between the axon terminals of the horizontal cells of the turtle retina (see Piccolino et al., 1984). In the present study we observed similar effects following the application of veratridine. The actions of all these drugs were prevented by dopamine antagonists acting on D1 receptors such as flupenthixol and SCH 23390. However, in contrast to dopamine, the actions of d-amphetamine, bicuculline, and veratridine were attenuated or abolished by pharmacological agents (such as 6-OH-dopamine, alpha-methyl-p-tyrosine, or reserpine) known to reduce the release of dopamine from dopaminergic neurons. Moreover, the actions of veratridine and bicuculline were prevented by tetrodotoxin, indicating that one or more neurons in the dopamine pathway are spike-generating. We conclude that d-amphetamine, bicuculline, and veratridine reduce electrical coupling between the axon terminals of the turtle horizontal cells by promoting the release of endogenous dopamine from the dopaminergic amacrine cells previously identified (Witkovsky et al., 1984). Electron-microscopic observations revealed that 6-OH-dopamine selectively attacked this population of amacrine cells. No degenerating terminals were found adjacent to the horizontal cell axon terminals. On this basis, we postulate that dopamine reaches the horizontal cell by diffusion through the extracellular space.

Animals↗
PubMed1985

Dopaminergic drugs improve human visual contrast sensitivity.

Effects of dopaminergic drugs (L-dopa plus benserazide, or nomifensine) on human visual function have been tested in healthy volunteers by measuring the psychophysical contrast sensitivity for sinusoidal gratings of various spatial frequencies. After drug administration the contrast sensitivity improved in all subjects over a limited range of medium to high spatial frequencies.

Adult↗
PubMed1984

Decrease of gap junction permeability induced by dopamine and cyclic adenosine 3':5'-monophosphate in horizontal cells of turtle retina.

The axon terminals of the H1 horizontal cells of the turtle retina are electrically coupled by extensive gap junctions. Dopamine (10 nM to 10 microM) induces a narrowing of the receptive field profile of the H1 horizontal cell axon terminals, increases the coupling resistance between them, and decreases the diffusion of the dye Lucifer Yellow in the network formed by the coupled axon terminals. These actions of dopamine involve the activation of D1 receptors located on the membrane of the H1 horizontal cell axon terminals proper. Increases of the intracellular cyclic AMP concentration induced by either stimulating the adenylate cyclase activity with forskolin or inhibiting the phosphodiesterase activity with isobutylmethylxanthine, theophylline, aminophylline, or compound RO 20-1724 elicit effects similar to those of dopamine on the receptive field profile of the H1 horizontal cell axon terminals, on their coupling resistance, and on the diffusion of Lucifer Yellow in the axon terminal network. It is concluded that dopamine decreases the permeability of the gap junctions between the axon terminals of the H1 horizontal cells of the turtle retina and that this action probably involves cyclic AMP as a second messenger.

Animals↗
PubMed1982

gamma-Aminobutyric acid antagonists decrease junctional communication between L-horizontal cells of the retina.

The antagonists of gamma-aminobutyric acid, bicuculline and picrotoxin, were found to narrow the receptive field profile of the large field horizontal cell (L1HC) in the turtle retina when added to the perfusion medium in micromolar concentrations. The coupling resistance between neighboring L1HCs was increased by bicuculline or picrotoxin. Under control conditions, the dye Lucifer yellow injected into one L1HC diffused into a large number of neighboring L1HCs; bicuculline or picrotoxin greatly restricted dye passage between these same cells. We conclude that antagonists of gamma-aminobutyric acid decrease the conductance of gap junctions between L1HCs.

Animals↗
PubMed1982

Processing of visual signals in vertebrate photoreceptors.

Photoreceptors of the vertebrate retina hyperpolarize in response to illumination. The conductance changes in the plasma membrane associated with the electrical response are the final step of chain of events initiated by light absorption at the outer segment of the visual cell. The mechanism whereby the free energy of photons in converted into neural information is largely unknown. Present knowledge is consistent with the idea that an internal transmitter is modulated by light and modifies the ionic permeability of the plasma membrane. As to the identity of the internal messenger two candidates have been proposed: Ca2+ and cyclic GMP respectively. Increasing evidence suggests that both substances may be involved in the process of phototransduction. The electrical response of photoreceptors does not simply reflect the light absorbed by the cell: complex interactions occurring between adjacent photoreceptors and between photoreceptors and second order neurons cooperate with the initial process in determining the final shape of the receptor message. Recurrent interactions involve particularly cones: their membrane potential can be modified at least by three distinct mechanisms; i) by light absorption at their outer segment; ii) by light absorption at the outer segment of neighbouring cones, and iii) by potential changes occurring in horizontal cells.

Adaptation, Physiological↗
PubMed1981

Involvement of small-field horizontal cells in feedback effects on green cones of turtle retina.

Light stimuli depolarize green cones of turtle retina through a circuit involving a feedback connection from luminosity horizontal cells (L-HC) to green cones. In turtle retina two types of L-HC have been distinguished: large-field L-HC and small-field L-HC. The spatial properties of the feedback depolarizations of green cones were compared with those of both large- and small-field L-HC. Green cones were found to be more effectively depolarized by relatively small spots of red light than by large red annuli. Moreover, red light stimulation of the periphery of the receptive field could reduce the depolarizing influence of central red stimuli. These spatial properties greatly differ from those of the large-field L-HC, whereas they strongly resemble those of the small-field L-HC. These results suggest that the small-field L-HC mediate the feedback action on green cones.

Animals↗
PubMed1981

Center-surround antagonistic organization in small-field luminosity horizontal cells of turtle retina.

1. The spatial properties of the small-field luminosity horizontal cell (L2-HC) were investigated in the retina of the turtle by using circular or annular light stimuli of varying dimensions. 2. The amplitude of the hyperpolarizing response induced by dim light spots decreased when the diameter of the spot was increased beyond about 1,000 micrometer. 3. With bright-light stimuli the peak amplitude of the light responses increased monotonically when increasing the illuminated area, but a delayed antagonistic effect appeared with spots of more than 1,000-micrometer diameter. 4. Depolarizing responses were observed if the periphery of the receptive field was stimulated with annuli of light in the presence of central background illumination. 5. The interaction of the inputs converging on the L2-HC from the peripheral and central regions of the receptive field was found to be nonlinear. The same peripheral stimulation could result either in an enhancement or in a depression of the central response according to the intensity of the central illumination. 6. By comparing the receptive-field properties of the L2-HC and the red cones a model is proposed that explains the antagonistic surround mechanism of the L2-HC on the basis of the antagonistic peripheral mechanism in cones. '

Animals↗
PubMed1980

Characteristics and ionic processes involved in feedback spikes of turtle cones.

In about 20% of the cones of untreated retinas of turtles, bright flash illumination of the periphery of their receptive field evokes a spike through the feedback mechanism from the L-horizontal cell. Such feedback spikes, never observed with central stimulation, are labile, but after they have disappeared they can be regained by depolarizing the cone. Feedback spikes are actual regenerative responses, since they show a critical threshold potential, are facilitated by cone depolarization and are blocked by hyperpolarization. They are associated with a membrane resistance decrease; tetrodotoxin (10(-5) M) does not block them. High Ca2+ media facilitate their appearance, but their effect is transient because of the cone hyperpolarization and the light response block that Ca2+ ions induce. Sr2+ ions (4-10 mM) facilitate the discharge of feedback spikes in response to peripheral illumination in every cone, whether or not it has previously shown feedback effects. In Sr2+ media, feedback spikes are stable and can be evoked by dim lights. Ba2+ (2-6 mM) also facilitates and stabilizes the discharge of feedback spikes. Co2+ and D-600 block the feedback spikes. Pharmacological agents that depolarize the L-horizontal cells, such as GABA, glutamate or nicotine, also block the feedback spikes. Both Sr2+ and Ba2+ also induce the appearance of spontaneous and off spikes, which are also blocked by Co2+, but these are not related to the feedback mechanism. These results strongly suggest that every turtle cone receives a feedback input from the L-horizontal cells, which would be able to induce an increase of the cone Ca2+ conductance, which may become regenerative.

Action Potentials↗
PubMed1980

Sustained feedback effects of L-horizontal cells on turtle cones.

Prolonged stimulation of the periphery of their receptive field can evoke in turtle cones sustained complex depolarizations or sustained membrane oscillations. In cones in which such effects of prolonged peripheral stimulation are not apparent, the injection of short depolarizing pulses can reveal a sustained increase of electrical excitability in response to prolonged peripheral illumination. The sustained effects of prolonged peripheral illumination have characteristics similar to those of the feedback depolarizations evoked by flash peripheral stimulation: they are labile in untreated retinas, can be blocked by either hyperpolarization, Co2+ or agents that depolarize the L-horizontal cells. They are associated with a decrease in the membrane input resistance. In retinas bathed in Sr2+- or Ba2+-containing media, prolonged peripheral illumination evokes a sustained repetitive discharge of spikes. These experiments demonstrate that the feedback effects of the L-horizontal cells on the cones are not only transient but also sustained and that the sustained effects of peripheral stimulations are associated with an increase in membrane Ca2+ conductance. The possible nature of the feedback connection between L-horizontal cells and the cones is discussed.

Animals↗