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N Bonaventure

Publications and source records attributed to N Bonaventure.

At least 37 records · Page 2Linked to original sources

Directional asymmetry of the horizontal monocular head and eye optokinetic nystagmus: effects of picrotoxin.

Frog monocular eye and head optokinetic nystagmus (OKN) were studied by coil recordings after intravitreal administration of picrotoxin into the closed eye. Before injection, the frog displayed an OKN only for stimulations in the temporo-nasal (T-N) direction. The injection of picrotoxin provoked the appearance of a N-T component of the head and eye OKN: the slow phase velocity gain and the resetting fast phase frequency were strongly and significantly increased. Thus, picrotoxin abolished the directional asymmetry of head and eye OKN, indicating the involvement of GABAergic mechanisms in the inhibition of the N-T component of the monocular eye and head OKN. Picrotoxin administration had an additional effect on the monocular head OKN only, the performances (measured by the velocity gain and the frequency of resetting fast phases) were markedly increased for both directions of stimulation, suggesting an effect of the drug upon the motor output of head movements.

Animals↗

Glutamatergic separation of ON and OFF retinal channels: possible modulation by glycine and acetylcholine.

When intravitreally injected into the frog in vivo, 2-amino-4-phosphonobutyrate (APB) and cis-2,3-piperidine dicarboxylic acid (PDA) showed opposite effects on ON and OFF retinal channels: APB abolished the ON responses in the electroretinogram and in ganglion cell activity, and increased OFF responses. At the same time the receptive field area was enlarged, and the inhibition exerted by the surround was suppressed. A cholinergic/glycinergic loop involving amacrine cells was suggested to be the pathway of the inhibitory ON input upon the OFF channel. PDA abolished the OFF responses in the ERG and in ganglion cell activity, while increasing the ON response in the ERG and decreasing the ganglion cell sensitivity at ON. The receptive field area was not modified, but the inhibition exerted by the surround was suppressed, probably by a blockade of horizontal cell glutamate receptors.

Acetylcholine↗

Is a retinal input involved in the generation of eye resetting fast phases in the frog eye optokinetic nystagmus?

An intravitreal injection of cis-2,3-piperidine dicarboxylic acid (PDA), a glutamate analog, in one eye only, decreased or even totally suppressed the eye resetting fast phases (ERFPs) of the frog optokinetic nystagmus (OKN) in monocular as in binocular situations. On the opposite, for low drum speeds, the slow phase eye velocity was not affected by PDA. Moreover, it seems that intravitreally injected PDA does not act upon central structures responsible for OKN. Our experiments suggest that a retinal input may be involved in triggering the ERFPs in the OKN.

Animals↗

Neurotransmission in the frog retina: possible physiological and histological correlations.

In the frog retina, extracellular recordings of transient ganglion cells have shown that the inhibitory surround of the receptive field of these cells was mediated by gamma-aminobutyric acid and acetylcholine (through the nicotinic receptors). Histoautoradiographic and immunocytochemical studies for the two respectively have shown that these neurotransmitters can act through horizontal and amacrine cells. The separation of the ON and OFF channels mediated by glutamate at the bipolar cell level may also be obtained by glycine and/or acetylcholine (through muscarinic receptors). Respective histoautoradiographic and immunocytochemical studies indicate that these neurotransmitters act at the amacrine cell level. These data are consistent with the functional separation of spatial and temporal organization of retinal information, with horizontal cells especially responsible for the spatial organization of the ganglion cell responses and amacrine cells involved in both spatial and temporal organization of the responses.

Acetylcholine↗

Electrooculographic study in the chicken after treatment with neurotoxin 6-hydroxydopamine.

The implication of dopamine in the modulation of the standing potential of the eye was tested in the chicken by an indirect electrooculogram (EOG) method. After a single rapid systemic injection of dopamine, a transient dose-dependent increase in the EOG voltage was observed. EOG recordings during light and dark adaptation were performed after retinal dopamine depletion was induced by intraocular injections of the neurotoxin 6-hydroxydopamine (6-OHDA). The eyes were injected on two successive days with a mixture of 6-OHDA (50 micrograms), pargyline (a monoamine oxidase inhibitor), and ascorbate added as an antioxidant. Following this treatment EOG recordings were performed 1, 4, and 8 days after the second injection. The electrophysiological changes appeared most spectacular on the fourth day: an important increase in the EOG basal values as well as of the amplitude of the light peak and of the dark trough were observed. Substantial reduction in retinal concentration of dopamine was found in treated retinas. These unexpected electrophysiological data offer additional evidence for the involvement of a catecholamine in the generation of the light peak and the dark trough of the EOG.

Animals↗

Involvement of ON and OFF retinal channels in the eye and head horizontal optokinetic nystagmus of the frog.

The specific role of ON and OFF retinal information channels in the generation of the horizontal optokinetic nystagmus (OKN) of the frog was studied. Coil recordings of monocular eye and head OKN were obtained before and after intravitreal injection of two drugs that block either ON or OFF channels. The intravitreal injection of 2-amino-4-phosphonobutyrate (APB), a glutamate analog that selectively blocks the ON retinal channel, strongly reduced or even cancelled the monocular OKN of the head and of the eye. The intravitreal injection of another glutamate analog, the cis-2,3-piperidine dicarboxylic acid (PDA) that especially blocks the OFF retinal channel, did not affect the gain velocity of the slow phase of both the horizontal monocular head and eye OKN, for low stimulus velocities. Our results suggest that the retinal ON information channel, but not the OFF channel, is involved in the generation of the slow phase of the OKN of the frog, at least at low drum velocities.

Aminobutyrates↗

GAD immunoreactivity in pretectal and accessory optic nuclei of the frog mesencephalon.

By an immunocytochemical technique using anti-GAD antibodies, we found a high density of GAD-immunoreactive puncta in the 5 pretectal nuclei and in the nucleus of the basal optic root. These results back up the suggestion that GABAergic modulation of the output of the visual pretectal relay nuclei might underlie the directional asymmetry of the horizontal optokinetic nystagmus and the directional selectivity of pretectal neurons.

Animals↗

On cholinergic mechanisms in the optokinetic nystagmus of the frog: antagonistic effects of muscarinic and nicotinic systems.

In a monocular situation, an intravitreal injection of acetylcholine (ACh) agonists (especially muscarinic agonists like muscarine or oxotremorine) provoked both the suppression of the optokinetic nystagmus (OKN) related to the injected eye, and the appearance of a nasal-temporal (N-T) component in the OKN triggered by the contralateral non-injected eye. These two effects were added in a binocular condition. Similar results were obtained with ACh nicotinic antagonists (D-tubocurarine, alpha-bungarotoxin, hexamethonium and gallamine). ACh muscarinic antagonists (atropine, scopolamine) had only moderate effects and failed to provoke an N-T component in the contralateral OKN. These data show that ACh mechanisms are involved in the control of the frog OKN, especially in directional asymmetry, nicotinic and muscarinic systems acting in an antagonistic way.

Animals↗

Physiological effects of muscarinic vs nicotinic ACh antagonists upon ganglion cell activity in the frog retina.

The intravitreal administration of ACh agonists (eserine, carbachol, oxotremorine) or that of ACh muscarinic antagonists (scopolamine, atropine) provoked a reduction of the On-Off ganglion cell discharges. The agonists depressed the Off discharges more than the On discharges, while the ACh muscarinic antagonists depressed the On- more than the Off discharges. These drugs did not modify the ganglion cell receptive field area; thus, the muscarinic cholinergic system seems not to be involved in the spatial organization of the On-Off ganglion cells, but rather seems to play an important part in the separation of On and Off information channels. ACh nicotinic antagonists [hexamethonium, D-tubocurarine (D-TC), alpha-bungarotoxin (alpha-BGTX)] provoked an increase of the receptive field area of On-Off ganglion cells, this enlargement being due to the suppression of the inhibition normally exerted by the surround upon the centre of the field. Moreover D-TC and alpha-BGTX, but but hexamethonium, increased the number of ganglion cell discharges. These data are analogous to those obtained after administration of GABA antagonists and show that through nicotinic receptors, ACh seems to be involved in the spatial organization of the On-Off ganglion cell.

Acetylcholine↗

[Contribution of internal layers of the retina to the genesis of the light peak in the electrooculogram in the chicken].

We report that in the Chicken retina, Na aspartate which selectively blocks signal transmission between the photoreceptors and second order neurons also largely modifies the EOG. In treated eyes, the standing potential is reduced and the LP which is very transient in the Chicken eye is substituted for by a reactivity to light with much slower rise and delayed culmination time. The data are discussed in terms of interaction between pigment epithelium and neuroretina in the pharmacological determinism of the LP.

Animals↗

Anisotropic inhibition in the receptive field surround of the frog retinal ganglion cells, evidenced by bicuculline and SR 95103, a new GABA antagonist.

When GABA antagonists (picrotoxin, bicuculline methiodide and SR 95103) were intravitreally injected in the frog, they increased the number of spikes of transient retinal ganglion cells, as well as the duration of the response. Thus, the transient pattern of the response became more sustained. GABA antagonists also provoked a marked increase in the size of the receptive field, which might be due to the abolition of the inhibition exerted by the surround upon the centre of the field. In fact, a stimulus applied to the surround of the field simultaneously with one applied to the centre no longer provoked the reduction of the field area nor that of the number of spikes. These are effects which were always observed before drug injection. After picrotoxin injection, the enlarged field was concentric with the initial one, both angular diameters doubled, whereas after bicuculline or SR 95103, the enlarged field was not concentric with the initial one and only one diameter increased. Thus, GABA inhibition appears to be distributed according to an anisotropic spatial pattern. Whether this anisotropy might be an input for direction selectivity in the frog visual system is a topic of discussion. With respect to SR 95103, this compound proved to act like a selective GABA antagonist with long lasting effects.

Animals↗

On GABAergic mechanisms in the optokinetic nystagmus of the frog: effects of bicuculline, allylglycine and SR 95103, a new GABA antagonist.

In a monocular situation, an intravitreal injection of the GABA antagonists, bicuculline or SR 95103 provoked both the suppression of the optokinetic nystagmus (OKN) related to the injected eye and the appearance of a Nasal-Temporal (N-T) component in the OKN triggered by the contralateral non-injected eye (this N-T component being absent in control OKN). These two effects were added in a binocular condition. Similar results were obtained with L-C allylglycine which reduces the endogenous GABA level, but these effects were delayed when compared to those of GABA antagonists. All these data are roughly analogous to those previously obtained with picrotoxin (a non-competitive GABA antagonist) and thus confirm that GABA mechanisms are involved in the control of the frog OKN. Furthermore, SR 95103 acted in this model as a potent selective GABA antagonist, as has been demonstrated in another system.

Allylglycine↗

Stereospecific effects of the alpha-aminoadipic acid on the retina: a morphological and electrophysiological study.

In both frog and chicken an intravitreal injection of the dextrorotatory (D)-isomer of alpha-aminoadipic acid (alpha-aaa) leads to a progressive disappearance of the ERG b-wave without affecting a and c components. Tectal evoked potentials (TEP) are no longer recorded. These physiological effects are concomitant with a specific glial cell damage, without any apparent damage to neurons. The levorotatory (L)-isomer at low concentrations is more gliotoxic than the D-isomer, the ERG b-wave is suppressed, while the amplitude of both a and c components is increased. TEPs are always recorded, i.e., a visual message is still generated in the retina and transmitted to the optic tectum when the Müller cells have been damaged and the b-wave is abolished. At higher concentrations the L-isomer suppresses TEPs and damages both glial and neuronal cells. Thus alpha-aaa appears to be a good tool for analyzing ERG components, especially subcomponents of the c-wave.

2-Aminoadipic Acid↗

Enhanced sensory convergence to the visual cortex in the rodless (rd/rd) mouse.

The rd/rd mutation provokes a specific degeneration of the photoreceptive cells in the mouse retina, without affecting other neuronal elements. This degeneration starts 8 to 10 days after birth. Discriminative learning experiments have shown the degenerated retina to remain light-sensitive, the sensitivity being reduced to 10(-5) of normal with a peak still at 500 nm. An ontogenetic study showed a progressive vanishing of visual potentials (electroretinogram and visual evoked potentials) during the third week of life. Potentials of auditory origin, which can be recorded from the visual cortex in normal mice, were found to be clearly facilitated by the absence of the visual input either because of retinal degeneration in rd mouse or provoked by enucleation at birth.

Animals↗

A cone-triggered c-wave in the chicken ERG time integration characteristics.

The c-waves recorded from the cone-dominant retina of the chicken proved to be cone-triggered. The time course and time integration properties of this retinal potential were compared with those of the rod-triggered c-wave recorded in the frog under scotopic conditions. The results clearly demonstrate that there is no evidence for time integration in cone-triggered c-waves but that rod-triggered c-waves follow the Bunsen-Roscoe law over more than 2 log units. We propose that these time-related differences may be used in other species as a differentiation criterion between cone-triggered and rod-triggered c-waves.

Animals↗

Photopic c-wave in the chicken ERG: sensitivity to sodium azide, epinephrine, sodium iodate, barbiturates, and other general anesthetics.

The c-wave recorded in the chicken electroretinogram proved to be a cone-triggered component. The questions arose whether its reactivity to various specific drugs (sodium iodate, sodium azide, epinephrine, or barbiturates) were similar to those described for classic rod-triggered c-waves. We also tested the sensitivity of the chicken c-wave to various general anesthetics. Urethane was found to be the drug that best preserves the c-wave in electrophysiological recordings.

Anesthetics↗

Evidence for both photopic and scotopic characteristics in the c-wave of chicken and frog ERG.

The electroretinographic c-wave was studied in two species with duplex retinas, the frog (rod-dominant) and the chicken (highly cone-dominant). In both species a cone driven c-wave was recorded in addition to the classical rod-driven c-wave. An attempt was made to specify the differential characteristics with respect to time-course, time integration, adaptational changes and spectral sensitivity of cone-driven vs rod-driven c-waves. These data confirm the generality of the c-wave generation by both rod and cone systems.

Adaptation, Ocular↗

[Pharmacological sensitivity of the photopic c-wave in the electroretinogram of the chicken. I. Effects of sodium azide, adrenaline, and a barbiturate].

The c-wave recorded in the chicken electroretinogram proved to be cone-triggered. The effect of various drugs active on pigment epithelium and on c-waves in scotopic retinas were tested in order to determine whether a similar mechanism may underlie both rod- and cone-triggered c-waves. Our results indeed point to such a similar reactivity of both types of c-waves. Pentothal, a short-acting barbiturate induced--as it does in the sheep--a transient disappearance of the c-wave. Sodium azide and adrenaline produced very similar effects: when injected i.v., these drugs produced a transient increase in the resting potential of the eye (the "azide potential"). When injected im or i.p., both drugs provoked--as they do in rabbit or in rat retinas--an increase in the voltage of the c-wave, but this increase was preceded in the chicken by a partial or total suppression of this component.

Animals↗