Involvement of NMDA in a plasticity phenomenon observed in the adult frog monocular optokinetic nystagmus.

The frog horizontal monocular optokinetic nystagmus (H-OKN) is asymmetrical, the reflex being evoked by a temporal-nasal (T-N) component, but not by a nasal-temporal (N-T) component. Coil recordings showed that, in adult animals, 8 days of monocular deprivation (by unilateral eyelid suture) provoked the appearance of a N-T component, the H-OKN becoming symmetrical, reacting for both directions of stimulation. This delay was shortened to 2 days following two successive unilateral pretectal administrations of NMDA or of LY 285 265, an NMDA agonist, the first 2 days of eyelid suture.

Different effects of dopamine and piribedil (a dopamine D2 agonist) on frog monocular optokinetic nystagmus asymmetry.

Frog monocular optokinetic nystagmus (OKN) displays a directional asymmetry, reacting only to stimulations in the temporal-nasal (T-N) direction. The nasal-temporal (N-T) component is almost absent. The systemic or intrapretectal injection of Piribedil, a D2 dopamine agonist, provokes the appearance of a N-T component suppressing the monocular OKN asymmetry.

Are retinal or mesencephalic dopaminergic systems involved in monocular optokinetic nystagmus asymmetry in frog?

In monocular vision, frogs display a unidirectional optokinetic horizontal nystagmus (H-OKN) reacting only to temporal-nasal (T-N) stimulation. The N-T component is almost absent. The analysis of search coil recordings after administration of dopamine into the viewing eye, the occluded eye or directly into the pretectum, hardly modifies the H-OKN triggered by the viewing eye irrespective of the concentration used.

N-methyl-D-aspartate antagonists suppress the development of frog symmetric monocular optokynetic nystagmus observed after unilateral visual deprivation.

In monocular vision, frogs display a unidirectional optokinetic nystagmus (OKN), reacting only to temporal-nasal (T-N) stimulation. The OKN N-T component is almost absent. However, prolonged monocular visual deprivation by unilateral eyelid suture provoked the appearance of the N-T component.

Pharmacological study of the chicken's monocular optokinetic nystagmus: involvement of the ON retinal channel evidenced by the glutamatergic separation of ON and OFF pathways.

The chicken's monocular optokinetic nystagmus (OKN), recorded by the magnetic search coil technique, displays a directional asymmetry, the temporal-nasal (T-N) stimulation being more efficient than the nasal-temporal (N-T) one to evoke the reflex. The intravitreal administration of APB, a glutamate agonist which selectively blocks the ON retinal channel strongly reduced the eye monocular OKN; it also induced spontaneous eye movements in the T-N direction. The intravitreal injection of PDA another glutamate analog, which reduces the OFF channel, while increasing the activity of the ON channel, induced a large increase in OKN velocity gain, especially for a N-T stimulation at the lowest drum speeds.

Pharmacological study of the chicken's monocular optokinetic nystagmus: effects of GABAergic agonist and antagonists.

When injected into the chicken open eye, the GABA-agonist THIP and the GABA-antagonists bicuculline and picrotoxin induced spontaneous eye movements in nasal-temporal (N-T) and in temporal-nasal (T-N) direction, respectively. These spontaneous movements were scarcely modulated by optokinetic stimulation, irrespective of the direction of stimulation. It is suggested that they are due to the suppression of directional selectivity of retinal ganglion cells.

Plasticity of the frog monocular OKN: involvement of pretectal GABAergic and cholinergic systems.

The frog horizontal monocular optokinetic nystagmus (OKN) is asymmetrical, the temporal-nasal (T-N) stimulation being the sole stimulation efficient to evoke the reflex, the nasal-temporal (N-T) component being almost absent. Coil recordings showed that, in adult animals, prolonged monocular visual deprivation by unilateral eyelid suture provoked the appearance of the N-T component. The OKN became symmetrical, reacting for both directions of stimulation.

Directional asymmetry of the frog monocular optokinetic nystagmus: cholinergic modulation.

The frog monocular optokinetic gaze nystagmus (OKN) was studied by coil recordings after intravitreal administration of cholinergic drugs into the closed eye. Before injection, the frog displayed OKN for stimulations in the temporo-nasal (T-N) direction only. The injection of muscarinic agonists, as well as that of nicotinic antagonists, provoked the appearance of a naso-temporal (N-T) component, the slow phase velocity gain then being strongly and significantly increased.

Possible involvement of cholinergic and glycinergic amacrine cells in the inhibition exerted by the ON retinal channel on the OFF retinal channel.

In the frog retina, the inhibition exerted by the ON channel on the OFF channel was evidenced by the increase in transient ganglion cell OFF responses, when the ON channel was blocked by 2-amino-4-phosphonobutyrate (APB). Intraocular administration of the neurotoxic choline analog ethylcholine mustard arizidinium ion (ECMA) also provoked an increase in the number of spikes of transient ganglion cell OFF responses, without suppressing the ON responses. APB, when administrated after ECMA, abolished the ON responses, but did not modify the OFF responses already increased by ECMA.

The pretectal cholinergic system is involved through two opposite ways in frog monocular OKN asymmetry.

Frog monocular horizontal optokinetic nystagmus (OKN) has been studied by coil recordings, before and after unilateral microinjection of cholinergic drugs into the pretectum. The recorded eye was either contralateral or ipsilateral to the injected structure. Before injection, monocular OKN displayed a directional asymmetry, reacting only to stimulations in the temporonasal (T-N) direction.

[Interactions between GABAergic and cholinergic mechanisms involved in monocular optokinetic nystagmus in frogs].

The systemic administration of atropine, a muscarinic cholinergic antagonist, was found to suppress the Nasal-Temporal (N-T) component of the frog monocular optokinetic nystagmus (OKN), which had appeared following a prior injection of bicuculline and which does not exist in the normal animal. On the contrary, the administration of a nicotinic cholinergic antagonist (D-TC, alpha-BGT, Hexamethonium) following that of bicuculline has prolonged the duration of the induced N-T component. Thus, ACh was shown to attenuate or to reinforce the GABAergic inhibition of the N-T component through muscarinic receptors or nicotinic receptors respectively.

Effects on the chicken monocular OKN of unilateral microinjections of GABAA antagonist into the mesencephalic structures responsible for OKN.

The SR 95531, a GABAA antagonist was microinjected into either the pretectum nuclei, (nucleus Superficialis Synencephali nSS) or the nBOR (nucleus Ectomammillaris nEM) of chickens. Monocular optokinetic nystamus (OKN) of each eye was recorded by the search coil technique before and after unilateral intracerebral drug administration. Before injection, monocular horizontal OKN in chickens, as in other lower vertebrates, displays a directional asymmetry: the stimulation in the Temporo-Nasal (T-N) direction is more efficient in evoking OKN than is stimulation in the Naso-Temporal (N-T) direction.

Unilateral pretectal microinjections of SR 95,531, a GABA A antagonist: effects on directional asymmetry of frog monocular OKN.

Monocular eye movements have been studied in frogs using the search coil technique before and after unilateral microinjection of SR 95,531, a GABA A antagonist, into the pretectal nuclei contralateral to the open eye. Before injection, monocular, horizontal optokinetic nystagmus (OKN) in frogs, as in other lower vertebrates, displays a directional asymmetry: the stimulation in the T-N (temporo-nasal) direction is more efficient in evoking OKN than is stimulation in the N-T (naso-temporal) direction. The N-T component is almost absent and displays only slow phases of very low speed.

Abolition of monocular optokinetic nystagmus directional asymmetry after unilateral visual deprivation in adult vertebrates: involvement of the GABAergic mechanism.

In lower vertebrates such as frogs and chickens, monocular optokinetic nystagmus (OKN) displays directional asymmetry, temporal-nasal (T-N) stimulation being more efficient in evoking this visuomotor reflex than N-T stimulation. The N-T component of monocular OKN is significantly weaker in chickens, while it is almost absent in frogs. Coil recordings showed that in adult frogs and chickens, prolonged monocular visual deprivation by unilateral eyelid suture provoked the appearance of the N-T component in frogs as well as its significant and progressive increase in both species.

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.

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).

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.

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.

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.

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).

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.

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.

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.