Biomedical subjects

N Bonaventure

Publications and source records attributed to N Bonaventure.

At least 19 recordsLinked to original sources

PubMed1997

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. The same results were obtained when chronic microinjections of NMDA or LY 285 265 were achieved, the frogs being maintained in total darkness during the week of eyelid suture. These data indicate that the plasticity phenomenon evidenced in the monocular frog H-OKN depends on the activation of the NMDA receptors of one pretectum. This activation was obtained either by a monocular light stimulation of 8 days duration, or by unilateral administration of drugs activating the NMDA glutamatergic pretectal system. In this last case, the light stimulation was no longer necessary.

Animals↗

PubMed1995

Protective role of excitatory amino acid antagonists in experimental retinal ischemia.

BACKGROUND: Excitatory amino acids and their analogues (NMDA, kainate and AMPA) are implicated in the pathogenesis of ischemic brain injury. In order to fully understand their involvement in the pathogenesis of retinal ischemic injury, we studied the electrophysiological and histopathological effects of two excitatory amino acid antagonists, cis-PDA and MK 801, in an experimental retinal ischemia model. METHODS: The two antagonists were injected intravitreously 15 min before ischemia was induced by elevatory intraocular pressure caused by external compression. Electrophysiological and histopathological evaluation was made 48 h after 45 min transient ischemia. RESULTS: The excitatory amino acid antagonists cis-PDA and MK 801 can partially protect against retinal ischemic injury; whereas the mean post-ischemic b-wave amplitude corresponded to 41% of the pre-ischemic value in the control group, it was 64% (P = 0.003) and 59% (P = 0.005) following administration of cis-PDA and MK 801 respectively. Histopathological study corroborated these data, showing significant differences for morphometric parameters (P = 0.011 and P = 0.007 respectively). CONCLUSION: These preliminary results suggest the possibility of limiting excito-toxicity, one of the lesion-forming mechanisms in ischemic retinal injury.

Animals↗

PubMed1995

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. Conversely, administration of Piribedil, a strong D2 dopamine agonist, provokes the appearance of a N-T component, suppressing the monocular H-OKN asymmetry, whether the drug is injected by intravitreal or intrapretectal route. It is suggested that Piribedil could also bind with receptors other than dopamine's.

Animals↗

PubMed1995

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. Conversely, dopamine or haloperidol (a dopamine antagonist, acting mainly on D2 receptors) have no effect upon the monocular OKN unidirectionality. The monocular OKN N-T component still appears after administration of Piribedil even if this injection is preceded by administration of haloperidol which blocks the dopaminergic D2 receptors. Moreover administration of atropine (a cholinergic muscarinic antagonist) following that of Piribedil suppresses the N-T component; when injected before Piribedil, atropine prevents the appearance of the N-T component. These results suggest that in our experiments, Piribedil binds with muscarinic receptors.

Animals↗

PubMed1993

Some biochemical and pathophysiological aspects of long-term elevation of brain ornithine concentrations.

Mice and chicken were given 5-fluoromethylornithine (5FMOrn), a selective inactivator of ornithine aminotransferase (OAT) over extended periods of time. This treatment allowed us to maintain elevated concentrations of ornithine in all tissues. Since gyrate atrophy, an autosomal recessive human disease, is characterized by the absence of OAT, special emphasis was put on the study of the visual system. Ophthalmoscopic and histologic examinations of the eye as well as electroretinograms and locomotor behaviour demonstrated an unimpaired visual system and brain. No toxic effects were observable in the treated mice. Likewise, chick embryo development was normal in spite of highly elevated brain and tissue ornithine concentrations. A likely explanation for the absence of toxic effects of 5FMOrn treatment, disregarding the non-toxicity of ornithine, is the fact that 10-20% of tissue OAT is refractory to inactivation by 5FMOrn. This residual activity may be sufficient to maintain vital functions.

Animals↗

PubMed1992

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. The analysis of search coil recordings showed that the slow phase velocity gain of both T-N and N-T components became similar. Chronic administration of N-methyl-D-aspartate (NMDA) antagonists for the duration of deprivation prevented the appearance of a symmetrical monocular OKN in frogs: following repeated intraperitoneal injections of either MK 801, CGS 19755 or intrapretectal microinjections of 2-amino-5-phosphonovalerate (APV), the N-T component did not appear, and OKN remained asymmetrical. Thus NMDA receptors appear to be involved in the control of the plasticity process which allows monocular OKN of adult lower vertebrates to become symmetrical.

2-Amino-5-phosphonovalerate↗

PubMed1992

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. Microinjection of either gamma-aminobutyric acid (GABAA) agonist 4,5,6,7-tetrahydroisoxazolo (5,4-C) Pyridin-3-ol (THIP) or muscarinic cholinergic antagonist atropine into the nucleus lentiformis mesencephali, the pretectal mesencephalic structure involved in OKN, transiently abolished the presence of N-T component. This result suggests that the phenomenon of visual plasticity, occurring after a week of monocular deprivation, can be due, at least partially, to reduction in pretectal GABAergic inhibition, and to concomitant activation of cholinergic muscarinic receptors.

Animals↗

PubMed1992

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. Neurons located in the inner part of the inner nuclear layer were histologically altered by the toxin, and choline acetyltransferase activity was significantly depressed in ECMA-treated retinas. A double immunostaining experiment showed that amacrine cells containing glycine bear muscarinic binding sites. These results confirm the participation of cholinergic neurons in the inhibition exerted by the ON retinal channel on the OFF retinal channel, and suggest the involvement of a cholinergic/glycinergic loop of amacrine cells in this mechanism.

Acetylcholine↗

PubMed1992

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 microinjections of SR 95531 into either the nSS or nEM induce a reversible increase of gain in OKN directed by the contralateral eye for both directions of stimulation. However administration into the nSS increased directional asymmetry by increasing the T-N component slow phase velocity more strongly than the N-T component slow phase velocity. On the other hand, the unilateral administration of the drug into the nEM suppressed the directional OKN asymmetry by increasing the N-T component slow phase velocity more strongly than the T-N component slow phase velocity. These results indicate that the drug suppresses GABAergic inhibition at the mesencephalic level. Moreover the nSS seems especially involved in monocular OKN in response to a T-N stimulation, while the nEM seems more involved in the OKN response to N-T stimulation. The increase in gain of OKN directed by the ipsilateral eye to microinjected nuclei could account for the strong interactions existing between these mesencephalic structures responsible for horizontal OKN.

Animals↗

PubMed1992

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. The intrapretectal administration of a cholinergic muscarinic agonist (oxotremorine), as well as that of a nicotinic antagonist (D-tubocurarine), abolished the monocular OKN asymmetry, inducing the appearance of the naso-temporal (N-T) component; the difference between the slow phase velocity gain of both components was no longer significant. These data suggest that acetylcholine (ACh), at the level of the pretectum, acts in opposite ways through muscarinic and nicotinic binding sites; monocular OKN asymmetry could result, at least partially, from a facilitating nicotinic effect and an inhibitory muscarinic effect. Possible interactions with other transmitter systems are discussed.

Animals↗

PubMed1992

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. These results indicate the main involvement of the ON retinal channel in the OKN genesis and the inhibitory effect of the OFF channel upon this oculomotor reflex.

Aminobutyrates↗

PubMed1992

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. When injected into the closed eye, GABAergic drugs did not produce spontaneous nystagmus. THIP provoked a reduction of the N-T component, without modifying the T-N one, while GABA antagonists induced a significant increase in OKN performance, especially for the N-T direction of stimulation. In these conditions, picrotoxin also provoked an increase in the duration of both components of optokinetic after nystagmus, indicating a direct effect of the drug upon the velocity-storage system.

Animals↗

PubMed1992

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. The abolition of the OKN directional asymmetry indicates that acetylcholine seems to act in opposite ways through muscarinic and nicotinic binding sites. The GABAergic and cholinergic systems may interact to generate and modulate OKN in the frog.

Acetylcholine↗

PubMed1992

[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. These data point to the existence of strong interactions between these two neurotransmission systems involved in frog monocular OKN.

Animals↗

PubMed1991

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. Unilateral SR 95,531 microinjection into the pretectum reversibly decreased the directional asymmetry of monocular horizontal OKN, by strongly increasing the N-T component slow phase velocity while the T-N slow phase velocity remained unchanged. These data show that SR 95,531 injected into the pretectum contralateral to the open eye reversibly decreased the inhibition upon the N-T component of monocular horizontal OKN, which suggests that a pretectal GABAergic system is involved in the directional asymmetry of monocular horizontal OKN in frogs.

Animals↗

PubMed1990

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. The administration of THIP, a GABAA agonist, abolished reversibly the increase of the N-T component in both species. This fact suggests that the GABAergic system could be involved in determining this plasticity process observed in adult lower vertebrates.

Animals↗

PubMed1990

EOG and ERG modifications induced in the chicken eye after blockade of catecholamine and 5-hydroxytryptamine biosynthesis.

The involvement of catecholaminergic and indoleaminergic systems in the modulation of the standing potential of the eye was tested in chickens by means of an indirect electrooculography method and direct current electroretinogram recordings. D,L alpha-monofluoromethyl dopa (MFMD), 50 and 100 nmol), a highly specific inactivator of aromatic L-amino acid decarboxylase, was injected intravitreally. This treatment is known to induce a selective and irreversible blockade of dopamine and 5-hydroxytryptamine biosynthesis. Five hours after drug injection an important increase in the standing potential appeared. The light peak was delayed by about 5 min but its amplitude was unchanged. The return of the standing potential to basal value during maintained illumination was delayed by 5-10 min. The time course of the dark trough was not modified. The intensity-voltage functions were also studied for the various electroretinogram components, 5 hr after MFMD. The voltage of the b-wave was reduced (by 65% with the highest intensity), while the other components were little affected. Substantial reduction in dopamine and 5-hydroxytryptamine concentrations were found in treated retinas. These data, together with previous results, suggest that the standing potential of the chicken eye may be modulated by a balance between catecholamine and indoleamine systems.

Animals↗

PubMed1990

Electrooculographic and electroretinographic study in the chicken after dopamine and haloperidol.

The implication of dopamine in the modulation of the standing potential of the eye was tested in the chicken through an indirect electrooculographic method and direct current electroretinogram (ERG) recording after haloperidol, a mixed D1-D2 antagonist. The standing potential of the eye was reduced within 15 min after intravitreal injection of the antagonist (150 micrograms). This effect is rapidly reversed by an application of dopamine. The fast oscillation was preserved but the light peak was either strongly reduced or abolished. The dark trough showed an apparently normal time course. The intensity-voltage function was studied for the various ERG components. After haloperidol the b-wave and the c-wave were strongly reduced, whereas the a-wave was little affected. Together with previous data obtained with intraocular injections of dopamine, our data suggest the involvement of dopamine in the modulation of the standing potential. They also support the hypothesis that the light peak, which is generated by a photoreceptor-pigment epithelium interaction, is influenced by dopamine or by a related substance. The modulatory effect could also be due to a balance between several neurotransmitter systems.

Animals↗