Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0028738 (nystagmus)
 7,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The anticonvulsant potency and neurological toxicity of two new catalytic inhibitors of GABA-transaminase have been assessed in acute experiments in baboons with a natural syndrome of photic epilepsy. gamma-Acetylenic GABA, 160--200 mg/kg, or gamma-vinyl GABA, 450--950 mg/kg, intravenously, gave complete protection against generalised myoclonus or seizure responses induced by photic stimulation (in baboons without or with priming with subconvulsant doses of allylglycine). The protection became maximal 1--3 h after injection, and continued for 7--24 h. Signs characteristic of the acute toxicity of anticonvulsant drugs (nystagmus and ataxia) were not seen. The potential use of these compounds in human epilepsy deserves investigation.
 ...
PMID:Blockade of epileptic responses in the photosensitive baboon, Papio papio, by two irreversible inhibitors of GABA-transaminase, gamma-acetylenic GABA (4-amino-hex-5-ynoic acid) and gamma-vinyl GABA (4-amino-hex-5-enoic acid). 10 Aug 12

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.
 ...
PMID:Pharmacological study of the chicken's monocular optokinetic nystagmus: effects of GABAergic agonist and antagonists. 132 44

1. Electrical stimulation of the nucleus of the optic tract (NOT) induced nystagmus and after-nystagmus with ipsilateral slow phases. The velocity characteristics of the nystagmus were similar to those of the slow component of optokinetic nystagmus (OKN) and to optokinetic after-nystagmus (OKAN), both of which are produced by velocity storage in the vestibular system. When NOT was destroyed, these components disappeared. This indicates that velocity storage is activated from the visual system through NOT. 2. Velocity storage produces compensatory eye-in-head and head-on-body movements through the vestibular system. The association of NOT with velocity storage implies that NOT helps stabilize gaze in space during both passive motion and active locomotion in light with an angular component. It has been suggested that "vestibular-only" neurons in the vestibular nuclei play an important role in generation of velocity storage. Similarities between the rise and fall times of eye velocity during OKN and OKAN to firing rates of vestibular-only neurons suggest that these cells may receive their visual input through NOT. 3. One NOT was injected with muscimol, a GABAA agonist. Ipsilateral OKN and OKAN were lost, suggesting that GABA, which is an inhibitory transmitter in NOT, acts on projection pathways to the brain stem. A striking finding was that visual suppression and habituation of contralateral slow phases of vestibular nystagmus were also abolished after muscimol injection. The latter implies that NOT plays an important role in producing visual suppression of the VOR and habituating its time constant. 4. Habituation is lost after nodulus and uvula lesions and visual suppression after lesions of the flocculus and paraflocculus. We postulate that the disappearance of vestibular habituation and of visual suppression of vestibular responses after muscimol injections was due to dysfacilitation of the prominent NOT-inferior olive pathway, inactivating climbing fibers from the dorsal cap to nodulouvular and flocculoparafloccular Purkinje cells. The prompt loss of habituation when NOT was inactivated, and its return when the GABAergic inhibition dissipated, suggests that although VOR habituation can be relatively permanent, it must be maintained continuously by activity of the vestibulocerebellum.
 ...
PMID:The nucleus of the optic tract. Its function in gaze stabilization and control of visual-vestibular interaction. 159 49

The GABAergic drug baclofen and the cholinergic drug physostigmine were administered to patients with upbeat and downbeat nystagmus. Baclofen (orally, 5 mg three times daily) reduced nystagmus slow phase velocity and distressing oscillopsia by 25-75% in four out of five patients (two upbeat nystagmus; two downbeat nystagmus). Physostigmine (1 mg single intravenous injection) increased nystagmus in five additional patients with downbeat (1) or positional downbeat nystagmus (4) for a duration of 15-20 minutes. The different interactions of baclofen and physostigmine on neurotransmission subserving vertical vestibulo-ocular reflex could account for these effects. The response to baclofen appears to be a GABA-B-ergic effect with augmentation of the physiological inhibitory influence of the vestibulo-cerebellum on the vestibular nuclei. Similarly baclofen has an inhibitory effect on the velocity storage mechanism. Cholinergic action may cause the increment of nystagmus by physostigmine.
 ...
PMID:The effects of baclofen and cholinergic drugs on upbeat and downbeat nystagmus. 165 96

1.) Eye movements were recorded in four Java monkeys (M. fascicularis) after unilateral microinjections (1 microliter, concentration 1 micrograms/microliter) of the GABA antagonist, bicuculline, and the GABA agonist, muscimol, into oculomotor related regions of the vestibular nuclei. Eye movements were investigated in the dark and light during spontaneous eye movements, vestibular stimulation (sinusoidal: 0.2 Hz, +/- 40 deg/s, and velocity trapezoid: 40 deg/s2 acceleration, 120 deg/s constant velocity), and visual-vestibular conflict stimulation. 2.) Bicuculline and muscimol injections consistently led to specific eye movement changes, which were maximal 5-10 min after bicuculline injection (muscimol 10-30 min), and lasted 90-120 min (muscimol 2-4 h). Control injections with NaCl (0.9%) into the responsive area and with bicuculline 2-3 mm more lateral showed no effect. 3.) Bicuculline induced a spontaneous nystagmus of 40.9 deg/s (average, range 10.5-93 deg/s), beating in 60% of the cases to the contralateral and in 40% to the ipsilateral side. The analysis of the slope of the slow phase gave no evidence for an additional gaze holding deficit. The VOR gain in the dark showed a slight decrease (pre: 0.96; post: 0.86) on average. The time constant of decay for slow phase nystagmus velocity after vestibular ramp stimulation was reduced, reflecting a 'velocity storage' deficit. After bicuculline injections nystagmus suppression in the light and during visual-vestibular conflict stimulation was generally well preserved. 4.) After muscimol injections horizontal gaze holding was severely affected. Each saccade was followed by an exponentially decreasing postsaccadic drift with a time constant as short as 250 ms (average 414 ms). The eyes always drifted towards a null-position, which generally did not coincide with the midposition of the eye. The null-position could move up to 35 deg to the contralateral or ipsilateral side. The highly distorted eye movements after muscimol injections prevented VOR-measurements based on eye velocity. Instead vestibular stimulation led to a shift of the null-position with an amplitude corresponding to a gain (eye position/stimulus position) of 0.17 (average) at 0.2 Hz (+/- 40 deg/s). Vertical eye movements did not show a major gaze holding deficit. 5.) From the experiments it can be concluded that the inhibitory transmitter GABA plays an important role for eye movement generation within the vestibular nuclei. Bicuculline induces mainly a vestibular imbalance with little evidence for a neural integrator deficit. In contrast unilateral muscimol injections lead to a complete, reversible loss of function for the common horizontal neural integrator, which converts eye velocity into eye position signals. The accompanying shift of the null-position reflects an additional vestibular imbalance.
 ...
PMID:Differential effects of bicuculline and muscimol microinjections into the vestibular nuclei on simian eye movements. 175 10

Behavioral and electrophysiological measures were used to elucidate the retinal modulation of oculomotor control in the turtle. Eye movements were recorded following intravitreal applications of 2-amino-4-phosphonobutyrate (APB) and the GABA antagonists picrotoxin and bicuculline. Visual responses of single basal optic nucleus (BON) neurons of the accessory optic system were studied in parallel experiments. The effectiveness of APB, a glutamate analog thought to act selectively on the retinal ON pathway, was assessed independently by recording electroretinograms or ganglion cell activity. Injections of APB into the turtle's eye reduced or blocked the injected eye's ability to drive horizontal optokinetic nystagmus, as also observed in rabbit and cat (Knapp et al., 1988; Yucel et al., 1989). Single-unit recordings from the BON during APB superfusion (50-200 microM APB) of the contralateral retina demonstrated that these cells, which are direction-sensitive and respond to the offset of light flashes, have their responses to moving stimuli blocked by APB. During the APB effect, GABA antagonists were applied to the same eye. Although moderate doses of APB were sufficient to block optokinetic or BON light responses, the addition of GABA blockers still elicited a spontaneous temporal-to-nasal nystagmus (Ariel, 1989) or visually responsive yet direction-insensitive responses from BON cells (Schuerger et al., 1990). These results are discussed in terms of the retinal output to pathways involved in oculomotor control of optokinetic nystagmus.
 ...
PMID:Effects of synaptic drugs on turtle optokinetic nystagmus and the spike responses of the basal optic nucleus. 176 13

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.
 ...
PMID:Unilateral pretectal microinjections of SR 95,531, a GABA A antagonist: effects on directional asymmetry of frog monocular OKN. 202 95

Large numbers of neurons were retrogradely labeled in both the dorsal and ventral medial terminal nucleus (MTN) after fluoro-gold injections into the rat pretectal nucleus of the optic tract/dorsal terminal nucleus (NOT/DTN). Fluorescence immunocytochemistry for GABA in the same brains revealed GABA-positive neurons distributed mainly in the dorsal MTN. Approximately half of all the GABAergic neurons in the MTN were double-labeled. Therefore, GABAergic neurons comprise a significant component of the MTN-NOT/DTN projection which most likely inhibits the pretectal pathway mediating horizontal optokinetic nystagmus.
 ...
PMID:The projection of GABA-ergic neurons of the medial terminal accessory optic nucleus to the pretectum in the rat. 213 69

Toluene, an aromatic solvent, prolongs the duration of nystagmus induced by a rotatory acceleration or by an optokinetic stimulation in the pigmented rat. Baclofen, an agonist of GABAB receptors, and 4,5,6,7-tetrahydroisoxazolo[5,4-c]-pyridin-3-ol (THIP), an agonist of GABAA receptors are able to block this toluene effect on the vestibular system. On the contrary diazepam, which by itself causes an evident reduction of the duration of acceleratory nystagmus, is not able to block the toluene effect. The results indicate that the toluene effect is related to GABA transmission and that the solvent interacts by a rather receptor specific mechanism of action.
 ...
PMID:The effect of toluene on the vestibulo- and opto-oculomotor system in rats, pretreated with GABAergic drugs. 216 15

The present experiment was designed to determine which neurotransmitter influences the burst pattern in the firing of the inhibitory burst neurons (IBN) during vestibular nystagmus. Cats were anesthetized with ether and mounted in a stereotaxic apparatus on a turntable, implanted stimulation electrodes, removed occipital bone and aspirated the vermal part of cerebellum. After the operation ether was discontinued. The recordings took place with the cats in an alert condition created by upper cervical cord transsection, artificial respiration and local anesthesia by infiltrating 0.5% lidocaine into the semilunar ganglions every two hours. We also employed iontophoretic application of the various drugs: GABA, muscimol, glycine, serotonin (5-HT) and bicuculline through seven-barrelled glass micropipettes. GABA or muscimol did not influence nystagmus rhythm, but both chemicals caused strong suppression of burst activities in IBN. Since this inhibitory effect of GABA was suppressed by the simultaneous application of bicuculline, IBNs appear to be controlled by GABAA receptor. Glycine and 5-HT did not change the firing pattern of IBN. Application of bicuculline itself caused an increase of tonic discharges of IBN. These findings suggest that IBN receive inhibitory impulses from the higher GABAergic neurons.
 ...
PMID:Neurotransmitter effects on inhibitory burst neurons in the cat. 257 38


1 2 3 4 5 Next >>