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)

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

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.
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PMID:Plasticity of the frog monocular OKN: involvement of pretectal GABAergic and cholinergic systems. 158 60

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.
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PMID:Abolition of monocular optokinetic nystagmus directional asymmetry after unilateral visual deprivation in adult vertebrates: involvement of the GABAergic mechanism. 235 90

This paper describes the EEG profiles, observed in rabbits, of drugs which affect GABA synaptic activity at GBB complex. Drugs which enhance GABA synaptic activity induce sedation associated with EEG synchronization. However, muscimol, THIP, GHB and baclofen induce signs of CNS stimulation (light tremors of the forelimbs, chewing, light nystagmus and hyperpnea) associated with EEG spikes. Signs of light stimulation (chewing and jerks of the head) also occur after BDZs and barbiturates, and are associated with the presence of 12-24 and 20-25 Hz waves, respectively. Drugs which reduce GABA synaptic activity (bicuculline, inverse BDZ agonists, PTZ, picrotoxin and Ro 5-3663) induce three dose-dependent stages of EEG changes: trains of slow waves, trains of spike-and-wave complexes and paroxysmal activity in the rostral encephalic structures without apparent changes of the electrical activity in the spinal cord. The first two stages are associated with a behavioral state of alert and the third stage with tonico-clonic convulsions. Among the inverse BDZ agonists, DMCM and beta-CCM elicit all three stages, whereas FG 7142 and beta-CCE induce only the first two and CGS 8216 only the first. The BDZ antagonists Ro 15-1788 and Ro 15-3505 (0.2-30 mg/kg IV) do not significantly affect the EEG pattern. However, they selectively inhibit the effects of diazepam and of the inverse BDZ agonists. In both cases, the inhibition is observed with doses as low as 0.2 mg/kg IV and leads to an EEG desynchronization. The possible involvement of the modifications of GABA synaptic activity in the etiology of both petit mal and grand mal epilepsies is discussed.
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PMID:Electroencephalographic investigations in rabbits of drugs acting at GABA-benzodiazepine-barbiturate/picrotoxin receptors complex. 299 34