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

Tryptamine alkaloid toxicosis (Phalaris staggers) was diagnosed in feedlot sheep. Clinical signs of toxicosis, which were exacerbated by excitement, included gait abnormalities, muscular tremors, nystagmus, and convulsions. An estimated 8% of the most severely affected lambs had clinical signs of toxicosis. Gross lesions detected in the brain of affected lambs consisted of focal gray-green discoloration in the brain stem and thalamus; these areas had microscopic evidence of intraneuronal pigment accumulation. Brain specimens obtained at slaughter indicated that 60% of the lambs had lesions consistent with tryptamine alkaloid toxicosis. Tryptamine alkaloids were found in low concentrations in the feed. Lambs exposed to these feeds had higher death losses than those that were not exposed to the feeds. Cobalt concentration in the feed was higher than that previously reported to be associated with Phalaris staggers.
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PMID:Tryptamine alkaloid toxicosis in feedlot sheep. 279 45

The effects of various lesions in the accessory optic system and pretectal area were studied on the horizontal optokinetic head nystagmus (OKN) in the frog Rana esculenta. For histological control the cobalt-filling technique and haematoxylineosin staining were used. Isolated complete transection of the basal optic root caused only a slight reduction in the frequency of the OKN. Transection of the marginal optic tract on one side reduced the frequency as if one eye had been removed. Electrolytic destruction of the basal optic nucleus on one side did not influence the optokinetic responses significantly. In monocular animals, however, an obvious reduction occurred in the frequency of the OKN when the basal optic nucleus corresponding to the seeing eye had been destroyed. If the lesion involved the brain tissue surrounding the basal optic nucleus, nystagmus could not be evoked. Complete destruction of the lateral pretectal neuropil, which receives retinal afferents, strongly reduced the frequency or abolished the OKN. We conclude that the pretectal region is the most important structure at the input side in the initiation of this visuomotor response. The basal optic nucleus together with the neighbouring tegmental area may also play some role in the regulation of the OKN.
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PMID:Re-investigation of the role of the accessory optic system and pretectum in the horizontal optokinetic head nystagmus of the frog. Lesion experiments. 623 33

Bilateral disruption, or one-sided transection of the basal optic root with a partial injury of this tract of retinal fibres on the other side, abolished vertical, but spared horizontal optokinetic head-nystagmus. Horizontal nystagmus could not be evoked when the ventral part of the pretectum was injured and the basal optic root was transected on the same side. The lesions were checked by the cobalt-filling technique. It is concluded that the basal optic nucleus mediates stimuli which evoke vertical optokinetic head-nystagmus in frogs.
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PMID:Transection of the basal optic root in the frog abolishes vertical optokinetic head-nystagmus. 660 69

It is still not established whether or not glucocorticoids are effective in the treatment of vestibular disorders such as dizziness and imbalance, although these drugs in combination with several others are used to treat dizziness and imbalance in some diseases. This study was undertaken to investigate the effects of a glucocorticoid, dexamethasone, on vestibular disorder following unilateral labyrinthectomy in pigmented rabbits. Neuronal activities of the medial vestibular nucleus (MVN) in alpha-chloralose-anesthetized cats were also investigated. Systemic injection of dexamethasone decreased the frequency of nystagmus and head deviation dose-dependently following hemilabyrinthectomy, and the rate of decrease was faster than that obtained by saline. In contrast, RU38486 (a glucocorticoid receptor antagonist) delayed the reduction of nystagmus and head deviation. Micro-iontophoretic application of dexamethasone rapidly enhanced the spontaneous firing of MVN neurons in a dose-dependent manner. These increases were blocked by RU38486, but not by GDEE (a glutamate receptor antagonist) or Co2+ (a Ca2+ channel blocker). These results suggest that dexamethasone directly activates the MVN neurons, thereby accelerating vestibular compensation.
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PMID:Role of glucocorticoid in vestibular compensation in relation to activation of vestibular nucleus neurons. 761 Aug 57

The purpose of the present study was to find out what particular stimulus features, in addition to the direction and velocity of motion, specifically activate neurons in the nucleus lentiformis mesencephali (nLM) in pigeons. Visual responses of 60 nLM cells to a variety of computer-generated stimuli were extracellularly recorded and quantitatively analyzed. Ten recording sites were histologically verified to be localized within nLM with cobalt sulfide markings. It was shown that the pigeon nLM cells were specifically sensitive to the leading edge moving at the optimal velocity in the preferred direction through their excitatory receptive fields (ERFs). Generally speaking, nLM cells preferred black edges to white ones. However, this preference cannot be explained by OFF-responses to a light spot. The edge sharpness was also an essential factor influencing the responsive strength, with blurred edges producing little or no visual responses at all. These neurons vigorously responded to black edge orientated perpendicular to, and moved in, the preferred direction; the magnitude of visual responses was reduced with changing orientation. The spatial summation occurred in all neurons tested, characterized by the finding that neuronal firings increased as the leading edge was lengthened until saturation was reached. On the other hand, it appeared that nLM neurons could not detect any differences in the shape and area of stimuli with an identical edge. These data suggested that feature extraction characteristics of nLM neurons may be specialized for detecting optokinetic stimuli, but not for realizing pattern recognition. This seems to be at least one of the reasons why large-field gratings or random-dot patterns have been used to study visual responses of accessory optic neurons and optokinetic nystagmus, because many high-contrast edges in these stimuli can activate a neuron to periodically discharge, or groups of neurons to simultaneously fire to elicit optokinetic reflex.
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PMID:Stimulus features eliciting visual responses from neurons in the nucleus lentiformis mesencephali in pigeons. 983 72

The effects of nociceptin (orphanin FQ) on medial vestibular nucleus (MVN) neurons in vitro, and on vestibulo-ocular reflex (VOR) function in vivo, were investigated in order to determine the role of 'opioid-like orphan' (ORL1) receptors in modulating vestibular reflex function in the rat. Nociceptin (100 nM-1 microM) potently inhibited the spontaneous discharge of the majority (86%) of MVN neurons tested in the rat dorsal brainstem slice preparation in vitro. This inhibition was dose-dependent and persisted after blockade of synaptic transmission in low Ca2+/Co2+ medium. The inhibitory effects were insensitive to the opioid antagonist naloxone, but were effectively antagonised by the selective ORL1 receptor antagonist, [Phe1Psi(CH2-NH)Gly2]Nociceptin(1-13)NH2. The majority of MVN neurons ( approximately 70%) were inhibited by both nociceptin and the delta-opioid receptor agonist, [D-ala2, D-leu5]-enkephalin (DADLE), while a minority of cells (approximately 30%) were selectively responsive either to DADLE or to nociceptin, but not both. Co-application of nociceptin and DADLE to neurons that were responsive to both agonists, resulted in an inhibitory response that was the same as or less than the inhibition evoked by either agonist alone. Intracellular whole-cell patch clamp recordings from identified Type A and Type B MVN cells showed that both these cell types are responsive to nociceptin, which induced membrane hyperpolarisation and decrease in input resistance consistent with its known effects on membrane K currents in other cell types. In alert rats, i.c.v. injection of nociceptin caused a significant decrease in the gain of the hVOR and resulted in a prolongation of post-rotatory nystagmus in darkness. The decrease in VOR gain and the increase in the VOR time-constant was significant even at low doses of nociceptin which did not cause other observable behavioural effects. These findings demonstrate that endogenously released nociceptin may have a hitherto unexplored role in the functional modulation of the neural pathways that mediate vestibular reflexes in vivo.
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PMID:Modulation of vestibular function by nociceptin/orphanin FQ: an in vivo and in vitro study. 1032 Jul 26