Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0278126 (loss of equilibrium)
 140 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A postural control system in the lamprey is driven by vestibular input and maintains a definite orientation of the animal during swimming. After a unilateral labyrinthectomy (UL), the lamprey continuously rolls toward the damaged side. Important elements of the postural network are the reticulospinal (RS) neurons that are driven by vestibular input and transmit commands for postural corrections to the spinal cord. We characterized the effect of UL on vestibular responses in RS neurons elicited by rotation of the animal in the pitch plane. The activity of RS neurons was recorded from their axons in the spinal cord before and after UL. The neurons can be classified into the Up and Down groups activated preferentially with nose-up or nose-down rotation, respectively. After UL, vestibular responses in the group Up changed only slightly on the damaged side and disappeared almost completely on the opposite side. In the group Down, responses on both sides persisted after UL. These results indicate that the left and right subgroups of the group Up neurons receive excitatory input mainly from the contralateral labyrinth. In contrast, the group Down neurons receive excitatory input from both labyrinths. We conclude that the UL-induced changes in vestibular responses to pitch tilt will disturb the normal activity of the postural control system. The UL-induced asymmetry in the bilateral activity of the group Up neurons seems to be an important factor contributing to the loss of equilibrium in UL animals and to their rotation during swimming.
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PMID:Asymmetry in the pitch control system of the lamprey caused by a unilateral labyrinthectomy. 1274 Mar 99

We investigated the temperature dependence of some physiological parameters of common eelpout (Zoarces viviparus) from different locations (North Sea, Baltic Sea and Norwegian Sea) on acclimation temperature (3 degrees C and 12 degrees C) and acute temperature variation. The lethal limit of 12 degrees C-acclimated eelpout was determined as the critical thermal maximum [loss of equilibrium (LE) and onset of muscular spasms (OS)] and it was found to be 26.6 degrees C for LE and 28.8 degrees C for OS for all populations. However, these parameters do not have any relevant ecological interpretation. We therefore investigated the effect of gradually increased water temperature on standard metabolic rate (measured as resting oxygen consumption Mo2) and critical oxygen concentration ([O2]c) of eelpouts. Acclimation to low temperature (3 degrees C) resulted in partial compensation of Mo2, paralleled by a decrease of activation energy for Mo2 (from 82 kJ mol(-1) at 12 degrees C to about 50 kJ mol(-1) at 3 degrees C) in North Sea and Baltic Sea eelpouts. At the same time, Norwegian eelpout showed no acclimation of oxygen demand to warm temperature (12 degrees C) at all. The scope for eelpout aerobic metabolism shrank considerably with increased acclimation temperature, as [O2]c approached water oxygen concentrations. At 22.5+/-1 degrees C the [O2]c reached air saturation, which is equivalent to the upper critical temperature (TcII) and at this temperature the aerobic scope for the metabolism completely disappeared. In line with previous insight, the comparative analysis of the temperature dependence of Mo2 of Z. viviparus from different populations suggests that a pejus (sub-critical) temperature for this species is about 13-15 degrees C. In conclusion, the capacity to adjust aerobic metabolism relates to thermal tolerance and the bio-geographical distribution of the species. Global warming would thus be likely to cause a shift in the distribution of this species to the North.
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PMID:Thermal physiology of the common eelpout (Zoarces viviparus). 1277 71

The effect of naringenin on the survival and morphogenesis of amphibian embryos was evaluated by means of the AMPHITOX test reporting early life stage and chronic toxicity effects. Lethality, malformation incidence and the degree of adverse effects were concentration-dependent. The Teratogenic Index (TI) for naringenin was 2 pointing out the high developmental hazard of this substance. For instance, 10 mg/l naringenin exerted 100% malformations while only 30% of the abnormal embryos died. Main abnormalities were reduced body size, axial curves, microcephaly, abdominal edema, underdeveloped gills and delayed development. Scanning electronic microscopy (SEM) showed alterations in epithelial cell shapes related to malformations. The results obtained by means of treatment of Bufo arenarum embryos with naringenin from complete operculum stage onwards show that at this final stage of development, the susceptibility of the embryos to this flavonoid is slightly lower for lethal effects but exerted sublethal adverse effects such as transient narcosis, abnormal contortions, loss of equilibrium, reduced motility and edema. Overall, amphibian early life stages appeared more susceptible to the embryotoxicity associated with exposure to naringenin, especially at concentrations greater than 5 mg/l. This increased susceptibility may result from the relatively high rates of cellular differentiation and morphogenesis that occur at this early stage of development.
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PMID:Lethal and teratogenic effects of naringenin evaluated by means of an amphibian embryo toxicity test (AMPHITOX). 1466 74

The stage dependent susceptibility to lead in amphibian development was studied by exposing Bufo arenarum embryos during neurulae, neuromuscular activity and gill circulation stages for twenty hours to 1 ppm Pb(2+). Survival, malformations and behavioral disorders were evaluated. The embryonic susceptibility to lead was markedly stage dependent. The survival at the neuromuscular activity stage was approximately half that of the other two periods; concerning malformations, the gill circulation stage was the least sensitive. The observed malformations consisted of failed closure of neural tube, hydropsy, small and cylindrical tails, reduced body size and incurvations in the body axis. Some alterations occurred in all experimental groups and therefore were considered non-dependent on the period of treatment. In all experimental embryos, neurological disorders such as trembles and loss of equilibrium were observed.
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PMID:Stage dependent susceptibility to lead in Bufo arenarum embryos. 1509 19

Removal of a vestibular organ (unilateral labyrinthectomy, UL) in the lamprey results in a loss of equilibrium, so that the animal rolls (rotates around its longitudinal axis) when swimming. Owing to vestibular compensation, UL animals gradually restore postural equilibrium and, in a few weeks, swim without rolling. Important elements of the postural network in the lamprey are the reticulospinal (RS) neurons, which are driven by vestibular input and transmit commands for postural corrections to the spinal cord. As shown previously, a loss of equilibrium after UL is associated with disappearance of vestibular responses in the contralateral group of RS neurons. Are these responses restored in animals after compensation? To answer this question, we recorded vestibular responses in RS neurons (elicited by rotation of the compensated animal in the roll plane) by means of chronically implanted electrodes. We found that the responses re-appeared in the compensated animals. This result supports the hypothesis that the loss of equilibrium after UL was caused by asymmetry in supraspinal motor commands, and the recovery of postural control in compensated animals was due to a restoration of symmetry.
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PMID:Vestibular compensation in lampreys: restoration of symmetry in reticulospinal commands. 1557 55

The cerebral cortical areas processing saccular information were investigated in human subjects using the fMRI method and loud clicks, which selectively activate the saccule. The results were compared with previous vestibular evoked potential (VEP) studies in anesthetized patients following vestibular nerve stimulation. Nine normal subjects participated in fMRI studies. By comparing the cortical areas activated by a click at 85 dB (auditory activation) with those activated by 102 dB (auditory plus saccular activation), the following cortical areas were selectively activated by saccular stimulation: intraparietal sulcus, frontal eye fields, prefrontal cortex, and postcentral gyrus, in addition to insula, supplementary motor area, and anterior and posterior cingulate cortex. Previous VEP studies also revealed similar activation areas by vestibular nerve stimulation with latencies at 6 ms, suggesting that the shortest pathways for activation of cerebral cortical neurons from the labyrinth are trisynaptic, with a relay in the thalamus. The activated areas are also consistent with results in previous studies using caloric stimulation, which primarily activates horizontal semicircular canals. These results suggest that canal and otolith information is processed largely by similar cortical areas in humans. Multiple cortical areas activated by these studies suggest that these areas are involved in different aspects of processing vestibular information. The saccular projections to the prefrontal and frontal cortex suggest that these areas are involved in planning motor synergies to counteract loss of equilibrium.
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PMID:Saccular projections in the human cerebral cortex. 1582 67

Static bioassays were made to determine acute toxicity of chlorpyrifos-methyl, a wide spectrum organophosphorus insecticide and potential toxic pollutant of aquatic ecosystem, Guppy fish (Poecilia reticulata). Bioassays were made at a regulated temperature of 22+/-1 degrees C and were repeated three times. Lethal doses of the insecticides were determined using LC50 software programme of U.S. EPA based on Finney's Probit Analysis statistical method. The 96 h LC50 value and 95% confidence limit of chlorpyrifos-methyl for Guppy was estimated as 1.79 (1.47-2.10) mg/l. The fish exposed to chlorpyrifos-methyl exhibited behavioral changes in the form of neurotoxin toxicity: less general activity than control group, loss of equilibrium, erratic swimming and staying motionless at a certain location generally at mid-water level for prolonged periods. The 1 mg/l (lowest) concentration had similar behavior (NOEC) with the control group.
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PMID:Investigation of acute toxicity of chlorpyrifos-methyl on guppy Poecilia reticulata. 1591 Sep 7

Petroleum products are known to have greater toxicity to the translucent embryos and larvae of aquatic organisms in the presence of ultraviolet radiation (UV) compared to toxicity determined in tests performed under standard laboratory lighting with minimal UV. This study assessed the acute phototoxicity of the water accommodated fractions of weathered Alaska North Slope crude oil (ANS) to juvenile pink salmon, which are a heavily pigmented life stage. Fish in the highest ANS treatments exhibited melanosis, less mobility, reduced startle response, erratic swimming, and loss of equilibrium. Gills from fish exposed to ANS had elevated levels of hydroperoxides in oil-only, UV-only, and oil+UV treatments compared to control fish, which was indicative of increased lipid peroxidation in gill tissue. Under the test conditions of moderate salinity, low UV and high short-term oil exposure there were no indications of photoenhanced toxicity as assessed by elevation of mortality, behavioral impairment, or gill lipid peroxidation in oil+UV treatments. The results of this study suggest that pink salmon may be at less risk from photoenhanced toxicity compared to the translucent early-life stages of several other Alaska species.
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PMID:Assessment of the phototoxicity of weathered Alaska North Slope crude oil to juvenile pink salmon. 1591 Sep 9

The toxicity of insecticide cypermethrin to the freshwater fish, Cirrhinus mrigala was studied using static bioassay method. The 96 h LC50 was found to be 5.13 microg/l. Increase in opercular movement, loss of equilibrium, increase in surface behaviour, change in body colour, increase secretion of mucus, irregular swimming activity, rapid jerk movement, 'S' jerky, partial jerk, and aggressiveness were observed in fish exposed to lethal concentration of cypermethrin. But in sub lethal concentration changes were observed from that of lethal and with the approach of 14 and 21 day, fish attained to normalcy.
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PMID:Behavioural changes in freshwater fish, Cirrhinus mrigala (Hamilton) exposed to cypermethrin. 1611 75

Some 2000 species of cyanobacteria (blue-green algae) occur globally in aquatic habitats. They are able to survive under a wide range of environmental conditions and some produce potent toxins. Toxin production is correlated with periods of rapid growth (blooms) and 25%-70% of blooms may be toxic. Anatoxin-a is an alkaloid neurotoxin that acts as a potent neuro-muscular blocking agent at the nicotinic receptor. Acute toxicity, following consumption of contaminated water, is characterized by rapid onset of paralysis, tremors, convulsions and death. Human exposures may occur from recreational water activities and dietary supplements, but are primarily through drinking water. The current studies were conducted to examine the effect of in utero exposure on postnatal viability, growth and neurodevelopment, to evaluate the potential of in vitro embryotoxicity, and to explore the synergistic relationship between anatoxin-a and the algal toxin microcystin-LR by the oral route. The results of preliminary studies on amphibian toxicity are also reported. Time-pregnant mice received 125 or 200 microg kg(-1) anatoxin-a by intraperitoneal injection on gestation days (GD) 8-12 or 13-17. Pup viability and weight were monitored over a 6-day period. Maternal toxicity (decreased motor activity) was observed at 200 microg kg(-1) in both treatment periods. There were no significant treatment-related effects on pup viability or weight on postnatal day (PND) 1 or 6. The GD 13-17 pups were evaluated on PND 6, 12 and 20 for standard markers of neurodevelopmental maturation (righting reflex, negative geotaxis and hanging grip time). No significant postnatal neurotoxicity was observed. In vitro developmental toxicity was evaluated in GD 8 mouse embryos exposed to 0.1-25 microm anatoxin-a for 26-28 h. Perturbations in mouse yolk sac vasculature were noted from the 1.0 microm concentration in the absence of significant embryonic dysmorphology. Potential algal toxin synergism was tested in mice receiving either 0, 500 or 1,000 microg kg(-1) microcystin-LR by gavage and approximately 50 min later receiving either 0, 500, 1,000 or 2,500 microg kg(-1) anatoxin-a by the same route. No deaths occurred at any dose and no definitive signs of intoxication were observed. Stages 17 and 25 toad embryos (Bufo arenarum) were exposed to 0.03-30.0 mg l(-1) of anatoxin-a for 10 days. Adverse effects included a dose-dependent transient narcosis, edema and loss of equilibrium. Most notable was the occurrence of 100% mortality at the high dose in both groups 6-13 days post-exposure. The observed delay between initial exposure and death is highly unusual for anatoxin-a.
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PMID:Potential developmental toxicity of anatoxin-a, a cyanobacterial toxin. 1612 66


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