Abnormal Swimming Behavior Research Articles

Acute, sublethal exposure to a pyrethroid insecticide alters behavior, growth, and predation risk in larvae of the fathead minnow (Pimephales promelas)

The present study determined the effects of environmentally relevant, short-term (4-h) exposure to the pyrethroid insecticide esfenvalerate on mortality, food consumption, growth, swimming ability, and predation risk in larvae of the fathead minnow (Pimephales promelas). Acute effect concentrations were determined, and in subsequent experiments, fish were exposed to the following measured sublethal concentrations: 0.072, 0.455, and 1.142 microg/L of esfenvalerate. To measure growth rates (% dry wt/d), 8-d-old fathead minnows were exposed to esfenvalerate for 4 h, then transferred to control water and held for 7 d. Food consumption and abnormal swimming behavior were recorded daily. Additional behavioral experiments were conducted to evaluate how esfenvalerate affects the optomotor response of the fish. To quantify predation risk, esfenvalerate-exposed fathead minnow larvae were transferred to 9.5-L aquaria, each containing one juvenile threespine stickleback (Gasterosteus aculeatus). Sticklebacks were allowed to feed for 45 min, after which the number of surviving minnows was recorded. No mortality occurred during 4-h exposures to esfenvalerate, even at nominal concentrations of greater than 20 microg/L. Delayed mortality (50%) was observed at 2 microg/L after an additional 20 h in clean water. Fish exposed to 0.455 and 1.142 microg/L of esfenvalerate exhibited impaired swimming and feeding ability as well as reduced growth compared to fish exposed to 0.072 microg/L and controls. Predation risk also was significantly increased for larvae exposed to 0.455 and 1.142 microg/L of esfenvalerate. These results demonstrate that larval fish experiencing acute exposures to sublethal concentrations of this insecticide exhibit significant behavioral impairment, leading to reduced growth and increased susceptibility to predation, with potentially severe consequences for their ecological fitness.

Proliferative Branchitis Associated with Pathognomonic, Atypical Gill Epithelial Cells in Cultured Ayu Plecoglossus altivelis

In 1998 and 1999, severe episodes of mortality, often reaching 90%, were recorded among cultured populations of ayu Plecoglossus altivelis reared in Japan. The diseased fish showed appetite reduction and abnormal swimming behavior. Histopathological examination revealed proliferative branchitis with enlarged and atypical epithelial cells. Abundant electron-dense, virus-like particles were observed within the cells under transmission electron microscopy. The particles had a cocoon-like shape and ranged in length from 200 to 300 nm, indicating a member of the poxvirus group. These findings suggest the possibility that the mortality events are related to infection of a poxvirus-like virus.

Nodavirus in farmed Atlantic cod Gadus morhua in Norway

Viral encephalopathy and retinopathy (VER) was diagnosed in 5 to 24 g sized farmed Atlantic cod Gadus morhua kept in sea cages at Parisvatn, Hordaland county, on the west coast of Norway. Moderate mortality (10 to 15%) was observed, along with anorexia and abnormal swimming behaviour, such as looping or spiral swimming and reduced coordination. Nodavirus was detected by 2 different real-time RT-PCR assays, and this was later confirmed by immunohistochemistry. This is the first report of an outbreak of VER in farmed cod in Norway, and the first report that VER affect cod exceeding 5 g in size.

A Piscirickettsiosis‐like Syndrome in Cultured Nile Tilapia in Latin America with Francisella spp. as the Pathogenic Agent

In 2004, cultured Nile tilapia Oreochromis niloticus in several Latin America farms began to succumb to a disease similar to the piscirickettsiosis-like syndrome previously reported in tilapia in Taiwan and the United States. Mortality increased during 2005; reductions in tilapia biomass ranged from 5% to 80% in individual ponds and averaged 50% overall. All ages of fish have been involved. Clinical signs include lethargy, loss of appetite, petechia, exophthalmia, and abnormal swimming behavior. Gross lesions have included splenomegaly, renomegaly, and numerous white nodules observed in the spleen, kidney, testes, heart, ovaries, and occasionally the liver. A previously unreported black granulomatous lesion was reported in up to 30% of the fillets. Histologically, granulomatous infiltrates were observed in the kidney, spleen, liver, testes, ovary, and choroid gland, and rarely in the brain and heart. A small pleomorphic bacterium was observed in Giemsa-stained blood smears and spleen imprints. The bacterium did not grow on standard microbiological media and has not been isolated in cell culture. We obtained a near-complete 16S ribosomal DNA sequence with high similarity to Francisella spp. sequences previously identified in tilapias Oreochromis spp. (Taiwan), Atlantic cod Gadus morhua (Norway), and three-line grunts Parapristipoma trilineatum (Japan).

Outbreaks of phaeohyphomycosis in the chinook salmon (Oncorhynchus tshawytscha) caused by Phoma herbarum

Phoma herbarum has been associated with two outbreaks of systemic mycosis in hatchery-reared chinook salmon (Oncorhynchus tshawytscha) fingerlings. Affected fish exhibited abnormal swimming behavior, exophthalmia, multiple rounded areas of muscle softening, protruded hemorrhagic vents, and abdominal swelling. In all affected fish, swimbladders were filled with whitish creamy viscous fungal mass, surrounded by dark red areas in swimbladder walls, kidneys, and musculature. Clinical and histopathological examinations suggest that the infection may have started primarily in the swimbladder and then spread to the kidneys, gastrointestinal tract, and surrounding musculature. Consistent microscopical findings included broad septate branched fungal hyaline hyphae, 5-12 microm in diameter within the swimbladder, stomach, and often within and adjacent to blood vessels. Profuse growths of woolly brown fungal colonies were obtained from swimbladders and kidneys on Sabouraud medium. On corn meal agar the formation of pycnidia, characteristic of Phoma spp., was detected within 10 days of incubation. Morphological and molecular analyses identified this fungus as Phoma herbarum. This report underscores systemic fungal infections as a threat to raceway-raised salmon.

Sublethal effects of lead on northern leopard frog (Rana pipiens) tadpoles

Northern leopard frogs (Rana pipiens) were exposed to environmentally relevant concentrations of lead in water (3, 10, and 100 microg/L as lead nitrate) from the embryonic stage to metamorphosis. Survival, growth, deformity, swimming ability, metamorphosis, and lead tissue concentrations were evaluated. Tadpole growth was significantly slower in the early stages (Gosner stages 25-30) in 100 microg/L treatment. More than 90% of tadpoles in the 100 microg/L treatment developed lateral spinal curvature, whereas almost all the tadpoles in the other groups were morphologically normal. Spinal deformity was associated with abnormal swimming behavior. Maximum swimming speed of tadpoles in the 100 microg/L treatment was significantly lower than that in the other groups. No significant effect of lead exposure was found on percentage metamorphosis, snout-vent length, mortality, and sex ratio of metamorphs. Time to metamorphosis was delayed in 100 microg/L treatment. Lead tissue concentrations in the tadpoles ranged from 0.1 to 224.5 mg/kg dry mass, were positively related to lead concentrations in the water, and fell within the range of tissue concentrations of wild tadpoles found in previous studies. According to our results, the current U.S. Environmental Protection Agency freshwater-quality chronic criterion for lead (2.5 microg/L) is appropriate to protect northern leopard frog larvae.

Pathological and epidemiological observations on rickettsiosis in cultured sea bass (Dicentrarchus labrax L.) from Greece

Summary A systemic infection of a Rickettsia-like organism (RLO) in cultured sea bass is described for the first time. In hatcheries, clinical signs were lethargy, inappetence and discoloration. Twenty days after transfer to sea cages from hatcheries where the disease existed, fish showed erratic and abnormal swimming behaviour, loss of orientation, and lethargy. Cumulative mortality in colder months of the year reached 30% in hatcheries and 80% in cages. Surviving fish in cages did not show any clinical signs of RLO infection in the subsequent year. Evidence for a systemic distribution of RLO was supported by histolopathological lesions in both infected hatchery and caged fish, where the lesion profile included cranial sensory, central nervous, integumental and alimentary organ systems. Intracranial lesions were primarily characterized by an ascending histiocytic perineuritis and necrotizing congestive meningoencephalitis, with evidence for transfer of infective agents across the blood–brain barrier confirmed by the presence of RLOs within capillary endothelium and histiocytes in inflamed regions of the optic tectum and the cerebellum. In the most severe cases, infection spread to the statoacoustical (semicircular) canal system and the ependymal lining of ventricles, with marked rickettsial-laden histiocytic infiltration of the canal lumen. Integumental lesions were restricted to the oral submucosa, nares and integumental dermis of the cranium. Alimentary lesions were noted in both the liver parenchyma and mucosa/submucosa of the stomach. In all affected organs the RLOs were found by immunohistochemistry to be related to Piscirickettsia salmonis.

Characterization of a new allele of Ames waltzer generated by ENU mutagenesis

Mutation in the protocadherin 15 (Pcdh15) gene causes hair cell dysfunction and is associated with abnormal stereocilia development. We have characterized the first allele (Pcdh15av-nmf19) of Ames waltzer (av) obtained by N-ethyl-N-nitrosourea (ENU) mutagenesis. Pcdh15av-nmf19 was generated in the Neuroscience Mutagenesis Facility (NMF) at The Jackson Lab (Bar Habor, USA). Pcdh15av-nmf19 mutants display circling and abnormal swimming behavior along with lack of auditory-evoked brainstem response at the highest intensities tested. Mutation analysis shows base substitution (A→G) in the consensus splice donor sequence linked to exon 14 resulting in the skipping of exon 14 and the splicing of exon 13–15. This results in the introduction of a stop codon in the coding sequence of exon 15 due to shift in the reading frame. The effect of nmf19 mutation is expected to be severe since the expressed Pcdh15 protein is predicted to truncate in the 5th cadherin domain. Abnormalities of cochlear hair cell stereocilia are apparent in Pcdh15av-nmf19 mutants near the time of birth and by about P15 (15 days after birth) there is evidence of sensory cell degeneration. Disorganization of outer hair cell stereocilia is observed as early as P2. Inner hair cell stereocilia are also affected, but less severely than those of the outer hair cells. These results are consistent with characteristics of the mutation in the Pcdh15av-nmf19 allele and they support our previous finding that Protocadherin 15 plays an important role in hair-bundle morphogenesis.

TBTCl이 구피(Poecilia reticulata)의 행동과 번식에 미치는 영향

TBTCl(0.1, 0.32, 1, 3.2, 10, 25, 32, 50, 75 및 100 <TEX>$\mug/l$</TEX>)을 구피에게 144시간 동안 노출시켜 TBTCl의 구피 생체 내 축적정도 및 구피의 번식과 행동에 미치는 영향에 대해서 조사하였다. 0.1 <TEX>$\mug/l$</TEX> 이상의 모든 TBTCl 실험군에서 <TEX>$\SigmaBTs\; (TBT:\SigmaBTs)$</TEX>가 67% 이상으로 매우 높았고, 고농도 실험군일수록 이 비율이 높아져, 고농도의 TBTCl에 노출될수록 구피의 대사능력이 저해됨을 알 수 있었다. 또한 TBTCl은 구피의 번식력을 약화시키고 행동이상을 유발함이 밝혀졌다. 즉, 0.1<TEX>$\mug/l$</TEX>의 실험군부터 수컷의 구애행동과 수출관 내 정포의 수가 감소되었고, 0.32∼10 <TEX>$\mug/l$</TEX>의 실험군에서는 정소 내 전체 생식세포낭에 대한 정포낭의 수도 점차 감소하여 TBTCl이 정자변태 과정에 영향을 미치는 내분비계 장애물질로서 작용하고 있음이 시사되었다. 더욱이 25 <TEX>$\mug/l$</TEX>이상의 고농도군에서는 단기간 내에 치사율이 증가하고, 생식세포가 괴사되고, 정소의 지지세포와 수출관 내의 상피세포가 상해되고, 유영행동 이상이 급증하고, 섭식이 중단되는 등 급성독성이 관찰되어, TBTCl이 구피의 번식 뿐 아니라 생존을 저해하고 있음이 시사되었다. Sexually matured guppies (Poeiria reticulata) were exposed to TBTCI (0.1, 0.32, 1, 3.2, 10, 25, 32, 50, 75 and 100 <TEX>$\mug/l$</TEX>) for 144 hours to determine the bioaccumulation rate and effects on the reproduction and behavior. The ratio of TBT residues to <TEX>$\SigmaBTs\; (TBT:\SigmaBTs)$</TEX> was 67% or higher in all the guppies exposed to TBTCl, and the higher the level of TBTCl exposed, the higher the ratio of TBT:∑BTs, suggesting that the higher the level of TBTCl exposed, the lower the metabolism rate of the fish. TBTCl exposure led to a poor reproductivity and an abnormal sexual behavior in the fish, i.e. a reduced number of the male sexual sigmoid display and of spermatophore in the efferent duct was observed in the fish exposed to 0.1 <TEX>$\mug/l$</TEX> and higher levels of TBTCl, and a decreasing ratio of the testicular spermatophore cyst to the whole germ cell cysts was observed in the fish exposed to 0.32∼10 <TEX>$\mug/l$</TEX>)of TBTCl. The reduced ratio of the spermatophore cyst seems to be an effect of the endocrine disrupter inhibiting spermiogenesis. In the fish exposed to 25 <TEX>$\mug/l$</TEX> and higher levels of TBTCl, more serious effects, such as a rapid increase of mortality, the necrosis of most of the germ cells, great damages in Sertoli cells and epithelial cells of the efferent duct, a significant increase of abnormal swimming behavior, and a cessation of feeding were observed, which suggest the acute toxicity of TBTCl inhibiting not only the reproduction and behavior but also the survival of the fish itself.

Mass Mortalities Associated with Viral Nervous Necrosis in Hatchery-Reared Sea Bass Lates calcarifer in the Philippines

Viral nervous necrosis (VNN), also known as viral encephalopathy and retinopathy (VER), is an emerging disease affecting larvae and juveniles of many farmed marine fish species in Asia, Australia, Europe and North America. Mass mortality occurred in 14-day old larval sea bass Lates calcarifer at a hatchery in the Philippines associated with clinical signs such as abnormal swimming behavior and pale-gray discoloration of the body. Histological investigations in moribund fish revealed marked vacuolation in the retina and brain. Cytopathic effects (CPE) were observed in SSN-1 cells inoculated with the tissue filtrate of affected sea bass. A piscine nodavirus, the causative agent of VNN, was detected in the affected tissues and SSN-1 cells inoculated with the tissue filtrate of affected fish by RT-PCR. Electron microscopy revealed non-enveloped viral particles, 22-28 nm in diameter, in the cytoplasm of the brain and retina of affected fish and in the cytoplasm of VNN-infected SSN-1 cells after CPE appeared. These results indicate that mass mortality of sea bass larvae in the Philippines was caused by a piscine nodavirus.

Pathology of heart and skeletal muscle inflammation (HSMI) in farmed Atlantic salmon Salmo salar

This is the first description of heart and skeletal muscle inflammation (HSMI), a novel disease affecting farmed Atlantic salmon Salmo salar in Norway. HSMI was first diagnosed in 1999, and there has since been a yearly increase in the number of recorded outbreaks. Atlantic salmon are commonly affected 5 to 9 mo after transfer to sea, but outbreaks have been recorded as early as 14 d following seawater transfer. Affected fish are anorexic and display abnormal swimming behaviour. Autopsy findings typically include a pale heart, yellow liver, ascites, swollen spleen and petechiae in the perivisceral fat. While mortality is variable (up to 20%), morbidity may be very high in affected cages. Until more accurate tests are available, HSMI is diagnosed on the basis of histopathology. The major pathological changes occur in the myocardium and red skeletal muscle, where extensive inflammation and multifocal necrosis of myocytes are evident. HSMI is transmissible and, although most likely caused by a virus, the causal agent has not yet been isolated. This paper describes clinical signs and pathology of HSMI from 3 field outbreaks in Norway. Microscopic lesions are compared and discussed in relation to published descriptions of pancreas disease (PD) and cardiomyopathy syndrome (CMS). It is concluded that HSMI is histopathologically distinguishable from PD and CMS.

Nodavirus Infection in Hatchery-Reared Orange-Spotted Grouper Epinephelus coioides: First Record of Viral Nervous Necrosis in the Philippines.

Mass mortality occurred in 34-day old larval orange-spotted grouper Epinephelus coioides reared at a hatchery in the Philippines with clinical signs such as anorexia and abnormal swimming behavior. Histopathology of moribund fish demonstrated marked vacuolation of the brain, spinal cord and retina. Cytopathic effects were observed in SSN-1 cells inoculated with the tissue filtrate of affected grouper. Electron microscopy revealed non-enveloped virus particles measuring 20 to 25 nm in diameter in the cytoplasm of degenerated SSN-1 cells. Piscine nodavirus (betanodavirus), the causative agent of viral nervous necrosis (VNN), was detected in the affected tissues and SSN-1 cells inoculated with the tissue filtrate of affected fish by RT-PCR. This is the first record of VNN in the Philippines.

The hook gene (flgE) is expressed from the flgBCDEF operon in Rhodobacter sphaeroides: study of an flgE mutant.

In this work we identified the flgE gene encoding the flagellar hook protein from Rhodobacter sphaeroides. Our results show that this gene is part of a flagellar cluster that includes the genes flgB, flgC, flgD, flgE, and flgF. Two different types of mutants in the flgE gene were isolated, and both showed a Fla(-) phenotype, indicating the functionality of this sequence. Complementation studies of these mutant strains suggest that flgE is included in a single transcriptional unit that starts in flgB and ends in flgF. In agreement with this possibility, a specific transcript of approximately 3.5 kb was identified by Northern blot. This mRNA is large enough to represent the complete flgBCDEF operon. FlgE showed a relatively high proline content; in particular, a region of 12 amino acids near the N terminus, in which four prolines were identified. Cells expressing a mutant FlgE protein lacking this region showed abnormal swimming behavior, and their hooks were curved. These results suggest that this region is involved in the characteristic quaternary structure of the hook of R. sphaeroides and also imply that a straight hook, or perhaps the rigidity associated with this feature, is important for an efficient swimming behavior in this bacterium.

Symposium on 'Morphology and Physiology of Semicircular Canal Ampulla'. Motion sickness and otolith asymmetry.

There is a highly scattered inter-individual susceptibility in man to motion sickness. It is discussed whether different masses of otoconias between right and left sides are responsible for a high susceptibility. In order to proof this theory, we measured the otoliths of fish (salmons, trouts, Xiphophorus Helleri; Sumatra barbes) and found big differences in the utricular stones up to 140%. The mass differences of the saccular stones were much smaller. In fish, showing abnormal swimming behavior during off-vertical axis rotation we found big mass differences compared to that of normal swimmers. This difference was only seen in the utricular and not in the saccular stones. We therefore assume, that a big mass difference is one of the factors to trigger motion sickness especially for the high susceptibility to it. The macula utriculi seem to be much more integrated in the vestibular sense than the macula sacculi.

Viral encephalopathy and retinopathy of farmed marine fish species in Italy

Viral encephalopathy and retinopathy, otherwise known as fish encephalitis or viral nervous necrosis (VNN), is an emerging problem in several farmed marine fish species in various geographic areas all over the world. Since summer 1995, heavy losses affecting mainly juvenile and adult sea bass ( Dicentrarchus labrax) have been observed in several on-growing facilities in Italy. Dying fish show abnormal swimming behaviour and, at temperatures higher than 20–22°C, mortality rates range between 15 and 50%. Neither significant external nor internal gross pathological signs, except frequent abnormal swim bladder hyperinflation, were detected. Histological investigations reveal vacuolations in the grey matter of the brain and spinal cord and in the granular layers of the retina. Serial tissue sections examined by an immunohistochemical method carried out with antisera against fish nodaviruses showed a positive reaction. Additionally, spherical virus-like particles 22–25 nm in diameter were detected by electron microscopy in negative stained preparations of brain tissues, and the same samples gave a positive reverse transcription–polymerase chain reaction (RT–PCR) for the T4 region of the fish nodavirus gene. These results indicate that both juvenile and adult sea bass subject to mass mortality in Italy since summer 1995 are infected with a fish nodavirus and strongly suggest that the identified virus is the cause of the observed mortality.

Pathogenicity of the Nodavirus Detected from Diseased Sevenband Grouper Epinephelus septemfasciatus.

Viral nervous necrosis (VNN) of sevenband grouper Epinephelus septemfasciatus at grow-out stages, which was characterized by upside down swimming or floating behavior, has been spreading in Japan. The present study describes pathogenicity of a nodavirus found in diseased sevenband grouper. When young sevenband grouper or juvenile redspotted grouper E. akaara were challenged by an intramuscular injection with the filtered homogenate of infected organs (brain and eye), abnormal swimming behavior and mortality were produced, but some affected fish recovered from the disease after exhibiting the characterized behavior. Necrosis and vacuolation of the brain and retinal tissues, characteristic to VNN, were produced in the dead and abnormally-swimming fish and the viral antigens were detected in the degenerated nerve cells by FAT with an anti-SJNNV (striped jack nervous necrosis virus) serum. The infection experiment with redspotted grouper also indicated that rearing water temperature (16-28°C ) influenced development of the disease : higher mortality and earlier appearance of the disease signs were observed at higher water temperatures.

Naturally Occurring Thiamine Deficiency Causing Reproductive Failure in Finger Lakes Atlantic Salmon and Great Lakes Lake Trout

Abstract A maternally transmitted, noninfectious disease known as the Cayuga syndrome caused 100% mortality in larval offspring of wild-caught landlocked Atlantic salmon Salmo salar from several of New York's Finger Lakes. Survival of lake trout Salvelinus namaycush from Lakes Erie and Ontario was also impaired, but not until yolk absorption was nearly complete; moreover, mortality was greatly reduced relative to that of the salmon (range: 5–87%). Tissue concentrations of thiamine hydrochloride were severely reduced in these salmonid fish relative to unaffected control stocks. Afflicted Atlantic salmon treated with thiamine by yolk-sac injection or by bath immersion recovered completely from the Cayuga syndrome, as evidenced by the quantified reversal of abnormal swimming behaviors only 2 d after treatment and by the excellent survival (>95%) of the treated Atlantic salmon through 1.5 months of feeding. These data represent the first evidence of a vitamin deficiency causing the complete reproductive failu...

Food Selection by Larval Paddlefish Polyodon spathula Supplied with Rice Bran to Promote Production of Live Foods, with Prepared Diets, or with their Combination in Earthen Ponds

AbstractFood selection of larval paddlefish Polyodon spathula was evaluated by gut analysis in nine 0.02‐ha ponds either fertilized with rice bran (RB) to promote zooplankton production, supplied with prepared diets (PD), or with a combination of rice bran and prepared diet (CB). After 40 d, mean fish yields in RB and CB ponds were significantly higher (P &lt; 0.05) than fish yield in PD ponds, but there was no significant difference (P &gt; 0.05) in survival among treatments. Cladocerans were the main Live food items selected by paddlefish in RB and CB ponds. Chironomid larvae were the main food items selected by paddlefish in PD ponds. Less than 10% of the food found in paddlefish guts was prepared diets in PD and CB ponds. Prepared diets apparently were not as available to the fish or were not as preferred by the fish as Live foods. Levels of un‐ionized ammonia were significantly greater in CB and PD ponds than that in RB ponds. Decomposition of uneaten high‐protein diets in PD and CB ponds probably led to production of ammonia. Elevated un‐ionized ammonia levels during week 5 caused abnormal swimming behavior and some paddlefish mortalities in PD and CB ponds. Based upon these results, use of RB or other organic fertilizers to promote zooplankton production is recommended over direct feeding or a combination of fertilization and feeding for larval paddlefish in earthen ponds.

Histopathology of Viral Deformity in Yellowtail Fingerling, Seriola quinqueradiata.

Histopathological changes assoicated with the infection of viral deformity virus (VDV) were described in yellowtail fingerlings, Seriola quinqueradiata, from a hatchery in Nagasaki Prefecture. Advanced congestion in the liver, edema and anemia in the kidney, anemia in the spleen and congestion in the various parts of the brain were observed in naturally diseased fish. Experimentally infected fish showed congestion and focal necrosis in the liver, vacuolar degeneration in tubular epithelial cells and edematous changes in the hematopoietic tissue of kidney, and extensive anemia and necrosis of the splenic tissues. In the brain of fish showing abnormal swimming behavior and deformity, advanced congestion and hemorrhage were found in all fish examined. Histopathological features in experimentally infected fish closely resembled those in naturally diseased fish. These findings suggest that lesions in the brain are related to abnormal swimming behavior and deformity of the diseased fish.

Quantitative and histochemical demonstration of mercury deposits in the inner ear of trout, Salmo trutta, exposed to dietary methylmercury and dissolved mercuric chloride

The deposition of organic and inorganic mercury compounds in the inner ear of trout, Salmo trutta was studied quantitatively and cytochemically. One group of trout was fed methylmercuric chloride (CH 3HgCl), equivalent to 2.5 μg Hg/g fish, once a week for four weeks. Another group of trout was exposed to dissolved mercuric chloride (HgCl 2, 150 μg Hg/l) for five days. 203Hg-labeled mercury was applied to quantify and to compare the accumulation of mercury in the inner ear with the accumulation in the whole fish and in 12 selected organs. The resulting order of mercury deposition differed in the two cases. Microscopic analysis, based on autometallographic silver enhancement, demonstrated a differential deposition of mercury in the utricular tissue of fish exposed to methylmercury and fish exposed to inorganic mercury. Thus, in the sensory epithelium of the trout treated with methylmercury, mercury deposits dominated in the apical part of both the receptor cells and the supporting cells, while the mercury deposits were located along the borders of neighboring cells in the sensory epithelium and along the basal membrane in the fish exposed to inorganic mercury. Below the sensory epithelium, both mercury compounds formed deposits in the endothelial cells of blood vessels and in the Schwann cells and endoneurium of the nerve fiber bundles. The results suggest that observed abnormal swimming behaviour and disequilibrium of mercury exposed fish may in part be due to an impaired inner ear function.