Acute Effects of Mercuric Chloride on the Olfactory Epithelium of Trichomycterus brasiliensis

Ribeiro, C.B.; Fernandes, Lucas Matos; Carvalho, C.S.; Cardoso, Renato; Turcatti, N.M.

doi:10.1006/eesa.1995.1049

Cited by 23 publications

(8 citation statements)

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“…6A–C; Tables 6A–C), perhaps abnormal growth within the telencephalon, especially the dorsal and lateral regions, contributed to the delay in spatial task learning. These conclusions do not rule out other mechanisms of the central or peripheral nervous systems, e.g., alterations in sensory neuron function [19, 57, 76–79], that could contribute to decreases in sensitivity to the mechanical, odor, or visual stimuli required for learning the spatial alternation task and/or information processing that would result in the appearance of a learning deficit. Reduced sensory neuron activation may lessen the fish’s ability to extract information about its environment and facilitating an appropriate decision-making process.…”

Section: Discussionmentioning

confidence: 99%

Developmental selenomethionine and methylmercury exposures affect zebrafish learning

Smith¹,

Carvan²,

Dellinger³

et al. 2010

Neurotoxicology and Teratology

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Methylmercury (MeHg) is a ubiquitous environmental pollutant and has been shown to affect learning in vertebrates following relatively low exposures. Zebrafish were used to model long-term learning deficits after developmental MeHg exposure. Selenomethionine (SeMet) co-exposure was used to evaluate its role in neuroprotection. Embryos were exposed from 2-24 hours post fertilization to (1) MeHg without SeMet, (2) SeMet without MeHg and (3) in combination of MeHg and SeMet. In case (1), the levels of MeHg were 0.00, 0.01, 0.03, 0.06, 0.10, 0.30 µM. In case (2), the levels of SeMet were 0.00. 0.03, 0.06, 0.10, 0.30 µM. In case (3), co-exposure levels of (MeHg, SeMet) were (0.03, 0.03), (0.03, 0.06), (0.03, 0.10), (0.03, 0.30), (0.10, 0.03), (0.10, 0.06), (0.10, 0.10), (0.10, 0.30) µM. Learning functions were tested in individual adults, four months after developmental exposure using a spatial alternation paradigm with food delivery on alternating sides of the aquarium. Low levels of MeHg (<0.1 µM) exposure delayed learning in treated fish; fish exposed to higher MeHg levels were unable to learn the task; SeMet co-exposure did not prevent this deficit. These data are consistent with findings in laboratory rodents. The dorsal and lateral telencephalon are the primary brain regions in fish involved in spatial learning and memory. Adult telencephalon cell body density decreased significantly at all MeHg exposures >0.01 µM MeHg. SeMet co-exposure ameliorated but did not prevent changes in telencephalon cell body density. In summary, MeHg affected both learning and brain structure, but SeMet only partially reversed the latter.Descriptors developmental exposure; learning; mercury; selenium; spatial alternation; zebrafish

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Section: Discussionmentioning

confidence: 99%

Developmental selenomethionine and methylmercury exposures affect zebrafish learning

Smith¹,

Carvan²,

Dellinger³

et al. 2010

Neurotoxicology and Teratology

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“…It is evident, therefore, that even sublethal exposures (<100 ppb Hg 2+ ) used in this study were able to induce delayed, subtle deficits in the M‐cell, lateral line and sensory neuron function and muscle activity. While most research on the effects of developmental mercury has focused on mammalian models, including human, changes in sensory function and locomotor activity of a number of fish species subjected to developmental mercury exposures have also been identified (Skak & Baatrup, 1993; Ribeiro et al , 1995; Weis & Weis, 1995; Ososkov & Weis, 1996; Smith & Weis, 1997; Fjeld et al , 1998; Webber & Haines, 2003).…”

Section: Discussionmentioning

confidence: 99%

Dose‐dependent effects of developmental mercury exposure on C‐start escape responses of larval zebrafishDanio rerio

Weber

2006

Journal of Fish Biology

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Zebrafish Danio rerio embryos were exposed to 0, 25, 50 or 75 ppb Hg 2þ from 0 to 24 h post-fertilization (hpf) then placed into Hg 2þ -free water. Inductively coupled plasma-mass spectrophotometer analysis of whole embryo Hg 2þ content at 24 hpf showed a positive correlation with exposure regime (Pearson's one-tailed, r 2 ¼ 0Á698, P < 0Á01); at 5 days posthatch (dph), whole larval Hg 2þ content was not detectable. Hg 2þ -induced behavioural deficits in larvae were, therefore, due to changes during embryogenesis and not to residual Hg 2þ in the larvae. At 5 dph, larvae were tested for responses to different frequencies but equal intensities of vibrational stimuli generated by a remotely controlled plastic hammer. Data were recorded by high-speed videography and computer-analysed for latency of response (ms), amplitude of the response as measured by maximum initial velocity [normalized as body (standard) lengths s ÿ1 ; V max ] and duration of behaviour from initial head movement to cessation of caudal tail movement (ms). A single mechanical stimulus resulted in behavioural outcomes that were related to embryonic Hg 2þ uptake. Response latency increased with exposure level and displayed an increase of Â1Á5-2Á5 over control values (ANOVA, P < 0Á01). The V max decreased with exposure level to a low of 71% of control at the highest Hg 2þ concentration (ANOVA, P < 0Á01). Duration of behaviour displayed a biphasic response pattern in which exposure to 0, 50 or 75 ppb Hg 2þ did not result in a significantly different response yet exposure to 25 ppb Hg 2þ caused a significantly longer time of active response (ANOVA, P < 0Á01). Repeated stimulation (1, 2 or 4 hits s ÿ1 ) resulted in a concentration-dependent increase in response failures. Regardless of stimulation frequency, larvae exposed to 0 or 25 ppb Hg 2þ as embryos maintained higher V max levels for longer intervals during the testing period than those exposed as embryos to either 50 or 75 ppb Hg 2þ .

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“…These authors report toxicity responses in fish olfactory epithelium, in particular clumping and loss of cilia. Damage and loss of cilia with retention of microvilli were also described by Ribeiro et al (1995) in Trichomycterus brasiliensis after Hg 2+ exposure and by Kolmakov et al (2009) in goldfish after Cu 2+ treatment. However, ultrastructural studies on zebrafish olfactory epithelium exposed to Hg 2+ ions are still missing.…”

Section: Discussionmentioning

confidence: 79%

“…Mercury is a diffuse neurotoxic agent affecting fish olfaction: in the Atlantic salmon, it was observed accumulation of mercuric chloride around the borders of OSNs (Tierney et al, 2010), while it caused cilia degeneration and cell death (both sensory and nonsensory) in the Indian major carp after extended exposure (15 and 30 days) to sublethal doses (Ghosh & Mandal, 2014). Unlike copper (Razmara et al, 2021), the mechanisms by which mercury affects olfaction are less known (Ribeiro et al, 1995). Indeed, nothing is reported about behavioral responses or adverse effects after short-term exposure (less than 7 days) in adult fish, so it is impossible to compare mercury effects with other metal toxicity.…”

Section: Introductionmentioning

confidence: 99%

Response of Olfactory Sensory Neurons to Mercury Ions in Zebrafish: An Immunohistochemical Study

et al. 2021

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Olfactory sensory neurons (OSNs) of fish belong to three main types: ciliated olfactory sensory neurons (cOSNs), microvillous olfactory sensory neurons (mOSNs), and crypt cells. Mercury is a toxic metal harmful for olfaction. We exposed the olfactory epithelium of zebrafish to three sublethal Hg2+ concentrations. Molecular markers specific for the different types of OSNs were immunohistochemically detected. Image analysis of treated sections enabled counting of marked cells and measurement of staining optical density indicative of the response of OSNs to Hg2+ exposure. The three types of OSNs reacted to mercury in a different way. Image analysis revealed that mOSNs are more susceptible to Hg2+ exposure than cOSNs and crypt cell density decreases. Moreover, while the ratio between sensory/nonsensory epithelium areas is unchanged, epithelium thickness drops, and dividing cells increase in the basal layer of the olfactory epithelium. Cell death but also reduction of apical processes and marker expression could account for changes in OSN immunostaining. Also, the differential results between dorsal and ventral halves of the olfactory rosette could derive from different water flows inside the olfactory chamber or different subpopulations in OSNs.

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Acute Effects of Mercuric Chloride on the Olfactory Epithelium of Trichomycterus brasiliensis

Cited by 23 publications

References 0 publications

Developmental selenomethionine and methylmercury exposures affect zebrafish learning

Developmental selenomethionine and methylmercury exposures affect zebrafish learning

Dose‐dependent effects of developmental mercury exposure on C‐start escape responses of larval zebrafishDanio rerio

Response of Olfactory Sensory Neurons to Mercury Ions in Zebrafish: An Immunohistochemical Study

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