PUBLICATION
Brief embryonic cadmium exposure induces a stress response and cell death in the developing olfactory system followed by long-term olfactory deficits in juvenile zebrafish
- Authors
- Blechinger, S.R., Kusch, R.C., Haugo, K., Matz, C., Chivers, D.P., and Krone, P.H.
- ID
- ZDB-PUB-070827-7
- Date
- 2007
- Source
- Toxicology and applied pharmacology 224(1): 72-80 (Journal)
- Registered Authors
- Krone, Patrick H.
- Keywords
- Olfactory epithelium, Zebrafish larvae, Cadmium, Alarm substance, Cell death, Lateral line
- MeSH Terms
-
- Animals
- Behavior, Animal/drug effects
- Cadmium/toxicity*
- Cell Death/drug effects*
- Embryo, Nonmammalian/physiology*
- Endpoint Determination
- HSP70 Heat-Shock Proteins/biosynthesis
- HSP70 Heat-Shock Proteins/genetics
- Image Processing, Computer-Assisted
- In Situ Hybridization
- In Situ Nick-End Labeling
- Indicators and Reagents
- Larva/physiology
- Lateral Line System/pathology
- Neurons, Afferent/drug effects
- Neurons, Afferent/metabolism
- Olfaction Disorders/chemically induced*
- Olfaction Disorders/psychology
- Olfactory Mucosa/pathology
- Predatory Behavior/drug effects
- Smell/drug effects*
- Stress, Physiological/pathology*
- Up-Regulation/drug effects
- Water Pollutants, Chemical/toxicity
- Zebrafish
- PubMed
- 17706735 Full text @ Tox. App. Pharmacol.
Citation
Blechinger, S.R., Kusch, R.C., Haugo, K., Matz, C., Chivers, D.P., and Krone, P.H. (2007) Brief embryonic cadmium exposure induces a stress response and cell death in the developing olfactory system followed by long-term olfactory deficits in juvenile zebrafish. Toxicology and applied pharmacology. 224(1):72-80.
Abstract
The toxic effects of cadmium and other metals have been well established. A primary target of these metals is known to be the olfactory system, and fish exposed to a number of different waterborne metals display deficiencies in olfaction. Importantly, exposure over embryonic/larval development periods can cause deficits in chemosensory function in juvenile fish, but the specific cell types affected are unknown. We have previously characterized a transgenic zebrafish strain expressing the green fluorescent protein (eGFP) gene linked to the hsp70 gene promoter, and shown it to be a useful tool for examining cell-specific toxicity in living embryos and larvae. Here we show that the hsp70/eGFP transgene is strongly and specifically upregulated within the olfactory sensory neurons (OSNs) of transgenic zebrafish larvae following a brief 3-h exposure to water-borne cadmium. This molecular response was closely correlated to an endpoint for tissue damage within the olfactory placode, namely cell death. Furthermore, cadmium-induced olfactory cytotoxicity in zebrafish larvae gives rise to more permanent effects. Juvenile zebrafish briefly exposed to cadmium during early larval development display deficits in olfactory-dependent predator avoidance behaviors 4-6 weeks after a return to clean water. Lateral line neuromasts of exposed zebrafish larvae also activate both the endogenous hsp70 gene and the hsp70/eGFP transgene. The data reveal that even a very brief exposure period that gives rise to cell death within the developing olfactory placode results in long-term deficits in olfaction, and that hsp70/eGFP may serve as an effective indicator of sublethal cadmium exposure in sensory cells.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping