Disease relevance of ache

• Toxicity of these pesticides has been correlated with their inhibitory effects on acetylcholinesterase activity [1].

High impact information on ache

• After release into the synaptic cleft, ACh is rapidly degraded by acetylcholinesterase (AChE) [2].
• Acetylcholinesterase is required for neuronal and muscular development in the zebrafish embryo [2].
• Young neurones within both the hindbrain and spinal cord were identified in live embryos using Nomarski optics, and histochemically by labelling for acetylcholinesterase activity and expression of an antigen recognized by the monoclonal antibody zn-1 [3].
• Compared with other vertebrate acetylcholinesterase genes, ache gene contains no alternative splicing at 5' or 3' ends where only a T exon is present [4].
• The enzyme acetylcholinesterase (AChE) terminates synaptic transmission at cholinergic synapses by hydrolyzing the neurotransmitter acetylcholine [5].

Chemical compound and disease context of ache

• Malathion's action as an acetylcholinesterase inhibitor and the toxicity of the metabolites of malathion may be responsible for malathion's teratogenic effects on fish development [6].
• Enzymological differences of AChE and diazinon hepatic metabolism: correlation of in vitro data with the selective toxicity of diazinon to fish species [7].

Biological context of ache

• Remarkably, the ratio of AAA/AChE activity decreased 210-fold from 4 to 144 h development, indicating a distinct embryonic role of AAA during early embryogenesis [8].
• Blocking acetylcholinesterase (AChE) with eserine had no effect on mEPC kinetics in embryos at 1 day and only partially slowed (by approximately 1/2) the decay rate in larvae at 6 days [9].
• The primary neurons appear to follow a common sequence of development consisting of a withdrawal from the cell division cycle, the expression of AChE, and axogenesis [10].
• Contrary to the predictions of this model, we find similar delay and onset kinetics of synaptic current at positive and negative muscle membrane potentials, even after inhibition of acetylcholinesterase [11].

Anatomical context of ache

• In contrast to previous results using a catalytic-inactive allele, our analysis demonstrates that AChE is dispensable for muscle fiber development and Rohon-Beard sensory neuron growth and survival [5].
• Moreover, we show that in the absence of AChE, acetylcholine receptor clusters at neuromuscular junctions initially assemble, but that these clusters are not maintained [5].
• Acetylcholinesterase function is dispensable for sensory neurite growth but is critical for neuromuscular synapse stability [5].
• ChAT-ir cells were restricted to the periventricular stratum of the optic tectum, but AChE-positive neurons were observed throughout the whole extension of the lamination except in the marginal stratum [12].
• Presumptive cranial ganglia transiently expressed AChE activity between 14 and 24 hours of development [10].

Associations of ache with chemical compounds

• Acetylcholinesterase inhibition and increased food consumption rate in the zebrafish, Danio rerio, after chronic exposure to parathion [13].
• The AAA activity was sensitive to eserine and serotonin, ensuring its association with AChE [8].
• The results showed that the observed cholinesterase activities in the whole embryo may be attributed mainly to acetylcholinesterase with a partial capability to use propionylthiocholine as a second substrate [14].
• Besides AChE activity, a variety of other parameters were measured: whole-body protein and lactate content, consumption rate, survival, growth and reproduction [13].
• Widespread innervation of the swim bladder was also indicated by acetylcholinesterase histochemistry, but choline acetyltransferase-immunoreactive (-IR) somata and fibers were limited to the junction of the pneumatic duct and esophagus [15].

Other interactions of ache

• Catalase, glutathione peroxidase, and superoxide dismutase activities and total glutathione content of hepatic extracts, as well as brain acetylcholinesterase activity and uranium bioaccumulation, were measured [16].

Analytical, diagnostic and therapeutic context of ache

• In situ hybridization and enzymatic activity detection on whole embryos confirmed early expression of the acetylcholinesterase gene in nervous and muscular tissues [4].
• Acute toxicity tests with fish have shown that high percentages of AChE inhibition are needed to cause detrimental effects, but not much is known about the consequences of chronic exposure to this group of chemicals for both AChE activity and higher levels of biological organisation [13].
• In zebrafish, the onset of acetylcholinesterase (AChE) expression was detected by RT-PCR at 4 hpf (hours post-fertilization) [8].
• Substantial differences in the ChAT and AChE distribution between zebrafish and other fish species were observed, which could be important because zebrafish is widely used as a genetic or developmental animal model [12].
• The cholinergic/cholinoceptive system of the zebrafish CNS was analyzed by using choline acetyltransferase (ChAT) immunohistochemistry and acetylcholinesterase (AChE) histochemistry in the brain, retina, and spinal cord [12].

References