Rat AChE(Acetylcholinesterase) ELISA Kit (E-EL-R0355)

This ELISA kit uses the Sandwich-ELISA principle. The micro ELISA plate provided in this kit has been pre-coated with an antibody specific to Rat AChE. Standards or samples are added to the micro ELISA plate wells and combined with the specific antibody. Then a biotinylated detection antibody specific for Rat AChE and Avidin-Horseradish Peroxidase (HRP) conjugate are added successively to each micro plate well and incubated. Free components are washed away. The substrate solution is added to each well. Only those wells that contain Rat AChE, biotinylated detection antibody and Avidin-HRP conjugate will appear blue in color. The enzyme-substrate reaction is terminated by the addition of stop solution and the color turns yellow. The optical density (OD) is measured spectrophotometrically at a wavelength of 450 nm ± 2 nm. The OD value is proportional to the concentration of Rat AChE. You can calculate the concentration of Rat AChE in the samples by comparing the OD of the samples to the standard curve.

Acetylcholinesterase (AChE) is a serine hydrolase that terminates cholinergic neurotransmission by rapidly hydrolyzing acetylcholine into choline and acetate at cholinergic synapses and the neuromuscular junction. Encoded by the ACHE gene, it occurs as several splice isoforms, including amphipathic, soluble monomeric and glycosylphosphatidylinositol (GPI)-anchored dimeric forms. Its catalytic rate is extremely high, clearing the transmitter within milliseconds, and the active-site serine is the target of numerous inhibitors. It is distributed in nervous tissue, skeletal muscle and peripheral organs. Functionally, AChE is indispensable for precise signaling: by limiting the duration of acetylcholine action it prevents sustained depolarization and receptor desensitization and ensures a discrete postsynaptic response to each nerve impulse. Acetylcholine acts not only at the neuromuscular junction but also at autonomic ganglia, parasympathetic nerve terminals and central synapses. AChE additionally participates in neuronal development and in the cholinergic anti-inflammatory pathway, through which vagal activity dampens systemic inflammatory responses. Inhibition of AChE causes acetylcholine accumulation and excessive receptor stimulation, the basis of organophosphate and carbamate toxicity, while controlled inhibition is exploited therapeutically by cholinesterase inhibitors used in dementia and myasthenia gravis. This ELISA kit enables quantitative determination of rat AChE in serum, plasma and tissue homogenates. In the rat it supports studies of cholinergic function, neurotoxicity and the cholinergic anti-inflammatory axis.