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What the hell is that and why does it sound so damn scary?

Well, like most things in life, too much or too little of something often carries bad consequences. Apparently there are proteins that are responsible for dopamine degradation after dopamine uptake. If you have a mutation that either prevents the formation of this protein (more likely than not this would be embryonically lethal) or that impairs the protein's function, then there will be an abnormally high level of dopamine. It's bad to have too little or too much of a neurotransmitter around.

Another example of something like this is cholinesterase. After the nerve impulse is transmitted, you want the acetylcholine broken down. If it's not broken down, then the nerve impulse continues to be triggered which could lead to unresolved trembling and twitching. In C. elegans, there are mutations in a subunit of the acetycholine receptor so that the receptors get continuously triggered leading to degeneration and the necrotic death of the neuron. In a genetic screen of these mutants it was noticed that there were some that appeared to be resistant. A further screen discovered that these mutants also had a mutation in another protein. Further investigation revealed that this protein was required for the maturation and expression of the acetylcholine receptor. If its role was inhibited by the mutation, then the defective subunit of the acetycholine receptor would never make it to the neuron cell surface. Apparently there is enough redundancy between acetylcholine receptors and other neurotransmitter-triggered receptors that the lack of the ACh receptor isn't lethal. My lab was working on finding out just what that protein (RIC-3, for Resistance to Inhibitors of Cholinesterase) did to get the acetylcholine receptor subunits from the endoplasmic reticulum, through assembly and transport, to cell-surface expression.