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Method for Improving Neurotransmission Failure Using a Novel Agent

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In central nervous system, synapses are important for conduction of nerve impulses. When these signals reach at the end of neurons, neurotransmitters are released to bind to receptors present on post-synaptic membrane to conduct the impulse to subsequent neurons. These neurotransmitters can include: acetylcholine, GABA, glutamic acid, serotonin, noradrenalin etc. Various abnormalities in these neurotransmitters can cause variety of diseases. Acetylcholine which is made up of two components i.e. acetyl co-A and choline, is found throughout the CNS. In PNS (peripheral nervous system) it is also being secreted. Similarly there are many other than acetylcholine whose proper transfer through these synaptic cleft is very important to operate nervous system within the body. There is another one, nitrogen monoxide which is thought to be a neurotransmitter but there is no specific receptor being detected for it yet. Though it is considered to be the control factor for flexibility of synaptic cleft.

Abnormalities in neurotransmitters and their effects

As these neurotransmitters are involved in various functions, any problem in their function can cause serious diseases. For instance, acetylcholine may be involved in various sympathetic, parasympathetic neurons, motor neurons, memory and learning behavior. So any defect in these signal transduction, or defects in ion channels or slow channels can cause various diseases such as Alzheimer, Autism, Huntington disease, Parkinson, Anxiety, and Depression. Various medications have been developed for improvement in treatment of various diseases such as in case of glaucoma, acetylcholine analogs are being used.

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Problem of conventional drugs being used for treatment of these diseases is that they have their own adverse effects. For instance, administration of excessive amount of anti-cholinestrerase can cause paralytic symptoms in muscles, or its long-term usage can cause alteration of receptors, fatal dysfunctioning of heart and lungs.Selenocysteine containing protein (Selenoprotein: SeP) as treatmentInventors have come up with the medication by improving signal transduction, behavior of acetylcholine and neurotransmission by nitrogen monoxide for treatment of neurotransmission dysfunction diseases. Inventors investigated selenoprotein P and found that they not only exhibit cell-death inhibitory function but also to treat neurotransmission function based on experiments performed on animals and have completed this invention.

Selenoproteins were first identified in 1977 as selenium-containing protein and in 1952 it was revealed that selenium was incorporated in the form of selenocysteine. In order to investigate whether this protein contain 10 selenocysteine residues, it was being cloned from cDNA of rats. Very little was known about it. There are many reports which report it as transporter of selenium to brain during its deficiency. Present inventors have investigated that addition of these selenoproteins to culture can enhance complexity in development.

Present inventors have also investigated that selenoprotein P also increases epilepsy symptoms. After performing experiments on rat, they found that selenoprotein P can accelerate synaptic formation, function of acetylcholine receptor, and activations of neurons by nitrogen monoxide, which can form basis of treatment of signal transduction dysfunction diseases. Selenium is a trace element, but its deficiency can cause serious diseases. It is essential for survival of cell.


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