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New Treatments for Neurochemistry and Neuropharmacology

Neurotransmission at cholinergic neurons; at first I will discuss neurologic transmitter. Neurotransmitter in cholinergic neuron involves synthesis of actylcholine esterase delays binding to that receptor, degradation and recapture and re-uptake. The synthesis of acetylcholine. Synthesis occurs by choline with acetyl coenzyme A. Choline acetyl transfer is capitilized the action and choline plus coenzyme A and choline. It is very important to know that choline is the direct limiting factor because in diseases such as Alzheimerís disease and other choline, acetylcholine deficit diseases we try to treat with supplementing choline.

Next esterase: acetyl choline, this is not very important but Iíll mention. Acetylcholine  into the vesicle by an active transport process which requires energy, and the mature vesicle is stored in the presynaptic terminal. Then release of acetylcholine. Release of acetylcholine is very, very important. Try to concentrate here. During the open and causes influx of calcium in the presynaptic area. When influx of calcium enters in the presynaptic area.

Then black widow spider venom causes explosive release of acetylcholine. It also acts in presynaptic area and black widow spider venom, which is a lactotoxin, there is only one toxin.

Binding to that receptor, after release from the presynaptic vesicle, it binds to the postsynaptic receptor and binding to that receptor leads to the biological response such as initiation of Funard impulse and activation of the specific enzyme. Itís only postsynaptic receptor. You can think it as a button on the computer. When button is pressed by acetylcholine action is generated, and there will be function.

The degradation of acetylcholine. Acetylcholine is rapidly hydrolyzed by choline estriol and in the synaptic cleft. This is also very important, but acetylycholine rapidly hydrolyzed by choline estriol in the synaptic cleft and here I mention acetylcholine, acetylcholine esterase. Here there are different kinds of medicine now and in the process of development and already developed to act on acetylcholine esterase to inhibit this process. And by that way we can increase the supply of estriol choline in the nerve terminal and memory will be improved.

Now acetylcholine receptors: there are two types of acetylcholine receptors, nicotinic receptor and muscarinic receptor. Nicotinic receptor has four types, actually, but I will not go into details of what are the functions of different types of nicotinic receptors because it is not relevant for the Board. I will discuss in general what is important. Nicotinic receptor exerts its effect.

Now nicotinic antagonist: there are two types of nicotinic antagonists, non-depolarizing or competitive antagonist, and a depolarizing antagonist, or non-competitive antagonist. Non-depolarizing antagonists are competitive and antagonists are tubocurarine. It binds to the nicotinic receptor and prevents the binding of acetylcholine. This is competitive blocker that is the function of competitive blocker, but it binds to the nicotinic receptor and prevents the binding of acetylcholine. It prevents depolarization and muscle contraction.

Then muscarinic receptor. Muscarinic receptor are more in the brain than nicotinic receptor. Nicotinic receptor mostly in neuromuscular junction and muscarinic receptor mostly in brain and sympathetic nerve terminal.