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Psychology and Biology - Essay Example

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This transmitter is degraded by the enzyme acetylcholinesterase (Wiener & Hoffman, 2004). A drug that would treat a psychological disorder related to acetylcholine deficiency…
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Psychology and Biology
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Psychology and Biology Assume that a psychological disorder is related to a deficiency of acetylcholine and you are creating a drug to treat this disorder, how might this drug work?Acetylcholine is an important neurotransmitter and in the brain it forms a vital synaptic transmitter. This transmitter is degraded by the enzyme acetylcholinesterase (Wiener & Hoffman, 2004). A drug that would treat a psychological disorder related to acetylcholine deficiency is one that would inhibit the activity of acetylcholinesterase enzyme.

This enzyme will prevent the acetylcholine degradation and thus prevent low levels of acetylcholine that is characteristic of a psychological disorder that can be attributed to a deficiency of acetylcholine. This will also prolong the action of acetylcholinesterase for a long duration. The drug should have a high specificity for the enzyme. This will ensure that it readily binds the enzyme. Moreover, its potency needs to be high in that the dissociation constant that gives the concentration required to inhibit enzyme activity.

This can be achieved via a combination of proteomics and bioinformatics. The final product should be highly effective with minimal side effects on the patients. 2. Speculate on what might occur if the receptors are blocked The acetylcholine receptor (AChR) is gated ligand ion channel whose opening is mediated by the binding of acetylcholine. This channel opening leads to ion flux thus neuromuscular transmission (Samson & Levitt, 2008). If these receptors are blocked the process of neurotransmission will be halted.

Acetylcholine fulfills the following functions: blood vessel dilation, heart rate decrease, bronchiole constriction, respiratory tract mucous production, intestinal contraction, pupil constriction and stimulated production of tears, sweat and saliva. Blockage of the AChR will lead to anticholinergic effects that arise in the absence of acetylcholine activity. These include blurred vision, increased heart rate, ulceration in the respiratory tract, blood vessel constriction, constipation, poor digestion and dry eyes.3. What effect does an inhibitor such as AChE-I have on AChE.

Acetylcholinesterase inhibitor(AChE-I) binds to acetylcholinesterase(AChE) thereby preventing the enzyme from degrading acetylcholine. AChE catalyzes the breakdown of Acetylcholine into choline and acetic acid (Wiener & Hoffman, 2004).Failure of acetylcholine breakdown leads to its accumulation in synapses with acetylcholine receptors and neuromuscular skeletal junction. 4. How could AChE-I be harmful?Acetylcholinesterase inhibitor leads to an increase in the level of acetylcholine in the brain (Wiener & Hoffman, 2004).

This also yields increased toxic levels of acetylcholine in sites of acetylcholine action in the bowels, intestines, eyes, respiratory tract, stomach etc. Therefore, the activity of acetylcholine in these areas will be heightened and the result will be great harm. For instance, acetylcholine causes intestinal contraction so stomach cramps are bound to arise in the presence of excessive acetylcholine. The patient is also likely to have diarrhea. In addition, acetylcholine will lead to excessive heart contraction.

This is dangerous and might lead to a coma and/or stroke. There can be increased tearing, saliva and production. There is also the possibility of suffocation as a result of increased bronchiole constriction. Other common drug side effects cannot be ruled out. This entails lethal drug-drug interactions if the patient is already under medication from another condition. Moreover, allergic reactions are also known to affect a given section of the population. Another plausible lethal effect of acetylcholinesterase inhibitors is toxicity of the central nervous system.

In essence, these effects are bound to arise from the combined action of excessive acetylcholine and prolonged acetylcholine activity.ReferencesSamson,A.O. & Levitt, M.(2008). Inhibition Mechanism of the Acetylcholine Receptor by R- Neurotoxins as Revealed by Normal-Mode Dynamics. Biochemistry, 47, 4065–4070.Wiener, S. W.& Hoffman, R.S.(2004). Nerve Agents: A Comprehensive Review. Journal of 200 Intensive Care Medicine, 19(1), 22-37.

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