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Example research essay topic: Amp Amp Neuromuscular Junction - 1,706 words

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... e effects would lead to a decrease in the safety factor for neuromuscular transmission. The safety factor is the difference between the threshold needed to elicit an action potential, which is usually around - 45 mV and the actual end-plate potential amplitude, which is usually 70 - 80 mV, this is shown in figure 5. As a result of the reduced number of functional A ChR, the skeletal muscle becomes weakened. This weakness has four special characteristics: 1. It generally affects the cranial muscles; e.

g. eyelids and the eye muscles, an example of this is shown in figure 6. 2. The severity of the symptoms varies in the course of a single day and over longer periods 3. There are no conventional clinical signs of d enervation 4.

Drugs that inhibit acetylcholinesterase, the enzyme that breaks down ACh, reverse the weakness. It was shown experimentally in animals that antibodies, which cause myasthenia are usually active against either of the two peptide sequences on the protein; the bungarotoxin-binding site or an area on the &# 945; -subunit termed the main immunogenic region. Circulating antibodies in humans are often directed against the main immunogenic region. It was found that the causative factor of myasthenia is found in the plasma, because draining of the lymph from the thoracic lymph ducts improves the symptoms in the patient, but if the patients own lymphatic fluid is re-injected into the patient the symptoms recur. Through experimentation it has been shown that antibodies to the &# 945; -subunit of ACh receptors have a pivotal role in the pathogenesis of myasthenia. However, questions still remain unanswered, like what stimulates production of the antibodies to the A ChR?

One theory is that viral or bacterial antigens may share epitopes with the A ChR. Therefore, when a person is infected with the bacteria or virus the antibodies produced also work on the A ChR. The molecular similarity of the antigens is called molecular mimicry. The way that myasthenia affects the neuromuscular junction is that it decreases the number of functional ACh receptors in the postsynaptic membrane as well as decreasing the geometry of the junctional folds and therefore reducing the area to insert new ACh receptors. This means that ACh only has a limited number of receptors to bind to and since the acetylcholinesterase is hydrolyzing it the neurotransmitter at the same time repeated stimulation means that the excitatory potential amplitude may not reach threshold to elicit an action potential.

There are two main ways to treat this disease; this first is by injecting acetylcholinesterase inhibitors, such as neostigmine into the muscle and therefore the ACh won't be degraded as quickly and there will be a higher concentration of the neurotransmitter in the synaptic cleft to bind to the receptors. The effectiveness of this treatment is shown in figure 4. Another way of treating the symptoms of myasthenia is by injecting antigens to the antibodies into the muscle. Soon after the identification of the disease it was found that in 15 % of the adult cases the patient also had a benign tumour of the thymus.

In 1939 Alfred Blalock reported that when the thoma was removed the patients symptoms improved. Later in the 1950 s Blalock and Harvey found that patients with myasthenia gravis experience improved symptoms with the removal of the thymus even if the patient didn't have a thoma. This procedure was known as a thymectomy and has become standard practice in the treatment of myasthenia gravis. The second and less common form of myasthenia is congenital myasthenia (CMS), which can arise from presynaptic, synaptic or postsynaptic defects. The effect of this form of myasthenia is similar to the autoimmune form in that the specific defect compromises the safety factor of neuromuscular transmission.

As already stated congenital myasthenic syndromes are heterogenous disorders, meaning there is a lot of variety with in the disease. It was found that mutations in the A ChR that increase or decrease the synaptic response to ACh are a common cause of the postsynaptic CMS. The increased response to ACh is called a slow channel mutation, which is characterized by prominent limb weakness with little weakness of the cranial muscles. There are eleven slow channel mutations to date. The consequences of slow channel CMS mutations, stem from prolonged opening periods of the A ChR ion channel. This causes (1) cationic overloading pf the junctional sarco plasm and an end plate myopathy with loss of A ChR due to the degradation of the junctional folds and (2) a depolarization block due to staircase summation of prolonged end plate potentials (Engel et al 1999, pp. 165).

The end plate potentials of the slow channel mutation are similar to that observed in AChE deficiency. A decreased response to ACh arises from a low affinity, fast channel mutation. In patients with this syndrome the response to ACh is markedly decreased, even though the number of A ChR per end plate is normal. Studies have shown that with this syndrome comes infrequent A ChR channel events, abnormally brief activation episodes due to decreased channel reopening's during ACh occupancy, and an increased resistance to desensitization by ACh.

CMS can also arise from AChE deficiency at the end plate. In this deficiency there is a detrimental response of the compound action potential evoked in muscle by repetitive stimulation of the nerve, the same as in the autoimmune form. However, the muscle responds repetitively to a single stimulus, a feature that is not observed in other conditions. There are also other abnormalities, including abnormalities of the presynaptic nerve terminal, this results in impaired release of ACh from the terminals, and the result of this is similar to that of fast channel mutations. Conclusion As can be seen from this report the formation of the neuromuscular junction is very well understood the most comprehensively understood of any nerve-to-target cell contact, but yet there is still much more to learn. We know that the protein again, which is synthesized in the motor axon, plays a major role in the formation of the synapse.

The muscle-specific kinase, MuSK, found on the muscle cells and concentrated at the synaptic site also plays a key role. Again triggers the aggregation of A ChR on the muscle cell at the synapse, an intracellular protein known as raison plays a pivotal role in this process. The motor axon also secreted neuregulin, which stimulates expression of the A ChR and its insertion into the postsynaptic membrane. There are also several diseases that affect the neuromuscular junction; the two that were concentrated on in this paper were the two forms of myasthenia; the autoimmune form and the congenital form. The autoimmune form is the more common of the two, and fits the criteria for an autoimmune disease perfectly, antibodies are produced that act against the A ChR and break them down. The symptoms of this disease vary greatly and misdiagnosis is common, it generally affects the cranial muscle and abnormal fatigability is a common symptom.

The result of this disorder is that the number of A ChR's on the postsynaptic membrane is decreased by increased breakdown of the receptors and degradation of the junctional folds, which decreases the surface area to insert the receptors. The symptoms of this disorder can be treated by injection of AChE inhibitors into the muscle. There is still a lot to learn about this disease, like why the antibodies are produced in the first place, there are theories to explain this, but there is no strong evidence to back them up. The second type of myasthenia is the less common congenital form, which can arise from presynaptic, synaptic or postsynaptic defects. Mutations in the A ChR can lead to an increase or a decrease in response of the receptor to ACh. A decreased response is known as a fast channel mutation, while an increased response is known as a slow channel mutation.

The congenital form of myasthenia can also arise from AChE deficiency and defects on the presynaptic membrane which inhibit the ACh being released. There are still many things that need to be known about the two diseases and the only way this can be done is with more research. References Boonyapisit, K. , Kaminski, H. J. & amp; Ruff, R. L. 1999, 'Disorders of Neuromuscular Junction Ion Channels', Vol. 106, no. 1, pp 97 - 113 Burden, S.

J. 1985, 'The sub synaptic 43 -kDa protein is concentrated at developing nerve-muscle synapse in vitro', Process of National Academic Science U. S. A. ' vol. 82, pp. 8270 - 8273 Engel, A. G. , Ohno, K. & amp; Sine, S.

M. 1999, 'Congenital Myathenic Syndromes: Recent Advances', Archives of Neurology, vol. 56, no. 2, pp. 163 - 167 Gautam, M. , Noakes, P. G. , Moscow, L. , Rupp, F. , Seller, R. H. , Merlie, J. P. & amp; Sane's, J. P. 1996, 'Defective neuromuscular synaptogenesis in again-deficient mutant mice', Cell, vol. 85, pp. 525 - 535 Gautam, M. , Noakes, P.

G. , Mudd, J. , Nichol, M. , Chu, G. C. , Sane's, J. R. & amp; Merlie, J. P. 1995, 'Failure of postsynaptic specialization to develop at neuromuscular junctions in raison-deficient mice', Nature vol. 377, p. 232 - 236 Kandel, E. R. , Schwartz, J. H. & amp; Jersey, T.

M. 2000, Principles of neural science, 4 th edn. , McGraw-Hill companies inc. , United States of America, pp. 1087 - 1100, 298 - 308 Litchtman, J. W. , Burden, S. J. , Culcian, S. M. & amp; Wong, R. O. L. 1999, 'Synapse formation and elimination', in Zigmond M.

J. , Bloom, F. E. , Landis S. C. , Roberts, J. L. & amp; Squire L. R. , 'Fundamental of Neuroscience', Academic Press, London, pp. 547 - 567 Liyanage, Y. , Hoch, W. , Beeson, D. & amp; Vincent, A. 20002, 'The again / muscle specific kinase pathway: New targets for autoimmune and genetic disorders at the neuromuscular junction', Muscle & amp; Nerve, vol. 25, pp. 4 - 16 Rest, N. E. , Were, M.

J. & amp; McMahan, U. J. 1992, 'Again released by motor neurons induces the aggregation of acetylcholine receptors at neuromuscular junctions', Neuron, vol. 8, pp. 865 - 868


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