Tyrosine came from the Greek word "tyros" which means cheese as it was discovered in cheese by Justus von Liebig, a German chemist in 1846. Tyrosine serves as the precursor for dopamine the neurotransmitter which is considered as the "reward or pleasure molecule" in our brain. It is also involved. in controlling the fine motor movement of our muscles such as those of our hands. Draw the titrimetric profile of tyrosine and calculate its isoelectric pH. [Note: The aromatic hydroxyl group is titratable]
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- Tyrosine came from the Greek word "tyros" which means cheese as it was discovered in cheese by Justus von Liebig, a German chemist in 1846. Tyrosine serves as the precursor for dopamine - the neurotransmitter which is considered as the "reward or pleasure molecule" in our brain. It is also involved in controlling the fine motor movement of our muscles such as those of our hands. Draw the titrimetric profile of tyrosine and calculate its isoelectric pH. [Note: The aromatic hydroxyl group is titratable]When the neurotransmitter acetylcholine (ACh) binds the acetylcholine receptor (a GPCR) on muscle cells, it causes them to contract. ZIGGY, a chemical analog of ACh, also binds to the same acetylcholine receptor on muscle cells, but instead causes the muscle cells to relax. For this reason, it is sometimes prescribed as a muscle relaxer. Explain in 3-4 sentences how ZIGGY could cause muscle relaxation. How can both ZIGGY and ACh bind the same GPCR? And then how can they have different effects on the cells, despite binding to the same receptor on the same cells?The neurotransmitter acetylcholine is released from presynaptic neurons in response to a nerve impulse and diffuses across the È synaptic cleft, or neuromuscular junction, to a receptor on another neuron or a muscle cell. The nicotinic acetylcholine receptor is a pentamer containing four types of subunits, azßys. Place the events in the correct order, from the release of acetylcholine from a neuron to receptor resensitization: -excited presynaptic neuron releases acetylcholine -acetylcholine diffuses across synaptic cleft or neuromuscular junction -acetylcholine is released from the binding sites -two acetylcholine bind to a receptor; the gate opens -small cations pass through the open pore of the receptor -the plasma membrane of the target cell is depolarized -two acetylcholine are tightly bound to a receptor; the gate is closed -one acetylcholine binds to a receptor; the gate is closed.
- L-Dopa One of the first medications developed to treat Parkinson's disease is a substance called L-DOPA (or Levodopa). This medication can be taken to reduce the motor symptoms of Parkinson's. Unfortunately there is no way to reverse or stop the death of the dopamine producing neurons, but L-DOPA is one of a few treatments that can help manage the symptoms. Your task is to investigate what L-DOPA is and explain why taking L-DOPA might reduce the symptoms of the disease. Write at least one paragraph (5 sentences) to explain your findings in the box below. Use the rubric here to make sure you are explaining the situation thoroughly. This should be entirely in your own words. Do not use phrases from the internet if you do not know what they mean. Rubric (use to check your work) Has major the main points misconceptions not understand of this topic Shows a Understands Clearly does complete understanding How do Neurons 100 85 70 50 use neurotransmitters like dopamine? What do neurons do when…Spastic paralysis (resulting from the failure of muscles to relax), induced by the neurotoxin strychnine, occurs when this poison blocks the binding of: the excitatory neurotransmitter acetylcholine to post-synaptic sodium channels the excitatory neurotransmitter glutamate to post-synaptic calcium channels the excitatory neurotransmitter serotonin to post-synaptic potassium channels the inhibitory neurotransmitter glycine to post-synaptic chloride channels the inhibitory neurotransmitter melatonin to post-synaptic bicarbonate channelsFlaccid paralysis (resulting from the failure of muscles to contract), induced by the neurotoxin tubocurarine, occurs when this poison blocks the binding of: the inhibitory neurotransmitter melatonin to post-synaptic bicarbonate channels the excitatory neurotransmitter glutamate to post-synaptic calcium channels the excitatory neurotransmitter acetylcholine to post-synaptic sodium channels the inhibitory neurotransmitter glycine to post-synaptic chloride channels the excitatory neurotransmitter serotonin to post-synaptic potassium channels
- In a cell line derived from normal rat thyroid, stimulation of the alpha1-adrenergic receptor increases both IP3 formation and release of arachidonic acid (AA). IP3 elevates cytosolic Ca, which mediates thyroxine efflux, whereas AA serves as a source of prostaglandin E2, which stimulates DNA synthesis. It is not clear how AA release is connected to the adrenergic receptor. AA could arise by cleavage from the DAG that accompanies IP3 production. Alternatively, AA could arise through an independent effect of the receptor on PLA2, which can directly release AA from intact phosphoglycerides. Consider the following experimental observations: a) Addition of noradrenaline to cell cultures stimulates production of both IP3 and AA. b) If the alpha1-adrenergic receptors are made unresponsive to noradrenaline by treatment with phorbol esters (which act through PKC to cause phosphorylation, and inactivation, of the receptor), addition of noradrenaline causes no increase in IP3 or AA. c) When…Which of the following structures has activity like acetylcholine? HyC H-C HC NMeg NMey D]A chemical synapse is a type of synapse that occurs between two neurons and between a motor neuron and skeletal muscle fibers (i.e. at a Neuromuscular junction, NMJ). Compare and contrast the specific events that occur at chemical synapses at these two sites. Describe clearly how they are similar and how they are different, starting at the arrival of a nerve impulse at the pre-synaptic neuron and ending up with the changes observed at the postsynaptic membranes.
- Vitamins B1, B6 and B12 are so-called "Neurotropic" vitamins. They may response to "Wallerian degeneration" in nerve system. Briefly describe"Wallerian degeneration" and how the "neurotropic" vitamins react with this process.I am confused about the process of rod cells in the dark. In the dark, rod cells are unstimulated and therefore the sodium is able to enter and depolarize the cell, stimulating the release of glutamate to the bipolar cell. However, this increase in glutamate in the bipolar cell inhibits the release of action potential from the bipolar cell to the ganglion cell. This doesn't make sense to me because shouldn't there be an increase in action potential since the rod cells are supposed to function in the dark?Epilepsy is often treated with a combination of drugs such as carbamazepine and phenytoin (polytherapy). CYP3A4 is induced by phenytoin and carbamazepine. Carbamzeipine is cleared by CYP3A4, but phenytoin is not cleared by CYP3A4. What problems might you expect if (a) carbamazepine is removed or (b) phenytoin is removed from this two-drug regimen.