Final answer:
To alleviate Devin's symptoms, drugs would need to increase the effects of serotonin, as SSRIs work by blocking serotonin reuptake, increasing its levels in the synaptic cleft. Dopamine binding to its receptor increases cAMP levels. Before phosphorylation of tyrosine on receptor tyrosine kinases, insulin binds to the receptor, causing it to dimerize and auto-phosphorylate.
Step-by-step explanation:
To directly alleviate Devin's symptoms, the drugs would need to increase the effects of one of the neurotransmitters listed. When considering treatments for depression, serotonin is often targeted because its low levels are commonly linked with depressive symptoms. Drugs like Selective serotonin reuptake inhibitors (SSRIs) are used to block the reuptake of serotonin into the presynaptic neuron, which causes an increase in serotonin levels in the synaptic cleft, thus helping to alleviate depression.
Regarding question 9: Upon the binding of dopamine to its receptor, it activates a G-protein, which in turn can stimulate the production of cyclic AMP (cAMP). Thus, we would expect the concentration of cAMP to increase after dopamine binds to its receptor.
For question 10: Prior to the phosphorylation of tyrosine residues on the receptor tyrosine kinase that insulin binds to, the activation of the receptor occurs when insulin binds to it, leading to the dimerization (pairing) of two receptor molecules and their subsequent auto-phosphorylation.
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