Final answer:
Dopamine is typically associated with long-term neuronal responses and, upon binding to its receptor, is expected to increase cAMP levels. Acetylcholine is the neurotransmitter released at the neuromuscular junction. Research on preventing excitotoxicity includes limiting glutamate binding to NMDA receptors, with a focus on the NR2B subunit to minimize side effects.
Step-by-step explanation:
The question is concerned with the initiation of the translational block for PKMz release. While the options provided include dopamine, serotonin, acetylcholine, and glutamate, the substance that is usually associated with long-term neuronal responses and interacts with G-protein-coupled receptors is dopamine. When dopamine binds to its receptor, one would expect an increase in the concentration of cyclic AMP (cAMP) as a second messenger system. This is because dopamine receptors are coupled with G-proteins that can activate adenylyl cyclase, which in turn synthesizes cAMP from ATP. Moving on to the specific neurotransmitter released at the neuromuscular junction, it is acetylcholine, not listed in the provided options, which are incorrect. Acetylcholine's release leads to the depolarization of muscle fiber membranes that ultimately results in muscle contraction. Regarding neuroprotection and the prevention of glutamate-mediated excitotoxicity, research suggests that limiting the release or binding of glutamate to its receptors, especially NMDA receptors, can be beneficial. Although the actions on the NR2B subunits of the NMDA receptors have shown promise in animal models, the results in human clinical trials have been more limited. Therefore, research continues to find more effective strategies with fewer side effects to prevent excitotoxicity-related damage.