Please explain the process of how an axon degenerates in the central nervous system following injury and how it affects the neuron/cell body, as well as presynaptic and postsynaptic neurons. Explain processes such as chromatolysis and how neurotrophin signaling works.
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Please explain the process of how an axon degenerates in the central nervous system following injury and how it affects the neuron/cell body, as well as presynaptic and postsynaptic neurons. Explain processes such as chromatolysis and how neurotrophin signaling works.
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- Choose a catecholamine neurotransmitter and describe/draw the components of the synapse important for its signaling including synthesis, packaging into vesicles, receptors, transporters/degradative enzymes. Describe 2 drugs that can act on this system.Indicate the correct order for the events that describe the activation of a g-protein coupled receptor, cAMP second messenger system. (not all options will be used) -cAMP is synthesized from ATP -Calcium binds to calmodulin -Ion Channels are opened and sodium and potassium affect the Vm -The G-protein activates Adenylate Cyclase or a similar protein -Activated kinases dephosphorylate proteins which change their activity and affects the cell. -Activate kinases phosphorylate proteins in the cell that cause intracellular changes. -The intracellular side of the receptor changes and activates a G-protein -cAMP is a second messenger that activates kinases like PKA Messenger binds to the transmembrane receptorWhat distinguishes a steroid receptor from a receptor tyrosine kinase receptor or a G-protein-coupled receptor?
- Figure 9.8 HER2 is a receptor tyrosine kinase. In 30 percent of human breast cancers, HER2 is permanently activated, resulting in unregulated cell division. Lapatinib, a drug used to treat breast cancer, inhibits HER2 receptor tyrosine kinase autophosphorylation (the process by which the receptor adds phosphates onto itself), thus reducing tumor growth by 50 percent. Besides autophosphorylation, which of the following steps would be inhibited by Lapatinib? Signaling molecule binding, dimerization, and the downstream cellular response. Dimerization, and the downstream cellular response. The downstream cellular response. Phosphatase activity, dimerization, and the downsteam cellular response.Outline the three general means by which binding of a water soluble extracellular chemical messenger to its matching surface membrane receptor brings about the desired intracellular response.You learned in this chapter that Na+/K+ active transport pumps in the plasma membrane of the axons are responsible for creating the imbalance between Na+ and K+ inside and outside of the neuron that produces the resting membrane potential. In early research studying the role of ions and the involvement of active transport of ions in neural signaling, investigators used the giant axon of a squid as a model. The diameter of a giant axon is far greater than that of a mammalian axon, which enabled researchers to isolate it easily and use it in in vitro experiments. In one early experiment, researchers investigated the active transport of Na+ out of the axon in response to the presence of cyanide. Experimentally they hooked up a section of axon to a syringe, immersed the axon in artificial seawater, introduced radioactive 22Na (as 22NaCl) into the axon, and then quantified the transport of 22Na out through the axons plasma membrane. The rate of 22Na transport out of the axon was determined by measuring the radioactivity released into the fluid sur- rounding the axon over a period of time. The Figure shows the results of the experiment. What is the effect of cyanide on Na1 transport out of the squid axon? How do the data show the effect? Source: P. C. Caldwell et al. 1960. The effects of injecting energy-rich phosphate compounds on the active transport of ions in the giant axons of Loligo. The Journal of Physiology 152:561590. Cengage Learning 2017
- Which of the following is incorrect about pathways activated by G-proteincoupled receptors? a. The extracellular signaling molecule is the first messenger. b. When activated, plasma membrane-bound G protein canswitch on an effector. c. Second messengers enter the nucleus. d. ATP converts to cAMP to activate protein kinases. e. Protein kinases phosphorylate molecules to change cellularactivity.What type of receptor requires an effector protein to initiate a signal? biogenic amine ionotropic receptor cholinergic system metabotropic receptorWhat effect will a cAMP inhibitor have on a peptide hormone-mediated signaling pathway? It will prevent the hormone from binding its receptor It will prevent activation of a G-protein It will prevent activation of adenylate cyclase It will prevent activation of protein kinases.
- The secretion of hormones by the pituitary gland is an example of.____ autocrine signaling paracrine signaling endocrine signaling direct signaling across gap junctionsVisit this site (http://openstaxcollege.org/l/neurolab) to see a virtual neurophysiology lab, and to observe electrophysiological processes in the nervous system, where scientists directly measure the electrical signals produced by neurons. Often, the action potentials occur so rapidly that watching a screen to see them occur is not helpful. A speaker is powered by the signals recorded from a neuron and it pops each time the neuron fires an action potential. These action potentials are firing so fast that it sounds like static on the radio. Electrophysiologists can recognize the patterns within that static to understand what is happening. Why is the leech model used for measuring the electrical activity of neurons instead of using humans?Assume presynaptic excitatory neuron A terminates on a postsynaptic cell near the axon hillock and presynaptic excitatory neuron B terminates on the same postsynaptic cell on a dendrite located on the side of the cell body opposite the axon hillock. Explain why rapid firing of presynaptic neuron A could bring the postsynaptic neuron to threshold through temporal summation, thus initiating an action potential, whereas firing of presynaptic neuron B at the same frequency and the same magnitude of EPSPs may not bring the postsynaptic neuron to threshold.
