AP151 Short Essays Exam 2

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AP151 LEC EXAM 2

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Can you describe the steps in the signaling that takes place in a G-protein coupled receptor that acts through cyclic AMP, and what is the function of acting through a second messenger system? 

A chemical messenger binds to a GPCR on the cell membrane. This activates a G protein inside the cell, which then activates the enzyme adenylate cyclase. Adenylate cyclase converts ATP into cyclic AMP (cAMP). cAMP acts as a second messenger by turning on protein kinases and other proteins that cause a cellular response. The second messenger system allows the signal to be amplified and coordinate multiple responses from just one messenger

2
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Need to know all the gory details of the production of an action potential? What is a threshold? What causes the different phases of the action potential? What are these phases called? Can you explain how an action potential propagates down the axon? Why can it only move unidirectionally? 

An action potential begins when the membrane reaches threshold, opening voltage-gated sodium channels. Depolarization occurs as sodium ions enter, making the inside of the cell more positive. Repolarization happens when potassium exits and sodium channels close. Hyperpolarization can occur briefly as potassium channels stay open longer. The action potential propagates down the axon because depolarization opens sodium channels in the next segment. It moves unidirectionally because the previous segment is in a refractory period

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What is the cue for the release of neurotransmitters? What proteins dock the vesicles? Can you describe the events that lead to the release of neurotransmitters?

The release of neurotransmitters occurs when an action potential reaches the presynaptic terminal, causing voltage-gated calcium channels to open. The influx of calcium ions signals the vesicles to prepare for release. SNARE proteins mediate the docking of these vesicles at the membrane. Once docked, the vesicles fuse with the presynaptic membrane in a calcium-dependent process, allowing neurotransmitters, such as ACh, to be released into the synaptic cleft. This release ensures that the signal can be transmitted to the postsynaptic cell, triggering a response.

4
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What are the different receptors that acetylcholine activates? What mechanism do they signal through? How is this neurotransmitter removed from the synaptic cleft?

Acetylcholine activates two types of receptors: nicotinic and muscarinic. Nicotinic receptors are ligand-gated ion channels that let sodium enter, causing depolarization and excitatory responses. Muscarinic receptors are G protein–coupled and can either excite or inhibit cells depending on the tissue. After acetylcholine acts on its receptors, it is broken down by acetylcholinesterase into acetate and choline. The choline is recycled to make more acetylcholine, allowing repeated signaling at the synapse

5
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Can you describe the process of long-term potentiation?  

Long-term potentiation is when repeated activity at a synapse makes the connection stronger over time. Glutamate from the presynaptic neuron activates AMPA and NMDA receptors on the postsynaptic neuron. Normally, NMDA is blocked by magnesium, but when the cell is depolarized, the block is removed and calcium flows in. This calcium signal causes the postsynaptic neuron to add more receptors and send signals back to the presynaptic neuron to release more glutamate. Together, these changes make the synapse stronger and more responsive.