What's the consequence of glutamate release when the postsynaptic membrane expresses NMDA but not AMPA receptors? a. NMDA receptors conduct sodium in the absence of a membrane depolarization b. NMDA receptors couple to G-proteins; activation opens up downstream sodium channels c. Calcium passively diffuses into the neuron triggering neurotransmitter release d. Magnesium blocks the pore of the NMDA channel prohibiting sodium influx

What's the consequence of glutamate release when the postsynaptic membrane expresses NMDA but not AMPA receptors? a. NMDA receptors conduct sodium in the absence of a membrane depolarization b. NMDA receptors couple to G-proteins; activation opens up downstream sodium channels c. Calcium passively diffuses into the neuron triggering neurotransmitter release d. Magnesium blocks the pore of the NMDA channel prohibiting sodium influx

BIOLOGY:CONCEPTS+APPL.(LOOSELEAF)

10th Edition

ISBN:9781305967359

Author:STARR

Publisher:STARR

Chapter29: Neural Control

Section: Chapter Questions

Problem 3SA: Action potentials occur when ______. a. potassium gates close b. a stimulus pushes membrane...

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Glutamate's effect when it binds with protein receptors on the post synaptic membrane is to: a. Initiate movement of potassium ions out of the membrane b. Initiate movement of sodium ions into the membrane c. Initiate movement of sodium ions out of the membrane d. Initiate movement of potassium ions into the membrane GABA is an example of an inhibitory neurotransmitter. Drugs that increase the level of GABA are used to treat diseases such as epilepsy where the signal transmission needs to be impaired. The effect of the inhibitory neurotransmitter on the postsynaptic membrane is to: a. hyperpolarize the postsynaptic membrane b. decrease the threshold level c. depolarize the postsynaptic membrane d. maintain the resting potential Calcium is vital for bone growth, but it's also an important part of neural transmission. Calcium is required for the axon terminal to: a. Reuptake the neurotransmitter via exocytosis b. The neurotransmitter to be released by endocytosis c. The neurotransmitter…
(b) Describe or draw the response you would observed in cell C if an action potential occurred in cel B, closely followed by an action potential in cell A. = glutamate = AMPA receptor = GABA, receptor = GABA
What does a ligand-gated channel require in order to open?a. increase in concentration of Na+ ionsb. binding of a neurotransmitterc. increase in concentration of K+ ionsd. depolarization of the membrane
There is a toxin extracted from pufferfish called tetrodotoxin (TTX), which completely inhibits (blocks) voltage-gated sodium channels. In low doses it can cause a slight numbness (people eat contaminated pufferfish sometimes!), in high doses it is lethal. Why is this the case? It prevents glutamate uptake and reuptake, causing seizures in the brain Ob. It causes excess neuronal activity, leading to excitotoxicity and cell death It destroys myelin around axons, slowing action potential propagation It prevents action potentials from being initiated, stopping all synaptic transmission O 0 o o
Action potentials propagate in one direction because of: O K+ Voltage-gated Channels become inactive for a while O Nat Voltage-gated Channels become inactive for a while O K+ nongated Channels become inactive for a while O Nat nongated Channels become inactive for a while
What is the difference between inactivate and closed Na+ channels?Explain how a salty flavor is transduced into an action potential. Describe each step in an action potential
A drug specifically blocks the Na+/K+ ATPase pump. What effect might this have on the action potential? O It will shorten the duration of the action potential as there will not be as many ions available to cross the membrane. None, as action potentials rely on channels for Na+ and K+ to cross the membrane, not pumps. It will not have an immediate effect, but eventually action potentials will stop as the Na+ and K+ gradients are depleted. It will make action potentials more likely to occur as the pump normally makes the cell more negative, so without it the membrane will reach threshold more easily.
Tetrodotoxin from pufferfish is a poison that blocks voltage-gated Na+ channels. Therefore it directly blocks exocytosis of neurotransmitter O action potentials excitatory graded potentials inhibitory graded potentials
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?
What causes NMDA receptors to open? Glutamate binding and depolarization of the membrane Glutamate binding O Depolarization of the membrane O GABA binding
"The local anesthetic, novacaine, used by most dentists blocks voltage-gated Na+ channels. Why would it result in numbness (loss of feeling)?" It prevents action potentials from occurring It prevents local potentials from occurring It prevents the membrane potential from returning to normal It prevents exocytosis of neurotransmitter O O
Which of the following events correctly ranks steps in an action potential? 1. Voltage-gated sodium and potassium channels transition from closed to open states allowing sodium ions to enter and potassium ions to exit. 2. Voltage-gated sodium channels transition from open to inactivated states. 3. Ligand-gated sodium channels are triggered to open. 4. Peak potassium permeability. 5. Peak sodium permeability. 6. Membranes hyperpolarize due to more potassium ions exiting cell and neuron enters refractory period. 7. Critical threshold is achieved. O 3, 1, 7, 5, 2, 4, 6 O 3, 7, 1, 5, 4, 6, 2 O 3, 4, 1, 2, 6, 7,5 O 6, 7, 3, 2, 5, 4, 1 O 7, 5, 3, 1, 4, 6, 2 4, 6, 3, 7, 5, 2, 1