In the glutamate-glutamine cycle, which of the following occurs?O Glutamate and GABA are released by astrocytes and taken up by nearby neuronsO Microglia scavenge glutamate and GABA from the synapseООAmmonia is produced by glia as a byproduct of the cycleO Glutamine is released by astrocytes and taken up by nearby neuronsGlutamine synthetase is found exclusively in microglia

The glutamate-glutamine cycle is a crucial metabolic pathway that occurs in the central nervous…

In the glutamate-glutamine cycle, which of the following occurs? Glutamate and GABA are released by astrocytes and taken up by nearby neurons Microglia scavenge glutamate and GABA from the synapse Ammonia is produced by glia as a byproduct of the cycle Glutamine is released by astrocytes and taken up by nearby neurons Glutamine synthetase is found exclusively in microglia

In the glutamate-glutamine cycle, which of the following occurs? Glutamate and GABA are released by astrocytes and taken up by nearby neurons Microglia scavenge glutamate and GABA from the synapse Ammonia is produced by glia as a byproduct of the cycle Glutamine is released by astrocytes and taken up by nearby neurons Glutamine synthetase is found exclusively in microglia

Anatomy & Physiology

1st Edition

ISBN:9781938168130

Author:Kelly A. Young, James A. Wise, Peter DeSaix, Dean H. Kruse, Brandon Poe, Eddie Johnson, Jody E. Johnson, Oksana Korol, J. Gordon Betts, Mark Womble

Publisher:Kelly A. Young, James A. Wise, Peter DeSaix, Dean H. Kruse, Brandon Poe, Eddie Johnson, Jody E. Johnson, Oksana Korol, J. Gordon Betts, Mark Womble

Chapter12: The Nervous System And Nervous Tissue

Section: Chapter Questions

Problem 7ILQ: Watch this video (http://openstaxcollege.org/l/summation) to learn about summation. The process of...

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Glutamate is the major excitatory neurotransmitter in the brain. Because too much glutamate can cause excess Ca+2/Na+2 influx and excitatory in post-synaptic cells, the balance between excitation and inhibition must be tightly regulated. Calling upon only mechanisms that are directly part of the glutamate life cycle, describe two ways that you could experimentally limit or prevent glutamate excitotoxicity.
mbing fiber depolarizes mbrane potential to en Ca2+ channels. tage-gated channel 2+ Ca²+ Release 2+ Ca²+ Endoplasmic reticulum removal of AMPA receptors from the postsynaptic membrane. insertion of AMPA receptors into the postsynaptic membrane O increase in intracellular Ca2+ via voltage-gated Ca2+ channels O DAG- and Ca2+-mediated activation of PKC increase in intracellular Ca2+ via endoplasmic reticulum IP3 receptors
Which statement is true regarding GABA and Glutamate? Glutamate signaling is only required for the development of glutamatergic synapses O GABA is always inhibitory Glutamate is recycled with the aid of glial cells at the synapse O Neither glutamate nor GABA are very prevalent in the CNS
Parkinson’s disease is a devastating, progressive disorder ofthe central nervous system. Damage to dopaminergic nervetracts in the brain causes tremors and impaired musclecoordination. An early-onset (inherited) form of the diseasehas been linked to a defective protein, now called parkin.Parkin has E3 activity. Describe, in general terms, howneurons with this defective protein are damaged.
Which of the following is true of ACh (acetylcholine)? O It cannot be degraded within the synaptic cleft to which it was released; it must be internalized and degraded by the cell that receives it O It is always excitatory because it causes the entrance of Na+ into a cell which leads to an increase in intracellular mV O It is released via exocytosis from the axon terminal of a somatic motor neuron O It is released via exocytosis from all pre-ganglionic motor neurons of the ANS
A quanta holds about 10,000 molecules of ACh. How many quanta are exocytosed during a single presynaptic AP? What controls or determines the total number of quanta released? Is this under physiological control?
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.
Watch this video (http://openstaxcollege.org/l/summation) to learn about summation. The process of converting electrical signals to chemical signals and back requires subtle changes that can result in transient increases or decreases in membrane voltage. To cause a lasting change in the target cell, multiple signals are usually added together, or summated. Does spatial summation have to happen all at once, or can the separate signals arrive on the postsynaptic neuron at slightly different times? Explain your answer.
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
Arrange following the boxed information in sequence regarding the dissociation and reassociation of G proteins following the activation of a G protein coupled receptor. GTP-bound Ga, dissociates from B and y cuhunits Gas exchanges GTP for GDP Gas reassociates with By subunits and the rorentor reforms Binding of the ligand to a G-protein rounled recentor GTP-bound Gas binds and activates adenvlul rurlase GTP is hydrolyzed and GDP bound Gas suhunit dissoriates Conformational change Increased synthesis of CAMP from ATP
Changes in intracellular Ca2+ is one of the main governing factors that determines the direction of plasticity (i.e., whether a synapse potentiates or depresses). Provide a general mechanism to explain how changes in intracellular Ca2+ can result in either synaptic depression or synaptic potentiation (refer to our discussion on kinases and phosphatases).
apucreceptors ava ble at the synapse are reflected in this number. Question 2: In this chapter, we discussed a GABA-gated ion channel that is permeable to Cl. GABA also activates a G-protein-coupled receptor called the GABA receptor, which causes potassium-selective B channels to open. What effect would GABAB receptor activation have on the membrane potential? GABAB receptor activation causes potassium-selective channels to open. As a result this bringhs the