9. A) What are two scaffolding proteins that localize NMDA and AMPA receptors at the post-synaptic membrane of excitatory glutamatergic synapses? | B) What are two synaptic proteins that interact with each other and span the synaptic cleft of excitatory and inhibitory synapses? C) What are two scaffolding proteins that localize Cys-loop GABA receptors at the post-synaptic membrane of inhibitory synapses? A. B. C.

9. A) What are two scaffolding proteins that localize NMDA and AMPA receptors at the post-synaptic membrane of excitatory glutamatergic synapses? | B) What are two synaptic proteins that interact with each other and span the synaptic cleft of excitatory and inhibitory synapses? C) What are two scaffolding proteins that localize Cys-loop GABA receptors at the post-synaptic membrane of inhibitory synapses? A. B. C.

Human Physiology: From Cells to Systems (MindTap Course List)

9th Edition

ISBN:9781285866932

Author:Lauralee Sherwood

Publisher:Lauralee Sherwood

Chapter4: Principles Of Neural And Hormonal Communication

Section: Chapter Questions

Problem 4TAHL: Assume presynaptic excitatory neuron A terminates on a postsynaptic cell near the axon hillock and...

See similar textbooks

Similar questions

Clostridium tetani toxin blocks the exocytosis of GABA. A. What anatomical part of a pre-synaptic neuron would be affected by this? B. How would a post-synaptic neuron’s likelihood of experiencing an action potential be affected by this toxin? C. Explain, using at least TWO of the following terms: threshold, depolarization, repolarization, hyperpolarization, summation, IPSP, EPSP, exocytosis
Calcium entry through NNDA receptor can potentiate synaptic transmission through the following mechanisms EXCEPT: a.) Insertion of AMPA receptors to postsynaptic membrane b.) Synthesis of NO to increase presynaptic transmitter release c.) Phosphorylation of AMPA receptors d.) Slowing down glutamate reupdate, so it remains longer in the synapse
a) Describe the behavior of an unaffected neuron sitting at its membrane resting potentialstimulated by a suprathreshold stimulus.b) Now, add the effects of the consumption of the Fugu toxin and stimulate that neuron with a supra-threshold stimulus.- Describe (and/or diagram) the effect on the membrane potential by supra-thresholdstimulation under this condition.c. Using any ONE (1) of the following three (3) means we have used to interpret the resultingmembrane potential for a neuron, describe the effect of the Fugu toxin on a neuron:i) Goldman’s equationii) “Driving” toward Ex of most permeable ioniii) Movement/flow of charge + charges
Why was the postsynaptic CA1 neuron voltage clamped to +30 mV? To stimulate insertion of AMPA receptors into the postsynaptic membrane To move NDA receptors into the synapse from an extrasynaptic site To cause coordination between the pre- and postsynaptic neuron To increase conductance of the NMDAR by removing the Mg?* block To stimulate AMPA receptors, which in turn activate NMDA Rs Explain the results obtained when AP5 was applied while the neuron was held at +30 mV. What is the interpretation of the result?
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.
3.) Signals are passed from axon to axon when neurotransmitter molecules are released from the presynaptic axon and diffuses across a small distance, called the synaptic cleft, to reach the post synaptic axon. If the neurotransmitter released by the presynaptic axon is dopamine and the diffusion distance across the synaptic cleft is 20 nm then how long will it take to pass the signal? The viscosity of the interstitial fluid in the synapse is 0.012 Pa*s. (You must look up dopamine properties to solve) Synapse Suiknce Facts aut Synaptic vesicle Voltage-gated Ca? /channel Presynaptic neuron Neurotransmitter molecules Synaptic cleft lon channel receptor Postsynaptic- neuron
Describe the 3 main steps for activation of receptor tyrosine kinases.
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).
Given the steps shown below, which of the following is the correct sequence for transmission at a chemical synapse? 1. neurotransmitter binds with receptor 2. sodium ions rush into neuron's cytoplasm 3. action potential depolarizes the presynaptic membrane 4. ion channel opens to allow particular ion to enter cell 5. synaptic vesicles release neurotransmitter into the synaptic cleft O 1, 2, 3, 4, 5 O 5, 1, 2, 4, 3 O 2, 3, 5, 4, 1 O4, 3, 1, 2, 5 O 3, 2, 5, 1, 4
Let’s say the synapses of a neuron’s dendrites are filled with glutamate-gated channels which, when activated by glutamate, cause an excitatory postsynaptic potential (EPSP) in the neuron. In one instance, glutamate is released at all of the synapses simultaneously and this leads to an action potential in the neuron. A) What type of summation of PSPs is this? Why? B) List the sequence of steps that occur starting from binding of glutamate to the glutamate-gated channels at the synapses and ending with the membrane potential at the axon hillock returning to resting potential at the end of the action potential. (Include all the changes in voltage-gated channels underlying the action potential.)
1.1 What would be the effect of blocking neurotransmitter degradation on neurotransmitter concentration at the synapse? 1.2You are studying an excitatory synapse that is not strong enough to evoke a postsynaptic action potential. Would the probability of a postsynaptic potential increase or decrease after blocking neurotransmitter degradation? 1.3 ) You are studying an excitatory synapse that evokes a postsynaptic action potential. Would the probability of a postsynaptic potential increase or decrease after blocking presynaptic voltage-gated calcium channels?
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?