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- Your current LTP experimental protocol is as follows: - Isolate a ‘silent synapse’ with only NMDA receptors in the postsynaptic membrane. - Induce LTP via low frequency presynaptic stimulation coupled with postsynaptic depolarization. You’re able to verify that the synapse has been potentiated, as there are now strong post-synaptic responses to presynaptic stimulation. But you’re unable to prove conclusively that this change was AMPA receptor-mediated. Explain how you will design an experiment to monitor the trafficking of AMPA receptors into the membrane during LTP using the electrophysiological tag, and how this technique works. Explain how your method utilizes 1) Visualization and 2) Electrophysiological recordings to quantify trafficking of AMPA receptors. Provide an example of how electrophysiological data can be interpreted support the hypothesis that LTP induction leads to the trafficking of AMPA receptors into the postsynaptic site.I have stimulated a neuron with dopamine for a second followed by treating it with cocaine and calcium chelating agent (which chelates out all calcium from the system making them unavailable for function), what will be the effect of such impulse on generating an action potential in the post-synaptic neuron? Will it be different if I pretreat the set of nerve cells with cocaine and calcium chelating agent followed by stimulating the neuron with dopamine? Justify your answer with proper reasoning in brief.discuss the excitatory NMDA receptor, the role of the Mg++ ion, and how NMDA activation can produce Long Term Potentiation (which could underlie memory). Finally, what is the seemingly unique involvement of neighboring glia cells in helping to regulate both GABA and Glutamate neurotransmission and why might that glia cell role occur
- 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).Reward-modulated spike-timing dependent plasticity (RSTDP) can be modelled as STDP with an eligibility trace. RSTDP provides an explanation for how a reward that occurs a short time after the stimulus (i.e., outside the STDP learning window) can nevertheless cause a change in the synaptic strengths. The activities of two neurons, labelled A and B, are being recorded and are observed to have similar average spiking rates. Both neurons are observed to change their firing rates in response to both a stimulus and a reward. Describe how the timing of the delivery of the reward could be manipulated so that, during the learning period, the activity of neuron A increased but the activity of neuron B decreased.what changes at the synapse underlie long-term potentiation. Select all that apply with explanation 1.A decreased number of receptors 2.An increase in transporters 3.An increased release of neurotransmitters 4.An increased number of receptors.
- Autnomic nervous system use arrows to show whether parasympathetic (p) or syspathic (s) fibers stimulate or inhibit or a dash for no parasympathetic interaction for each of the following construction of blood vessels of skin and abdominal viscera 2, salivation and digestive organ contractions 3,Erection or engorgement of genitalia 4, dilation of bronchioles for easier breathing 5, contraction of bladder and relaxation 6,contractions of arrector pill of hair arrector pill of hair follicles causing goose bumps 7,increase in blood glucose level by pancreatic serection coling with stress fight or fight responseAnswer the following questions regarding conduction of action potentials using the velocities given on p. 100: a. How long would it take for an action potential to travel 0.6 m along the axon of an unmyelinated neuron of the digestive tract? b. How long would it take for an action potential to travel the same distance along the axon of a large myelinated neuron innervating a skeletal muscle? c. Suppose there were two synapses in a 0.6 m nerve tract and the delay at each synapse is 1 msec. How long would it take an action potential and chemical signal to travel the 0.6 m now, for both the myelinated and unmyelinated neurons? d. What if there were five synapses?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.
- 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 theMatching (may not use al choices; may use some choices more than once) Sección 79. Site of action potential propagation 80. Myelin is found here 81. Voltage gated calcium channels are found here 82. Site of temporal summation 83. Structure involved with signal reception 84. Location of EPSPS Post-synaptic membrane Site of salutatory Conduction 85. 86. 87. Site of spatial summation 88. Ligand (chemical) gated channels are found here 89. _Pre-synaptic membrane Salto de columna A. Dendrites B. Soma C. Axon Hillock D. Aхon E. Synaptic knobWhat type of synaptic potential (if any; be sure to indicate if any modification is occurring as well) would occur if: a.) An MAO inhibitor type of antidepressant is functioning at an active dopaminergic synapse that increases the rate of sodium flowing into the cell. b.) Prozac is present at an active serotonin synapse where receptor activation increases the flow of potassium out of the cell.