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- What 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.71) Figure below illustrates the data from one of the original experiments that showed evidence for 'silent synapses'. Stimulation of CA3 axons resulted in no postsynaptic response when the CA1 neuron was voltage-clamped at -60 mV. +30 mV 30 response amplitude (PA) 20 10 Isnos 0 -10 -20 -60 mV 0 100 200 300 stimulus number AP5 400 600 700 a) Why was the postsynaptic CA1 neuron voltage clamped to +30 mV? (a) To stimulate insertion of AMPA receptors into the postsynaptic membrane (b) To move NMDA receptors into the synapse from an extrasynaptic site (c) To cause coordination between the pre- and postsynaptic neuron (d) To increase conductance of the NMDAR by removing the Mg2+ block (e) To stimulate AMPA receptors, which in turn activate NMDA Rs b) Explain the results obtained when AP5 was applied while the neuron was held at +30 mV. What is the interpretation of the result? (2-3 sentences.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
- Consider the circuit from Q5 (above). We want to add another inhibitory neuron to this circuit to increase the likelihood that neuron D will have an action potential. With which cell (A, B, C or D) should our new inhibitory neuron make a synapse to make it more likely that the post - synaptic neuron will have anaction potential?The diagram below shows a simple neural circuit with three pre - synaptic cells labelled 'A', 'B' and 'C', and a post - synaptic cell labelled 'D ' (see image below). Assume neurons A and B each have outputs of +2 and neuron C has output of -1.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 + chargesapucreceptors 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
- 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, exocytosis1.1 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?An effector neuron is a motor neuron that transmits impulses from the CNS to an effector (muscle or gland).In an experiment, it was determined that the effector neuron for muscle fibre 1 had a threshold level of –5 mV. The effector neuron for muscle fibre 2 had a threshold level of –16 mV. An electrical probe was used to stimulate these two effector neurons of the muscle fibres. Which of the following rows correctly identifies the reaction of each muscle fibre based on the applied stimulus voltage? Stimulus Voltage Muscle Fibre 1 Muscle Fibre 2 –20 mV Relaxed Contracted b. Stimulus Voltage Muscle Fibre 1 Muscle Fibre 2 –20 mV Contracted Relaxed c. Stimulus Voltage Muscle Fibre 1 Muscle Fibre 2 –10 mV Contracted Relaxed d. Stimulus Voltage Muscle Fibre 1 Muscle Fibre 2 –10 mV Relaxed Contracted
- Describe at least 2 processes at the synapse that shift the effect of an action potential of a pre synaptic cell on the response of a post synaptic cell.At the peak of the neuronal action potential, Vm is approximately +50 mV. Assuming normal intracellular and extracellular K+ concentrations ( [K+]o = 4 mM, [K+]i = 150 mM ), what is the driving force (in mV) that acts on K+ ions at the peak of the action potential?Depression is a condition in which sufferers may feel low mood, lack of motivation and sleep. It is caused by a lack of serotonin in the synaptic cleft of neurone pathways. Serotonin is a neurotransmitter. a) Describe how serotonin acts as a neurotransmitter. Using your understanding of synaptic transmission, explain how communication between neurones in serotonin pathways of the brain would be affected in someone with depression. b) Doctors use tubocurarine drug as an anaesthetic as it temporarily paralyses muscles. It blocks receptors at neuromuscular junctions. Why does this lead to paralysis?