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.
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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.
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- The following diagram represents a typical serotonergic synapse. Where, specifically, do antidepressants work (e.g. SSRI)? Neurotransmitter Neurotransmitter transporter Аxon Synaptic vesicle terminal Voltage- gated Ca?+ channel Synaptic cleft Receptor Postsynaptic density Dendrite Neurotransmitter Synaptic Vesicle Neurotransmitter transporter (aka Reuptake transporter) Receptor O All of the aboveLet’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.)Besides the standard post- and pre-synapse that exchange information, non neuronal cell types also play a role in synaptic transmission. One of those are called astrocytes and can form a tripartite synapse. Explain the roles of astrocytes in synaptic transmission.
- 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?Give a detailed, step-by-step description of the stages of an action potential, including a description of and explanation for the refractory periods and the rising and falling phases as well as return to rest. In your explanation, make sure to include 1) summation principles, 2) key membrane potentials (values), 3) location of voltage changes along the membrane, 4) states of the various voltage-gated channels. The more detail, the better. There are 5 main steps.which one of the following statements is incorrect? a. temporal summation occurs when a single synaptic input is activated twice in succession, with the second postsynaptic potential occurring before the first postsynaptic potential is over. b. blocking voltage-gated k* channels in the presynaptic membrane of a typical chemical synapse is likely to reduce the amount of neurotransmitter released in response to a single action potential in the presynaptic axon. c. in the optic tectum of the hunting rattlesnake, spatial summation is used to combine inputs from visual and thermoreceptive layers in order to make a decision whether to strike at a mouse-like object. d. a single type of neurotransmitter can have different postsynaptic actions depending on the type of receptor to which it binds.
- Which of the following statements concerning synapses is FALSE? O A) Modulation of synaptic strength can be presynaptic of postsynaptic B) High frequency stimulation in the presynaptic neuron often leads to DECREASED neurotransmitter release O C) Modulation of synaptic strength can either be short term, lasting seconds, or long term, lasting as long as a lifetime. D) Agonists are drugs that mimic neurotransmitters and antagonists are drugs that block the action of neurotransmitters O E) Certain drugs prevent the reuptake of neurotransmitter from the synapseThere are a broad range of anti-epileptic medications currently on the market, with different therapies prescribed for different types and severities of the condition. Given what you have learned about synaptic transmission, which of the following could be a potential therapeutic approach to prevent the spreading of neuronal excitation? (3 correct answers, select all that apply) O A voltage-gated calcium channel blocker/inhibitor selective to glutamate-releasing neurons. O A voltage-gated calcium channel blocker/inhibitor selective to GABA-releasing neurons. O A glutamate receptor blocker (antagonist). O A GABA receptor antagonist. O A glutamate reuptake inhibitor. O A GABA reuptake inhibitor.Imagine that a toxin creates pores that are permeable to Ca2+. Describe its immediate effect on the resting potential of the neuron: identify which ions diffuse across the membrane, which direction they diffuse (and why), and whether this brings the neuron closer to or further from threshold potential. asap please
- Draw details of the repolarization phase of an action potential from the following descriptions of the sequences of AfterHyperPolarization (AHP) and AfterDePolarization (ADP) sequences. Make the distinct phases clear and noticeable (5 % each) A complex AHP consisting of a first component AHP, an ADP, and a second component AHP before repolarization to resting membrane potential a first fast AHP component, followed by a slower AHP, followed by a fast ADP, and a second late AHP component before repolarization to restIn the figure to the left, name the 4 phases of the action potential (Note: you have to write in where phase 4 occurs). Describe what happens in each phase with a focus on Na+ and K+ flow through channels and the membrane potential. Discuss the importance of threshold. How does this relate to the concept of APs being all or none?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. thanks a lot in advance:)