Assuming that ESre is a functioning neurotransmitter, what other ESre-specific components would we expect to find (and where) and what purpose do they serve (think about the entire process of synaptic transmission when answering)?
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- 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.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.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?A postsynaptic neuron has three presynaptic inputs from neurons X, Y, and Z. When X and Y are stimulated simultaneously and repeatedly, the postsynaptic neuron reaches threshold and undergoes an action potential. When X and Z are stimulated simultaneously, however, there is no change in the membrane potential of the postsynaptic neuron. Which of the following is correct? Select one: A. The simultaneous stimulation of X and Z is an example of temporal summation. O B. The simultaneous stimulation of X and Y is an example of temporal summation. O C. The repeated rapid stimulation of X is an example of spatial summation. O D. The stimulation of Y causes an IPSP in the postsynaptic neuron. O E. The stimulation of Z causes a hyperpolarization in the postsynaptic neuron.Would anyone be able to explain these different channels? I would like an explanation as to why voltage gated membranes are associated with axon membranes (although it's prob because of membrane potential differences and depolarization/hyperpolarization?), why ligand gated channels are primarily at synapses (via neurotransmitters?), etc.
- When an impulse arrives at the synapse, the synaptic vesicles open and release neurotransmitters into the cleft within a thousandth of a second. Within another ten thousandth of a second, these molecules have diffused across the cleft and bound to receptor sites in the effector cell. In what two ways is transmission across a synapse terminated so that the neuron’s signal is concluded?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.)Photoreceptor cells form glutamatergic synapses onto bipolar cells and when photoreceptor cells are depolarized the release of glutamate into the synapse is increased. One class of bipolar cells, (called OFF bipolar cells) have excitatory glutamate receptors in their post-synaptic specialization. What happens to the membrane potential of OFF bipolar cells when photoreceptors are illuminated?
- A chemical synapse is a type of synapse that occurs between two neurons and between a motor neuron and skeletal muscle fibers (i.e. at a Neuromuscular junction, NMJ). Compare and contrast the specific events that occur at chemical synapses at these two sites. Describe clearly how they are similar and how they are different, starting at the arrival of a nerve impulse at the pre-synaptic neuron and ending up with the changes observed at the postsynaptic membranes.During excitatory synaptic transmission, the electrical signal carried along the axon of a presynaptic neuron causes the release of neurotransmitters into the synapse and its sub- sequent reception by receptors on the postsynaptic neurons. The activation of receptors on the postsynaptic neurons then triggers the generation of the new action potential in that neuron. Both chemical and electrical neuronal signals are mediated by the movement of ions across the neuronal membrane. Which of the following correctly describes the movement of ions across neuronal membranes as an action potential is conducted down the neuron? A B с D At rest, the internal side of the membrane has an overall positive charge, but as the ac- tion potential moves down the neuron, more ions flow out of the neuron to neutralize the membrane. At rest, the internal side of the membrane has an overall positive charge, but as the ac- tion potential moves down the neuron, more ions flow into the neuron making the membrane…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).
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