Briefly describe how silent glutamatergic synapses become activated during long term potentiation, describing all of the key neurotransmitters and their post-synaptic receptors and events that give rise to the process.
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Briefly describe how silent glutamatergic synapses become activated during long term potentiation, describing all of the key neurotransmitters and their post-synaptic receptors and events that give rise to the process.
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- 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 occurWhat 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.The correlation between neurons can explain the basis of the synaptic modification, that is, how much they can connect to each other or if they are not synchronized, how much they can lose or weaken their connections. Draw a picture of an excitatory synapse such as glutamatergic with its receptors between the pre- and postsynaptic neuron.
- The therapeutic effect of Aricept (generic donepezil) is due toA: binding of the drug to voltage-gated sodium channels.C: the drug producing an IPSP on the postsynaptic membrane.D: the drug causing the reuptake of acetylcholine at the synapse.E: the drug maintaining higher concentrations of acetylcholine at synapseNervous system functions that directly employ acetylcholine neurotransmitters are referred to as cholinergic. Drugs that might be therapeutic in treating the symptoms of dopamine loss in Parkinson’s disease could include multiple choice 1 dopaminergic agonists and cholinergic antagonists. dopaminergic antagonists and cholinergic antagonists. dopaminergic antagonists and cholinergic agonists. dopaminergic agonists and cholinergic agonists. 2. From the information provided, drugs used to treat Parkinson’s disease symptoms will act at which location? multiple choice 2 The globus pallidus The substantia nigra The striatum 3. Which of the following might be therapeutic in the treatment of Parkinson’s disease symptoms? multiple choice 3 all of these choices listed may be therapeutic increasing dopamine receptor responsiveness monoamine oxidase inhibition increasing dopamine release decreasing dopamine…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:)
- 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?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 abovePhotoreceptor 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?
- Explain how the binding of heroin to presynaptic neurones raises the probability of action potentials in the postsynaptic neurone. asap typed onlyThere 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.explain the simplified version of the synaptic process resulting in long-term potentiationand explain the roles of AMPA and NMDA receptors; glutamate; sodium, calcium, and magnesium ions in strengthening a synapse.