Question 1: What does quantum release of neurotransmitters mean?
Answer: The basic unit of neurotransmitter release is the contents of a synaptic vesicle. Each vesicle contains several thousand transmitter molecules. The total amount of transmitter released at a synapse is a multiple of this number, depending on how many vesicles release their contents into the synaptic cleft. The amplitude of the postsynaptic EPSP is a multiple of the response to the contents of a vesicle. It reflects the number of transmitter molecules in a synaptic vesicle and the number of postsynaptic receptors available at the synapse.
Question 2: You apply acetylcholine and activate nicotine receptors on muscle cells. When Vm=-60mV, in which way will the current pass through the receptor channel? When Vm = 0 mV? When Vm = is 60 mV? Why
Answer: Neurotonic acetylcholine receptors are permeable to both sodium and potassium. When Vm = -60mV, the net current through the ach-gated ion channel is inward, toward the equilibrium potential of sodium, resulting in depolarization. At Vm = 60 mV, the net current through the ach-gated ion channel is directed outward, toward the equilibrium potential of potassium, causing the membrane potential to decrease positively. The critical value of the membrane potential when the direction of current flow is reversed is called the reversal potential. In this case, the reversal potential is 0 mV because this is the value between the equilibrium potentials of sodium and potassium. At 0 mV, no current flows.
Question 3: In this chapter, we discussed a GABA-gated ion channel that is permeable to Cl-. GABA can also activate a G-protein-coupled receptor called the GABAB receptor, causing potassium-selective channels to open. What effect does activation of GABAB receptors have on membrane potential?
Answer: The activated gaba-gated Cl- ion channel causes the cell membrane to reach the equilibrium potential of Cl-, which is -65mV. When the transmitter is released, the membrane potential is less negative than -65mV, and activation causes hyperpolarization. Activation of GABAB receptors results in the opening of potassium ion-selective channels. Therefore, activation of GABAB brings the membrane potential close to the equilibrium potential of potassium, which is -80 mV. When the transmitter is released, the negative value of the membrane potential is less than -80mV, and activation will also cause hyperpolarization. This channel may also affect neurons through shunt inhibition, allowing depolarizing currents from excitatory synapses to leak out. This in turn reduces the likelihood of action potentials occurring. However, G protein-coupled receptors act more slowly than GABA-gated Cl channels or typical excitatory synapses. Therefore, its effects will be slower and last longer.
Question 4: You think you have discovered a new neurotransmitter, and you are studying its effects on neurons. The response reversal potential induced by the new chemical was -60mV. Is the substance excitatory or inhibitory? Why
Answer: If a new chemical has a reversal potential of -60mV, it is likely to be inhibitory. The reversal potential reflects the types of ions that are permeable to the cell membrane after neurotransmitter application. A reversal potential of -60mV indicates that neurotransmitters activate ion channels, making the cell membrane more negative. If a neurotransmitter causes the cell membrane to move toward a more negative value than the action potential threshold, the neuron is less likely to fire the action potential, meaning it is inhibited.
Question 5: A drug called strinine, isolated from the seeds of a tree native to India and commonly used as a rat poison, blocks the action of glycine. Is strychnine an agonist or antagonist of glycine receptors?
Answer: Stychnine is an antagonist of glycine receptors. Mild phloemine intoxication can enhance startle and other reflexes, similar to euphoria. High doses abolish glycine-mediated inhibition in spinal cord and brainstem circuits. This results in uncontrollable seizures and uncontrolled muscle contractions, spasms, and paralysis of respiratory muscles. It can ultimately lead to a painful, painful death from suffocation. Question 6: How does nerve gas cause respiratory paralysis?
Answer: Nerve gases interfere with synaptic transmission at the neuromuscular junction by inhibiting acetylcholinesterase. Uninterrupted exposure to high concentrations of acetylcholine for just a few seconds causes a process called desensitization. During this process, the transmitter-gated channel remains closed despite the continued presence of acetylcholine. Normally, rapid destruction of acetylcholine by acetylcholinesterase prevents desensitization. However, if acetylcholinesterase is inhibited by nerve gas, acetylcholinesterase receptors will be desensitized and neuromuscular transmission will fail, resulting in respiratory paralysis.
Question 7: Why are excitatory synapses on the soma more effective at evoking action potentials in postsynaptic neurons than excitatory synapses on the dendritic tips?
Answer: Current entering a synaptic contact site must spread to the spike initiation zone, which must be depolarized beyond its threshold to generate an action potential. Furthermore, depolarization decreases with distance along the dendrite. Therefore, the effectiveness of excitatory synapses in triggering action potentials depends on how far away they are.
Synapses originate from the spike initiation region. Because the soma is closer to the spike initiation zone, excitatory synapses on the soma evoke action potentials more efficiently than excitatory synapses on the dendritic tips.
Question 8: What are the steps that lead to the increase in neuronal excitability when NE is released presynaptically?
Answer: When NE is released presynaptically, the steps to increase the excitability of a neuron are:
1. The NE receptor binding to the b receptor activates the g protein on the cell membrane.
2. The g protein activates adenylate cyclase.
3. Adenylyl cyclase converts ATP into the second messenger cAMP.
4. cAMP activates a protein, a kinase.
5. Kinase closes the potassium channel by attaching a phosphate group to the potassium channel. This causes a small change in membrane potential but increases membrane resistance, increasing the length constant of the dendrites. This enhances the response generated at a weak or distal excitatory synapse. This effect can outlive the transmitter.