Bio Systems (Neurons) Mastering Bio

25 July 2022
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question
Neuron Structure
Neuron Structure
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Axon hillock: where axon connects to cell body ligand-gated channels: connects synaptic terminal to another cell Synaptic terminal: End of axon (deditos) voltage-gated channels: between myelin sheath The structures of a neuron play specific roles in receiving information from one cell, generating and propagating an action potential (sometimes over very long distances), and then passing the information along to another cell.
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Ion Movements at resting potential
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Voltage gated Na+ and K+ closed. Sodium-potassium pump: Na+ out and K+ in Non-gated K+: K+ out Non-gated Na+: Na+ in At resting potential, the membrane potential remains constant at about -70 mV. This means that there is no net movement of ions across the membrane. Assuming that Na+ and K+ are the only ions that move at resting potential, Na+ movement out of the cell through the sodium-potassium pump is balanced by an influx of Na+ through the non-gated Na+ channels. Conversely, K+ movement into the cell through the sodium-potassium pump is balanced by an outward movement of K+ through the non-gated K+ channels.
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Suppose that an artificial non-gated K+ channel could be inserted into the plasma membrane of an axon at resting potential (membrane potential = -70 mV). Assume that the axon has not recently produced an action potential. What would happen when an artificial K+ channel is inserted into an axon membrane at resting potential? (next 3 Qs) In what direction will the K+ ions move through the artificial channel
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Out of the cell
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Does the K+ concentration gradient promote or impede the movement of K+ ions through the artificial channel?
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promote
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Does the membrane potential promote or impede the movement of K+ ions throught the artificial channel
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impede
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How does the movement of K+ ions through the artificial channel affect the membrane potential?
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causes a hyperpolarization At resting potential, the pumping of K+ ions into the cell by the sodium-potassium pump is balanced by the movement of K+ ions out of the cell through non-gated K+ channels. If an artificial K+ channel is inserted into the membrane at resting potential, K+ ions will also move out of the cell through that channel. The K+ ions moving through the artificial channel move along their concentration gradient, but against the membrane potential. The K+ movement further decreases the positive charge inside the cell, so the membrane potential becomes more negative (hyperpolarization).
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Under most circumstances, once an axon's membrane potential reaches threshold (about -55 mV in mammals), an action potential is automatically triggered. The graph below shows the changes in membrane potential that occur in an axon membrane that is initially at resting potential. In response to a stimulus, the membrane slowly depolarizes until the membrane potential reaches a particular value, called threshold. At threshold, a rapid depolarization of the membrane occurs and an action potential is initiated. Sequence of events:
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1. membrane potential reaches threshold 2. many voltage-gated Na+ channels open 3. Na+ ions rush into the cell 4. membrane potential rises (depolarizes) rapidly Once the membrane potential reaches threshold, the voltage-gated Na+ channels open and the Na+ ions move into the cell (moving down their electrochemical gradient). This influx of positive ions makes the inside of the cell less negative compared to the outside, and the membrane potential rises (depolarizes) rapidly.
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The fixed pattern of changes in membrane potential during an action potential is coordinated by the sequential opening and closing of voltage-gated ion channels. Can you identify the status (open/closed) of the voltage-gated Na+ and K+ channels during each phase of an action potential?
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a. resting potentialL: Na+ and K+ cahnnels closed b. rising phase: Na+ open; K+ closed c. falling phase: Na+closed; K+ open d. undershoot: Na+ closed; K+ open e. resting potential: Na+ and K+ closed During the rising phase, the membrane potential becomes less negative because voltage-gated Na+ channels are open and Na+ ions enter the cell. During the falling and undershoot phases, the membrane potential becomes more negative because voltage-gated K+ channels are open (while voltage-gated Na+ channels are closed) and K+ ions leave the cell. At resting potential, both types of voltage-gated channels are closed and no ions move through the voltage-gated channels.
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The strength of a stimulus (for example, whether you feel a slight pain versus an intense pain) determines the number of action potentials sent along an axon. As the graphs show, a strong stimulus produces more action potentials spaced more closely together than a weak stimulus. The time between when a first action potential ends and a second action potential can be triggered is determined by the axon's refractory period. A second action potential cannot be triggered until the end of the refractory period. Which determines when refractory period ends?
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how long it takes for the voltage-gated Na+ channels to reactivate at the end of an action potential During the refractory period, an action potential cannot be triggered even if the membrane potential reaches threshold because the voltage-gated Na+ channels are inactive. The Na+ channels must reactivate before Na+ ions can move into the cell again, and the rising phase of the second action potential can begin. In this way, the refractory period determines how closely one action potential can follow another.
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An action potential moves along an axon due to the sequential opening of voltage-gated Na+ channels. The diagram below shows voltage-gated Na+ channels separated by a short distance in the plasma membrane of an axon. Initially (left panel), only channel (a) is open. Within a very short time (right panel), channel (b) also opens. What causes the second voltage-gated Na+ channel to open?
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After the first channel opens, the movement of many types of ions (both inside and outside the cell) alters the distribution of charges near the second channel, causing it to open. When Na+ ions enter the cell through the first channel, the charge distribution across the membrane changes. Inside the cell, the increase in Na+ ions near the first channel makes that region more positive; as a result, negative ions are attracted to the region, while positive ions are repelled. Conversely, outside of the cell, the loss of Na+ ions makes the region near the first channel more negative; as a result, positive ions are attracted to that region, while negative ions are repelled. Together, all of these ion movements alter the charge (and thus the membrane potential) at the neighboring channel, allowing it to reach threshold.
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There are two properties that affect the conduction speed of an action potential along an axon: the axon's diameter and whether or not the axon is myelinated. Slowest --> Fastest conduction speed
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1. Non-myelinated invertebrate axon (20 diameter) 2. Non-myelinated invertebrate axon (30 diameter) 3. Non-myelinated invertebrate axon (40 diameter) 4. Myelinated vertebrate axon (30 diameter) For non-myelinated axons, the larger the diameter of the axon, the faster the conduction speed of an action potential. However, even the smallest myelinated axons are much faster than the largest non-myelinated axons (the squid axon, for example).
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Chemical synapses transmit information from the sending (presynaptic) cell to the receiving (postsynaptic) cell in the form of neurotransmitters. The release of neurotransmitter into the synaptic cleft and the resulting changes in the membrane potential of the postsynaptic cell (postsynaptic potentials) all depend on the presence of several different types of gated ion channels and the distribution of these channels in the pre- and postsynaptic cells. The image here illustrates a chemical synapse.
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Presynaptic Cell: a) synaptic terminal: Voltage gated Na+ & K+ b) presynaptic membrane: voltage gated Na+; K+ and Ca2+ Postsynaptic Cell: c) postsynaptic membrane: ligand-gated d) plasma membrane of cell body: none e) axon hilloc: Voltage gated Na+ and K+ Voltage-gated Na+ and K+ channels are found only in membranes that propagate action potentials. Membranes found in a chemical synapse that propagate action potentials are the membrane of the synaptic terminal, including the presynaptic membrane, and the membrane of the axon hillock (and axon) of the postsynaptic neuron. Voltage-gated Ca2+ channels, which help regulate the release of neurotransmitter from the presynaptic neuron, are found only in the presynaptic membrane. Ligand-gated ion channels, which open in response to neurotransmitter in the synaptic cleft, are found only in the postsynaptic membrane. Finally, there are no gated ion channels in the plasma membrane of the cell body of the postsynaptic cell. For this reason, postsynaptic potentials are not propagated along the membrane of the postsynaptic cell in the same way that an action potential is propagated along a membrane containing voltage-gated Na+ and K+ channels.
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All chemical synapses exhibit the same general sequence of events during the transmission of information across the synaptic cleft. This sequence is always initiated by an action potential that travels down the presynaptic cell (the sending neuron) to its synaptic terminal(s). Sequence of events?
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Action potential enters the presynaptic membrane: a) Ca2+ channels in presynaptic membrane open briefly b) Ca2+ ions enter presynaptic cell c) neurotransmitter-containing vesicles fuse with presynaptic membrane d) neurotransmitter released into presynaptic cleft e) neurotransmitter binds to ligand-gated ion channels in postsynaptic membrane; channels open f) neurotransmitter degraded or removed from cleft; ligan-gated ion channels close The sequence of events at a chemical synapse is centered around the release of neurotransmitter into the synaptic cleft, in response to an action potential in the presynaptic cell. Recall that it is the neurotransmitter that "transmits" information from the presynaptic cell to the postsynaptic cell. The following steps occur as a result of an action potential reaching a synaptic terminal of the presynaptic cell. The diagram below indicates where each step occurs in a chemical synapse. Presynaptic cell 1. Voltage-gated Ca2+ channels in the presynaptic membrane open briefly, allowing Ca2+ ions to enter the cell. 2. This higher cytosolic Ca2+ concentration in the synaptic terminal causes some synaptic vesicles to fuse with the presynaptic membrane. 3. By fusing with the presynaptic membrane, the synaptic vesicles release neurotransmitter into the synaptic cleft. Postsynaptic cell 4. The increased concentration of neurotransmitter in the synaptic cleft causes it to bind to ligand-gated ion channels in the postsynaptic membrane. As a result, the channels open. Ions may then diffuse through the channels, causing a change in the membrane potential of the postsynaptic cell. 5. Quickly, the neurotransmitter concentration in the synaptic cleft falls (due to degradation or removal), causing the release of neurotransmitter from the ligand-gated ion channels. As a result, the channels close.
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The binding of neurotransmitter to ligand-gated ion channels in the postsynaptic membrane causes these channels to open. As soon as the neurotransmitter is removed from the synaptic cleft, the ligand-gated ion channels close. In the brief time these channels are open, ions are able to diffuse across the postsynaptic membrane down their electrochemical gradient. The result is a postsynaptic potential, a brief change in the membrane potential of the dendrites and cell body of the postsynaptic cell. There are two types of postsynaptic potentials: excitatory postsynaptic potentials (EPSPs) and inhibitory postsynaptic potentials (IPSPs). An EPSP is excitatory because it makes it more likely that the axon of the postsynaptic cell will trigger an action potential. Conversely, an IPSP is inhibitory because it makes it less likely that the axon of the postsynaptic cell will trigger an action potential.
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excitatory postsynaptic potential (EPSP): -brings the postsynaptic membrane potential closer to threshold -depolarizes the postsynaptic membrane -results from the movement of Na+ ions into postsynaptic cell inhibitory postsynaptic potential (IPSP): -moves the postsynaptic membrane potential farther away from threshold -hyperpolarizes the postsynaptic membrane -results from the movement of K+ ions out of the postsynaptic cell both: -it is a graded potential Excitatory postsynaptic potentials (EPSPs) are excitatory because they make the postsynaptic neuron more likely to generate an action potential by depolarizing the membrane (making the membrane potential less negative) and bringing the membrane potential closer to threshold. This is often accomplished by opening ligand-gated Na+ channels in the postsynaptic membrane, which allows Na+ ions to enter the cell. In contrast, inhibitory postsynaptic potentials (IPSPs) make it more difficult for the postsynaptic neuron to produce an action potential by hyperpolarizing the membrane (making the membrane potential more negative) and moving the membrane potential farther from threshold. This is often accomplished by opening ligand-gated K+ channels in the postsynaptic membrane, which allows K+ ions to leave the cell. Regardless of whether they are excitatory or inhibitory, all postsynaptic potentials are graded, meaning that their magnitudes are variable. (Action potentials, on the other hand, are all-or-none events.) And because a postsynaptic potential is not propagated like an action potential, its magnitude decreases with distance from the synapse along the cell body.
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The graph below shows the membrane potential measured at the axon hillock of the postsynaptic neuron. Each target indicates a change in the membrane potential at the axon hillock caused by a postsynaptic potential at one of the four synapses. Summation occurs when two or more postsynaptic potentials overlap in time; that is, one postsynaptic potential begins before the membrane has returned to resting potential after a previous postsynaptic potential. When such overlap occurs, the membrane potential measured at the axon hillock is the sum of the two (or more) overlapping postsynaptic potentials.
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a) I2 b) E2 c) E1 d) I1 e) E2 f) E1 By analyzing each change in the membrane potential at the axon hillock of the postsynaptic neuron, you can tell which presynaptic neuron produced the change. For example, when the membrane potential at the axon hillock becomes more negative (hyperpolarizes), you know that an inhibitory postsynaptic potential (IPSP) was produced at the synapse. Conversely, when the membrane potential at the axon hillock becomes less negative (depolarizes), you know that an excitatory postsynaptic potential (EPSP) was produced at the synapse. Because postsynaptic potentials decrease in magnitude with distance from the synapse, a smaller change in the axon hillock's membrane potential indicates that the presynaptic neuron that produced that potential is farther away. Conversely, a presynaptic neuron nearer the axon hillock will produce a larger change in the axon hillock's membrane potential. Finally, an action potential is generated in the postsynaptic cell only when the membrane potential at the axon hillock reaches threshold. In this example, both presynaptic neurons that produce EPSPs must produce potentials nearly simultaneously in order to bring the membrane potential at the axon hillock to threshold. This effect is called summation.
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Drug Opiate Lowest Concentration That Blocked Naloxone Binding Morphine Yes 6 × 10-9 M Methadone Yes 2 × 10-8 M Levorphanol Yes 2 × 10-9 M Phenobarbital No No effect at 10-4 M Atropine No No effect at 10-4 M Serotonin No No effect at 10-4 M (Next 6Q) The data from this experiment are expressed using scientific notation: a numerical factor times a power of 10. Remember that a negative power of 10 means a number less than 1. For example, the concentration 10-1 M (molar) can also be written as 0.1 M. What is the lowest concentration of morphine that blocked naloxone binding, in standard notation?
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0.000000006 M
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What result did the researchers obtain for atropine, in standard notation?
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no effect at 0.0001 M 10-4 is 0.0001.
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Compare the concentrations for methadone (2 × 10-8 M) and phenobarbital (10-4 M). Which concentration is higher and by how much?
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Phenobarbital's concentration is 5,000 times higher. The concentration of phenobarbital is 10-4 M, whereas the concentration of methadone is 2 × 10-8 M. The concentration of phenobarbital is higher by 10-4/(2 × 10-8) = 5 × 103 or 5,000 times.
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Which drugs blocked naloxone binding in this experiment?
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morphine, methadone, and levorphanol only
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Would phenobarbital, atropine, or serotonin have blocked naloxone binding at a concentration of 10-5 M?
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None of these drugs would have blocked naloxone binding at 10-5 M. None of these drugs had an effect at a concentration of 10-4 M, which is higher than 10-5 M. If they had no effect at the higher concentration, they would certainly not have had an effect at the lower concentration.
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Morphine, methadone, and levorphanol blocked naloxone binding in this experiment. What do these results indicate about the brain receptors for naloxone?
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They are specific for opiate drugs The three opiates blocked naloxone binding, whereas the three non-opiates did not block naloxone binding. These results indicate that the receptors for naloxone are specific for opiates.
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When the researchers repeated the experiment using tissue from mammalian intestinal muscles rather than brains, they found no naloxone binding. What does this result suggest about opiate receptors in mammalian intestinal muscle tissue?
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There are no opiate receptors in mammalian intestinal muscle tissue.