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Nervous System AQs
Terms in this set (56)
What are the two divisions of the CNS? The PNS? In which division would sensory receptors be appropriately categorized? What is your rationale?
In the CNS, the brain and spinal cord. In the PNS, the cranial nerves and spinal nerves. Sensory receptors would be categorized in the PNS because sensory organs are the most peripheral extensions of sensory neurons.
How is it that brain cancer is fairly common, yet like muscle (myocytes) and fat cells (adipocytes), neurons do not mitotically divide? How does chemotherapy work?
Brain cancer is typically caused by glial cells, not neurons. Glial cells rapidly divide in the brain and they are more abundant, thus cancer may occur. Chemotherapy (taxol) works by targeting dividing cells (mitotic spindle apparatus) and halting cell division.
What glial cells in the PNS has a similar function to the astrocyte in the CNS? What is a node of Ranvier? Are they found in the CNS and PNS?
Glial cells in the PNS that have a similar function to astrocytes are satellite cells. A node of Ranvier is the region of an axon between myelinated regions (internodes). Nodes of Ranvier are found in both the CNS and PNS.
Comparing a neuron (specifically the axon portion) to the charging cord for your cell phone, what biological material surrounding an axon would be analogous to the plastic/rubber coating surrounding the wire of the cord itself? What is the portion of this material surrounding axons in humans?
Myelin sheaths surround our "wires" (axons). It insulates the neurons and increases action potential velocity.
Of the three structural classes of neurons, which are sensory? Motor? Which conduct information afferently? Efferently? What percentage of all neurons are interneurons? Where are they located?
Bipolar neurons are sensory afferent neurons (special senses). Unipolar neurons are sensory afferent neurons (somatic senses) and multipolar neurons are motor efferent neurons. 99% of all CNS neurons are interneurons.
What are dendritic spines? What is a soma? What is a nerve fiber? What are synaptic knobs?
Dendritic spines are elevations of dendrites where presynaptic neurons form a synapse. A soma is the cell body of a neuron. A nerve fiber is an axon. And a synaptic knob is the terminal end of an axon where neurotransmitters are stored and released.
What are the three components of a synapse? The synaptic cleft is nothing more than what? How is information transferred from the presynaptic cell to the postsynaptic cell?
The three components of a synapse are the presynaptic cell, synaptic cleft, and postsynaptic cell. The synaptic cleft is nothing more than extracellular fluid (space). The information is transferred from the presynaptic cell to the postsynaptic cell in the form of neurotransmitters.
In a disease such as multiple sclerosis where the immune system attacks myelin-synthesizing cells, which property or properties of neurons would be affected? How so?
The properties of neurons affected are action potential conduction. In demyelinating disorders there is damage to the myelin sheath and the axolemma since the immune system attacks these cells/membranes (autoimmune disease). Currents will leak out of the axon and result in a short of the signal (drop in action potential propagation).
Which MAP transports recycled vesicles from the axon terminal knob to the soma? Is this in the positive or negative direction? Which MAP transports secretory vesicles from the soma to the terminal knobs? Is this in the positive or negative direction? Which of the three components of the cytoskeleton do these MAPs "walk" along?
Dynein transports recycled vesicles from the axon terminal knob to the soma in the negative direction. Kinesin transports secretory vesicles from the soma to the terminal knobs in the positive direction. MAPs walk along microtubules.
In which portion of a neuron does a resting membrane potential (RMP) exist? In which portion of a neuron do graded (local) potentials occur? In which portion of a neuron do action potentials occur?
RMPs exist in all portions of a neuron. Graded (local) potentials occur in cell bodies, dendrites, internodes, and terminal knobs. Action potentials occur only in the nodes of Ranvier.
What is an equilibrium potential? What is the equilibrium potential value for NA? For K? How do these equilibrium potentials relate to the RMP? In other words, how did we experimentally determine that K is the ion primarily responsible for the establishment of an RMP?
The equilibrium potential is the membrane potential at which an ion is in equilibrium across the plasma membrane. The equilibrium potential for NA is +60 mV and -90 mV for Ca. If the only ions across the cell membrane are K ions, the resultant membrane potential would be -90 mV, which is very close to the actual membrane potential of the neuron (-70 mV).
What is the primary mechanism responsible for establishing an RMP? Hypothetically, how would your cells' RMP be affected if this mechanism went off-line (stopped working)?
The K leak channels are the primary mechanism responsible for establishing an RMP. If the K leak channels stopped working, the RMP would be very positive as the K would build up in the cell via the action of the Na/K pump.
What is the most abundant intracellular cation? What is the most abundant extracellular cation? What cation has the steepest concentration gradiant across the plasma membrane? Why is it crucial that there is a 1 mOsm difference in plasma solute concentration between our blood plasma and interstitial fluid?
The most abundant intracellular cation is K. The most abundant extracellular cation is Na. Ca2+ has the steepest concentration gradiant across the plasma membrane. It is crucial to have this difference in plasma solute concentration between our blood plasma and IF so that water will go into our blood stream to keep blood volume and blood pressure up.
If a cell at rest is -70 mV, what happens when Na+ enters it? K+ leaves it? Chloride enters it? If a cell goes from -70 mV to -60 mV is that a reduction or increase in membrane potential? Why? What is the TMP when a cell is at 0 mV?
As Na enters it, the cell becomes more positive and depolarized. If K leaves it, the cell becomes more negative or hyperpolarized. If chloride enters the cell, the cell becomes more negative, or hyperpolarized. If a cell goes from -70 to -60 this is a reduction in membrane potential because the cell is becoming less negative, so the polarity is being reduced. The TMP when is cell is at 0 mV there is no polarity across the membrane.
What is depolarization? How can it be achieved? What is a hyperpolarization? How can it be achieved? What is repolarization? How does this term relate to depolarization, hyperpolarization, and resting membrane potential?
A depolarization is a decrease in membrane potential. The membrane potential is becoming less negative or more positive. This can occur by Na or Ca2+ entering the cell. Hyperpolarization is an increase in membrane potential. The membrane potential is becoming more negative. This can occur by Cl- ions entering the cell or K ions exiting the cell. Repolarization is returning the RMP after a depolarization. A neuron becomes depolarized, fires an action potential, reaches RMP, and is hyperpolarized shortly.
Graded potentials are also referred to as local potentials. Why are these potentials referred to as "graded" potentials? Local potentials? What does it mean that the magnitude (amplitude) of a graded potential is variable? What does it mean that the change in membrane potential is directly proportional to the size of the stimulus? What does it mean that graded potentials are distance-limited?
The change in membrane potential is directly proportional to the magnitude of the stimulus. Graded potentials are also called local potentials because they only occur over small regions of the plasma membrane. If there is a greater stimulus (more ions entering the cell) there will be a greater change in membrane potential. Therefore, the change in membrane potential is directly proportional to the stimulus. Graded potentials are distance limited because diffusion is distance limited.
For a patient with hyper-neuronal activity (anxiety or PTSD), what could you inhibit/block to stop their neurons from generating the graded potentials thereby preventing their neurons from firing (undergoing action potentials)?
Receptors in the neuron that when opened, lead to EPSPs.
What does it mean that action potentials are variable in frequency? Fixed in magnitude? Can you compare and contrast the major differences between graded potentials and action potentials?
The frequency of action potentials along an axon is a major way in which information is coded. In general, a strong stimulus would have a greater action potential frequency than a weak one. The amplitude of an action potential is fixed for a specific neuron. Graded potentials may be depolarizing or hyperpolarizing depending on the stimuli where action potentials always are depolarizing. In graded potentials the amplitude is proportional to the stimuli where in action potentials is fixed.
What is the RMP value of a typical neuron? What is a threshold potential (TP)? What is a TP value for a typical neuron? What is the peak amplitude (in mV) of a typical neuron?
The RMP of a typical neuron is -70 mV. A threshold potential, which must be achieved in the axon hillock, is the potential at which the neuron will fire an action potential. The TP value for a typical neuron is -60 mV. The peak amplitude of a typical neuron is +30 mV.
I like to think of dendrites and the cell body of a neuron as AM receivers and the axon as an FM transmitter. Can you explain my rationale for this comparison based on AM/FM radio waves and neuron function?
Dendrites and cell body are like AM receivers since they receive sensory information and the amplitude of the graded potentials is modulated. The axon is like an FM transmitter since it transmits the information efferently and the frequency of this information is what is modulated.
Can you explain what a generator potential is? Receptor potential? How do the two differ from one another? What structural class of neurons do these potentials occur in?
A generator potential occurs at the end of a neuron that has ligand or mechanically gated channels that cause voltage gated channels to open, thus creating action potentials. A receptor potential involves two cells, a neuron with voltage gated sodium channels and an independent cell that generates some graded potential, the cell releases neurotransmitters. These types of potentials occur in sensory neurons.
What portion of a neuron can other neurons from synapses with? What is an excitatory postsynaptic potential (EPSP)? An inhibitory postsynaptic potential (IPSP)? In general, what types of potentials are EPSPs and IPSPs?
The cell body and dendrites are the portions of a neuron that other neurons can form synapses with. An EPSP is a depolarization while an IPSP is a hyperpolarization. EPSPs and IPSPs are graded (local) potentials.
What type of channels are involved in EPSPs? Neurotransmitters? Ions? What type of channels are involved in IPSPs? Neurotransmitters? Ions?
EPSPs use ligand-gated channels. The neurotransmitters are glutamate and the ions are Na+ or Ca2+. IPSPs are ligand-gated channels that use the neurotransmitter GABA and the ion Cl-.
What are the two regions of the spike initiation zone of a neuron? What types of channels are located in each area? What type of potentials occur in each area?
The axon hillock and the initial segment of an axon are the regions of a spike initiation zone. The axon hillock has ligand-gated Na channels. The initial segment has voltage-gated Na channels and voltage-gated K channels. The axon hillock undergoes graded potentials and the initial segment undergoes action potentials.
How does the brain of a neuron work? In other words, can you explain how temporal and spatial summation affect the threshold potential? Where does the action potential first occur in a neuron? What are the events that lead up to the action potential occurring? If a postsynaptic cell synapses with 32 different EPSPs totaling 42 mV, and one IPSP of -32 mV, would the initial segment of the axon fire and action potential? Why?
The brain of a neuron is a calculator that does addition. It adds incoming positive charge to incoming negative charge. Temporal summation is when one presynaptic neuron is fired repeatedly over time. Spatial summation is when several presynaptic neurons fire simultaneously. In either case, many ions accumulate in the postsynaptic cell. Positive charge pushes K towards the axon hillock. Negative charge draws K away from the axon hillock. The action potential first occurs in the initial segment of an axon. If the current reaching the axon hillock changes the membrane potential there to -60 mV, current will spread to the initial segment and open voltage-gated Na channels at -60 mV. Action potentials will then ensue. If a postsynaptic cell synapses with 32 different EPSPs totaling 42 mV, and on IPSP at -32 mV, the initial segment of the axon would fire an action potential.
What channels are involved in an AP? At which voltages do they open? Close? What are the three conformations of the voltage-gated sodium channels?
Voltage-gated sodium channels and voltage-gated calcium channels are involved in action potentials. They open at -60 mV (voltage-gated Na channels) and close at +30 mV (voltage-gated calcium channels). Three conformations of the voltage-gated Na channels are open (-60), closed (-70) and inactivated (+30).
During a minor hand surgery, a local anesthetic (e.g., lidocaine) is used to numb the patient's hand. What is the mechanism by which this drug works?
Lidocaine inhibits voltage-gated Na+ channels. Neurons are still activated but the voltage-gated Na+c channels can't open, so there is no action potentials and therefore no pain signal reaching the brain. Therefore, the perception of pain never occurs in the brain.
During depolarization in an action potential, what channel is open and what channel is closed? During repolarization in an action potential, what channel is open and what channel is closed? What are the conformations of the two channels at -70mv and at +30mv?
Voltage-gated Na+ channels are open and voltage-gated K+ channels are closed during depolarization. During repolarization, voltage-gated K+ channels are open and voltage-gated Na+ channels are closed (actually they are inactivated). -70 mV: voltage-gated Na+ channels are closed and voltage-gated K+ channels are closed. +30 mV: voltage-gated Na+ channels are inactivated and voltage-gated K+ channels are open.
Hypothetically, if cell's TMP was 0 mV, what would happen to its TMP if both voltage-gated Na+ and K+ channels were blocked and incapable of opening? Could threshold be met?
No, threshold would not be able to meet since the cell would not be able to depolarize.
Can a cell fire a second action potential after threshold has been met but the TMP has not yet reached 30 mV? Why? What about during the relaitve refractory period? Why?
No, because voltage-gated Na+ channels would already be open from the first action potential. During the relative refractory period potentially yes, but the stimulus would have to be greater than norma as the cell is hyperpolarized during this period.
Why is it important the the heart's action potential frequency is about 1 action potential per 200 ms vs. skeletal muscle, which has a frequency of about 1 action potential per 5 ms?
With a greater action potential frequency, muscles can summate muscle tension forming what is known as a tetanus, or sustained contraction. Heart cell action potential frequency is markedly decreased, making it impossible for the summation of muscle tension. Therefore, the heart cannot undergo a sustained contraction.
Action potential propagation along a myelinated neuron can be described as a series of successively regenerated action potentials linked by a series of successively regenerated graded potentials. Starting with a neuron reaching threshold in the axon hillock, can you provide a more detailed explanation of how an action potential arises in the initial segment and then how the signal is propagated along a neuron? Is the same action potential that is generated in the initial segment the signal that is propagated along the entire neuron?
Ac action potential arises in the initial segment when enough Na+ comes into the cell to bring it from -70 mv to -60 mv, here depolarization happens and this activates voltage-gated Na+ channels. Na+ flows in until the cell reaches +30 mv, where voltage-gated Na+ channels inactivate and voltage-gated K+ channels open. K+ leaves the cell until it reaches -90 mv where voltage-gated K+ channels close and the cell returns to its normal state. This process repeats itself as action potential propagation continues.
Where are voltage-gated Na+ and K+ channels found in myelinated axons versus unmyelinated? What other protein must be present in the axolemma for action potential formation and propagation?
Voltage-gated Na+ and K+ channels are found in nodes of Ranvier in myelinated axons and down in the axon in unmyelinated axons. The Na/K pump must be presnt for an action potential to occur.
What type of conduction occurs in myelinated nerve fibers? Unmyelinated? What are the relative speeds of conduction? Which is faster, myelinated or unmyelinated? Nerve fibers are much like electrical wires. Current in electrical wires is generated by the flow of electrons. What is flowing in nerve fibers creates the current of your neurons?
Saltatory (100 m/s) conduction occurs in myelinated nerve fibers and continuous (1 m/s) conduction occurs in unmyelinated nerve fibers. K is flowing through your nerve fibers that creates current.
You are creating a human-like android. You want to create an android that can react, move and think faster than yourself. How would you construct neurons for your android so that they propagate action potentials with a greater velocity than your own neurons?
Make the nodes of Ranvier closer together.
The internodes of an axon are a defined length. What is the reason they evolved to be the length that they are? What would happen if they were shorter? Longer?
Diffusion is distance limited. If the nodes were further apart, the graded potentials in the internodes would be too weak to reach the nodes. The action potential in the initial segment could not be regenerated along the axon if they were longer.
A friend explains to you that multiple sclerosis is analogous to have a phone charging cord that has a broken coating and is frayed. He also explains how some electricity from the outlet is lost through these frayed spots on its way to charge the phone. In other words, there is a short in the wire. How do you compare this to a neuron that is damaged due to multiple sclerosis?
This is analogosu to multiple sclerosi since the myelin sheath is attacked by the wire immune system. The myelin sheath acts as the rubber coating to a wire, and when this sheath is attacked by the immune system breaks down over time. Without this sheath, information/current will leak out of our cells (K+), thus creating a 'short' in our wires.
What are the three components of a synapse? What portion of a neuron do other neurons form synapse with? In an ax-dendritic synapse, where an axon of one neuron synapses with the dendrite of another, what is the presynaptic cell? Postsynaptic?
The three components of a synapse are the presynaptic membrane, synaptic cleft, and postsynaptic membrane. The cell body and dendrites are the portion of neurons that other neurons form synapses with. In an ax-dendritic synapse the presynaptic cell is the axon terminal and the postsynaptic cell is the dendrite.
What kind of potential occurs in a terminal knob? This change in membrane potential in the synaptic terminal leads to the opening of what type of channels? What happens as the result of the influx of these ions into the terminal knob?
Local potentials occur in the terminal knob and this change in membrane potentials leads to the opening of voltage-gate Ca2+ channels. As a result of ions coming in the synaptic vesicles undergo exocytosis.
In a synapse, we often say that information is communicated from one neuron to the next in the following way: electrical to chemical to electrical. Can you explain what this means in neurophysiological terms.
The presynaptic neuron undergoes action potentials (electrical) and releases neurotransmitters (chemicals) that stimulate the postsynaptic neuron to undergo action potentials (electrical).
What kind of gated channels are located in dendrites? Soma? Axons?
Dendrites and soma are ligand-gated channels. Axons are voltage-gated channels.
What is an excitatory postsynaptic potential (EPSP)? An inhibitory postsynaptic potential (IPSP)? Is an EPSP a depolarizing or hyperpolarizing stimulus? Is an IPSP a depolarizing or hyperpolarizing stimulus?
An EPSP is an excitatory (depolarizing) potential. An IPSP is an inhibitory (hyperpolarizing) potential.
How does an electrical synapse differ from a chemical synapse? Which is more common? What does it mean that electrical synapses signal transfer occurs with 100% fidelity? How do chemical synapses differ in this regard?
In an electrical synapse, the presynaptic and postsynaptic membranes are coupled via gap junctions (there is no synaptic clef). A chemical synapse is not physically couple together (there is a synaptic cleft). Chemical synapses are more common. In electrical synapses, the presynaptic neuron will always propogate its signal to the postsynaptic neuron, this is what 100% fidelity means. In chemical synapses, the presynaptic neuron may or may not propogate its signal to the postsynaptic neuron.
The fields of pharmacology and pharmaceutical sciences are all about chemical synapses. Why is this the case?
Because synapses are where chemical information is transferred between two cells and manipulating synapses will alter this information, thus giving different physiological responses.
How does signal transfer occur in electrical synapses? Chemical? Can EPSPs occur in postsynaptic neurons in an electrical synapse? IPSPs?
In electrical synapse, signal transfer is direct ion transfer. In chemical synapses, signal transfer is mediated by neurotransmitters. EPSPs can occur in postsynaptic neurons in an electrical synapse and so can IPSPs.
What is a ligand? Agonist? Antagonist?
A ligand is an ion/molecule that binds to a receptor. An agonist is an ion/molecule that binds to a receptor and enhances that receptors activity or response. An antagonist is an ion/molecule that binds to a receptor and resists that receptors activity or response.
What is a cholinergic synapse? What is/are the ligands? What are the different types of cholinergic receptors?
A cholinergic synapse contains acetycholine and may be excitatory or inhibitory. These are abundant in the brain and neuromuscular junctions. The different types are niotinic (ionotropic - permissive to ions) and muscarinic (metabotropic - metabolic changes).
What does ionotropic mean? What type of cholinergic receptors are ionotropic? What does metabotropic mean? What type of cholinergic receptors are metabotropic?
Ionotropic means a channel will open and become permissive to ions (nicotinic cholinergic receptors). Metabotropic means it causes metabolic change in the postsynaptic cell (muscarinic cholinergic receptors).
Can you provide an example of an excitatory cholinergic synapse and explain how it works? Inhibitory?
Excitatory cholinergic synapse: NMJ of skeletal muscle. ACh binds to muscle cells and opens nicotinic receptors and causes a change in membrane potential of the muscle cell membrane.
Inhibitory cholinergic synapse: SA node on the heart is regulated by the ANS; ACh hyperpolarizes pacemaker cells and thus slows our heart rate down.
What would happen if ACh was not tonically dripped on the heart's SA node? What would happen if epinephrine (adrenaline) was dripped on the SA node instead of ACh? Would heart rate increase or decrease if cAMP levels in the SA node increased?
If ACh stopped dripping on the SA node, our heart rate would increase to 110 bpm. If epinephrine was dripped on the SA node, our heart rate would increase dramatically since it speeds the rate of our action potentials. If cAMP levels increased in the SA node, heart rate would increase.
What is a GABAergic synapse? What is/are the ligands? What are the different types of GABAergic receptors? Which one is ionotropic? Metabotropic? Is diazepam (valium) an agonist or antagonist? For which receptor?
A GABAergic synapse contains y-aminobutyric acid (GABA) which is an inhibitory neurotransmitter in the brain. This is exclusively inhibitory. The ligands are GABA. The different types of receptors are GABAa which is ionotropic and GABAb which is metabotrpic. Valium is an agonist for GABAa.
What is an adrenergic synapse? What is/are the ligands? What is a catecholamine? What are the different types of adrenergic receptors?
An adrenergic synapse contains catecholamines (norepinephrine and epinephrine). The different types are alpha (1 and 2) and beta (1 and 2) adrenergic receptors.
What is a glutamatergic synapse? What is/are the ligands? What are the different types of glutamatergic receptors? How is AMPA gated? NMDA? Can you describe how the AMPA and NMDA receptors work together to mediate the postsynaptic response? Is ketamine an agonist or antagonist. For which receptor?
A glutamatergic synapse contains glutamate (excitatory neuron in the brain). The ligands are glutamate. The different types are NMDA and AMPA. AMPA is a ligand-gated Na+ channel and NMDA is a ligand-gated Ca2+ channel but also a voltage-gated channel as well. Na+ entering AMPA depolarizes the cell which ejects the Mg2+ ion in the center of the NMDA. Ketamine antagonizes the NMDA receptor.
What type of channel would you antagonize to treat depression? Anxiety? If you wanted to treat two patients, one with depression and one with anxiety, what types of synapses would you influence in each individual if you could only employ antagonists.
You will want to inhibit selective serotonin receptors to treat depreession and for anxiety you want to agonize GABA receptors.
What is the Gs G protein-coupled receptor signaling pathway? Gi? Gq?
Gs: stimulatory pathway. The neurotransmitter binds to a receptor attached to a G-protein and activates G-protein that will then activate the enzyme adrenylyl cyclase in the membrane. This converts ATP to cAMP and thus activates the protein kinase A, which phosphorylates proteins inside the cell and changes the cells metabolism.
Gi: inhibitory pathway. Activates G-protein and causes adenylyl cyclase activity to decrease (cAMP and protein kinase levels go down, decreasing phosphorylation).
Gq: activates phospholipase C producing diacylglyceral (DAG) and IP3. DAG activates protein kinase C, which phosphorylates proteins inside the cell and changes the cells metabolism. IP3 increases Ca2+ and calcium in the cell.
What are the various mechanisms involved in the cessation of a nerve signal? What is AChE? What is its function? What is a selective serotonin reuptake inhibitor (SSRI)? What is it used to treat? What is its mechanism of action?
1. Cessation of firing of the signal from the presynaptic neuron.
2. Ligand-receptor binding is temporary.
3. Neurotransmitter diffuses out of synaptic cleft; peripheral glial cells can absorb them.
4. Neurotransmitter can be degraded in the synaptic cleft.
5. Presynaptic knob reabsorbs neurotransmitter and their degraded constituents.
AChE is the enzyme anticholinesterase, which degrades ACh to acetate and choline; this can be resynthesized in the terminal knob.
SSRI is selective serotinin reputake inhibitor - reabsorbs serotinin in the presynaptic terminals. SSRIs treat depression by increasing serotonin levels by limiting serotonin reabsorption into presynatpic cells, increasing its levels in the cleft and thus more is able to bind to the postsynaptic receptors.
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