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70 Cards in this Set
- Front
- Back
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what are the four types of potentials in the nervous system? Of these, which are amplitude modulated (not all or none)? Of these which is propagated actively (potential moved bc of potential)? Which can be spatially summed? Which can be temporally summed?
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receptor, presynaptic, postsynaptic, and action. receptor, pre and post synaptic potentials are amplitude modulated. AP's are propagated actively. Receptor and postsynaptic potentials can be spatially summed. Receptor, pre and post synaptics can be temporally summed.
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in the knee jerk reflex, a depolarizing receptor potential is generated by a patellar lig tap, how and where is the amplitude (measures length of stretch from tap) converted into AP's?What is the threshold receptor potential that will illicit an AP?
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at the initial segment of the stretch receptor axon (analagous to the axon hillock of motor neurons), one or more AP's are generated encoding the receptor potential amplitude into AP number/frequency. -50 mV is the threshold potential.
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in the knee jerk reflex, where are the "hot spots" of voltage sensitive Na channels? what is their function?
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the nodes of ranvier hold these channels and they ensure conduction all the way to the spinal cord without decrement.
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knee jerk reflex: AP's reach the cord and synapse with (1.what and where?).
2. In this synapse what type of channels illicit the presynaptic potential and what is special about their speed of opening? 3. How is a frequency modulated signal transformed back into an amplitude modulated? 4. what NT is released and what kind of post synaptic potential does it create. |
1. alpha motor neurons for the same muscle in the anterior horn (also an interneuron for inhibition of knee flexion... on later card)
2. Ca+ channels are stimulated, but they are slow openers, thus they can be temporally summed. 3. More AP's means more Ca+ influx bc they are slow openers and thus more Ca++ means more NT 4. glutamate is the excitatory NT we use here, and it creates varying amplitudes of EPSP's depending on the amount released from the presynaptic axon. |
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describe the events of the inhibitory neuron on the flexor alpha motor neuron in the knee jerk reflex.
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the inhibitory neuron is stimulated by the afferent was signalled from the ligament stretch by glutamate. The inhibitory neuron then synapses on the flexor motor neuron with the NT glycine which cause postsynaptic Cl- channels to open, thus hyperpolarizing the post synaptic cell and creating an IPSP.
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What is the potential on a muscle called that is stimulated by a motor neuron?
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end plate potential which is analagous to an EPSP in neurons.
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what properties of membranes allow signals to propagate?
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Cm (membrane capacitance): charge seperation across the membrane
Rm (membrane resistance): density of permeant ion channels that are open (usually K leak channels) Ra: (axial resistance) which is cytoplasmic resistance that is determined by the diameter of the neural process. |
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what are local circuit currents and how are they propagated?
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currents that are initiated on a nerve cell process that travels without the help of voltage sensitive ion channels. They are propagated passively
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current must flow how?
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in all directions, if it comes into the cell, then it must go out
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what are orthodromic and antidromic directions? how would antidromic be stimulated?
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orthodromic is the normal direction toward the terminal while antidromic is toward the soma. absolute refractory period prevents antidromic flow when an AP is stimulated at the synapse, but if the nerve is stimulated in the middle, current can flow in both directions
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total membrane current is equal to what?
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capacitance current plus ionic current (ionic current is the current that flows through the membrane and axial resistances)
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how is the membrane capacitance discharged? what does this create?
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cations move from the influx of cations upstream to the originally negative cytosolic side of the membrane, thus repelling the positive charges extracellularly. The capacitance is reversed thus creating a moving capacitance current that must precede the ionic current flow. NOTE this current is not due to flow of ions through the membrane.
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which currents repolarize the membrane and recharge the capacitance?
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capacitance current recharges the membrane capacitance first, then the ionic current (K+ outflow) repolarizes the membrane
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when does the membrane start to depolarize? when does it repolarize?
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the capacitance current (at its initial peak) created by the discharging of the membrane capacitance causes the membrane to depolarize, the discharge of the reversed capacitance causes the mebrance to repolarize.
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what is the significance of the membrane capacitance discharge causing membrane depolarization?
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TIME that it takes for the capacitor to discharge and thus the time for the membrane to depolarize.
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what passive membrane properties affect how fast signals rise and fall? how far they propagate? conduction velocity?
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Rm and Cm, Rm and Ra, Ra and Cm
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any site on the neuron that does not voltage sensitive ion channels will exhibit what kind of signal propagation?
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passive signal that is decremental bc the voltage channels are not there to "boost the amp" back up.
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define the time constant.
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the time it takes for the max membrane change to decay by 63% OR Rm X Cm
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what is the advantage of a long time constant? disadvantage? what receptors would have a long time constant? short?
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increases effective temporal summation, decreases temporal resolution (ability to feel multiple quick stimuli), deep sensory receptors have long time constant to tell us intensity of the pain, finger tips have short time constant so they can "flutter" and distinguish indentions over a surface quickly.
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lenght constant is defined how?
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the distance it takes for the max membrane change to decay by 63% OR square root of (Rm/Ra). Note no Cm bc that would bring in TIME.
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what are the advantages and disadvantages of longer length constants?
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spatial summation is increased (signals add easily from different sites), but spatial resolution decreases (ability to detect signals from different sites)
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why does increasing diameter of an axon increase the conduction velocity (do not worry about myelination here).
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there is a higher volume of cytoplasm thu more intracellular ions to carry current and less resistance to current flow (lower Ra). Thus local current spreads faster.
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Conduction velocity is inversely proportional to what? why then does an increase in diameter increase conduction velocity?
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Ra X Cm, Ra is decreased as diameter is increased (greater volume means less Ra) while Cm is only slightly increased (it depends on surface area which does not increase as much as the volume does).
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how does myelin increase conduction velocity?
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it greatly decreases ionic attraction across the membrane and therefore decreases Cm. It also increases Rm and effective spread of local currents
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moderate demyelination results in what?
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decreased conduction velocity and temporal dispersion (slowed and inconsistent AP timing)
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demyelination affects what axons first?
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the largest and fastest axons
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large myelinated axons are said to have what in terms of current threshold? what does this mean?
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they have a low current threshold that can capture more extracellular current and respond to smaller shocks due to its larger size and higher Rm.
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demyelination does what to the membrane resistance? how does it do this?
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it reduces the membrane resistance by exposing more leak channels thus increasing the current threshold (need more stimulus AKA current to make an AP)
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why does parasthesia result from demyelination?
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demyelinated axons in a nerve near myelinated axons are exposed to ephaptic transmission (electrical cross talk), the demylinated axon is excited by extracellular portions of local circuit currents of nearby normal axons bc the demyelinated axon is no longer insulated.
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what is the most severe consequence of demyelinating disease and how does it occur?
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conduction block of the AP at a node. The membrane capacitance is too high bc of little myelin thus most of the current is used in trying to reverse the membrane capacitance. This is a very rare event however.
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mammalian myelinated axons use what kinds of ion channels to repolarize the membrane? what do other animal axons use? what is the consequence and benefit to mammals then?
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they use K+ passive channels instead of voltage sensitive K+ channels AKA delayed rectifiers. Delayed rectifyers have two effects: they increase the relative refractory period and extend the length of the AP. Thus mammals have shorter APs and relative refractory periods. This means more frequent AP's. Mammalian axons are also more energy effivients bc they are only generated at nodes and thus the Na+/K+ demand is much lower (less ATP used).
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define saltatory conduction.
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AP's are sequentially generated at the nodes of Ranvier
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for a single AP, how many nodes are usually activated?
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about 30
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demyelination of a few nodes typically does not cause conduction block bc...? but what does occur?
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the current generated by an AP is huge, thus they have a high safety factor to correct for the loss of current due to demyelination. But slower conduction velocity and temporal dispersion do occur.
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How do you determine the safety factor, and what is the safety factor of normal mammalian axons?
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take peak voltage of AP and divide it by the AP threshold voltage. It is about 5 in mammalian axons (100 mV divided by 20 mV)
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multiple sclerosis usually demyelinates where? Guillain Barre'?
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CNS, PNS
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what are the four neurophysiological symptoms of demyelination and what will cause these symptoms to worsen and why?
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slowed conduction velocity, temporal dispersion, conduction block, and paresthesias. Elevated body temp worsens these bc the gates of the ion channels are proteins and thus the activating gates are activated faster and the inactivating gates are activated faster when the temp is higher.
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why does intermittent improvement occur in the demyelinating diseases?
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insertion of internodal V sensitive Na+ channels and remyelination (usually not permanent in MS)
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chronic demyelination leads to what?
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axonal degeneration
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why are demyelinating diseases progressive and irreversible?
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new lesions occur leading to demyelination and for some reason quick degeneration instead of chronic thus irreversible axon disability.
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Why is it that remyelination in Guillian Barre lasts longer than in MS?
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remyelination by schwann cells, PNS, lasts longer than the remyelination in the CNS.
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what often precedes GBS?
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infection with campylobacter jejuni
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what are the therapies for MS and GBS?
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immunotherapy to block the immun response to myelin and now there is research on promoting remyelination and repair
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what are the gene mutations seen in Charcot-Marie-Tooth disease? What are the symptoms?
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Type 1b is point mutations in a peripheral myelin protein, type 1a is AD resulting in over-expression of a peripheral myelin protein. The X linked mutation is a defect in a connexin, gap junction protein, of the myelin lamellae. The symptoms include reduced conduction velocity, cyclical demyelination and myelination, and impaired gait and pes cavus (deformed contracted foot) with chronic disease.
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what are some genetic demyelinating diseases?
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charcot-marie-tooth, leukodystrophies (CNS myelin is affected), and Pelizaeus-Merzbacher (affects proteolipid protein)
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what is the structure and characteristics of an electrical synapse?
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the two cells are connected via gap junctions (made by connexin molecules) and the signal goes straight through with no complex signal integration (NT's, summation... etc) or synaptic delay.
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what are the two broad types of postsynaptic receptors of chemical synapses and their respective characteristics?
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ionotropic postsynaptic receptors directly gate the ion channels, thus they have minimal synaptic delay while metabotropic receptors indirectly gate ion channels via G proteins and thus have longer synaptic delay. Metabotropic receptors can activate second messenger cascades that can amplify signals far from receptors
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NT's effects depend upon what?
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the type of receptor (for example, it is incorrect to say that GLU is ALWAYS excitatory bc one of its metabotropic receptors in the eye is inhibitory), presynaptic potential (from Ca influx, depending upon frequency and # of presynaptic AP's), amount of NT released, driving force for ionic flux, if channel opens or closes, and temporal/spatial summation (remember can have additive or subtractive potentials summing depending upon if they are inhibitory or excitatory)
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what are the characteristics of the GABAa receptors?
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they are ionotropic, which opening allows influx of chlorine resulting in hyperpolarization (IPSP)
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what are the characteristics of the glycine receptors?
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they are ionotropic and opening allows influx of Cl- resulting in hyperpolarization (IPSP)
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what are the characteristics of nicotinic ACH receptors?
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they are ionotropic which open to allow influc of Na+ and a little efflux of K+ causing a depolarization resulting in EPSP, EPP, or MEPP
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What are the characteristics of the GLU (AMPA) receptors?
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ionotropic channels that allow Na+ influx and small K+ efflux and some Ca++ influx resulting in a depolarization and thus EPSP.
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What are the characteristics of the GLU (NMDA) receptors?
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they are ionotropic which open to allow Na+ influx, Ca++ influx, and K+ efflux resulting in a depolarization and EPSP, BUT they will only open if they themselves are depolarized when GLU binds thus they are ligand and voltage sensitive.
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what are the characteristics of the GABAb receptor?
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it is metabotropic which will allow K+ efflux on a post synaptic membrane when it is opended. The result is a hyperpolarization. The second messenger used is Gi. Thus a SLOW IPSP is created.
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what are the characteristics of the muscarinic ACH receptors (non M type)?
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they are metabotropic and allow K+ efflux when opened. They use Gi as a second messenger, are hyperpolarizing and are found in the heart, specefically GIRK channels. They allow a SLOW IPSP since they are metabotropic.
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What are the characteristics of the muscarinic ACH receptor M type?
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It is metabotropic and found in sympathetic ganglia. When ligand is bound, the G protein causes the receptor to CLOSE thus stopping K+ efflux. This causes a depolarization resulting in a slow EPSP from the Na+ leak current.
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describe the EPSP created by the closing of the M type K+ channel.
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It is slower than the first EPSP initiated by other receptors opening (due to the fact that the M type EPSP is from slow leak of Na+ inside the cell and not a barage of it) and it is long and slow thus modulating the resting membrane potential and making the neuron more excitatory in this state.
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in the CNS post synaptic potentials must generally do what to illicit an AP?
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usually be summed bc PSP's are very small singly.
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multi-synaptic integration depends upon what?
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PSP amplitude, time constant and length constant
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inhibitory synapses are often positioned where on a dendrite in order to "shunt" or short circuit EPSP's?
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Closer to the trigger zone of the AP.
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why do infants suffer more seizures than when they are adults?
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their chloride pumps that establish the chloride equilibrium (Eion Cl- is -75mV) does not work yet. Thus signals that are supposed to be inhibitory maybe excitatory bc of the different Cl- concentrations and where it wants to flow
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what are the normal electrical potentials K+, Na+, Cl-, and Ca++ usually seek?
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-90mv, +60mV, -75mV, and +120 mV
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describe the activities and results of pre-synaptic inhibition and pre-synaptic facilitation.
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pre-synaptic inhibition depresses transmission by an inhibitory signal from another neuron acting upon the presynaptic neuron before it synapses. Presynaptic facilitation enhances transmission of signal by another neuron synapsing on the presynaptic axon to increase the signal. This is commonly mediated by axoaxonix synapses.
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what receptors mediate long term potentiation and what is long term potentiation?
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NMDA receptors in the hippocampus, which are usually blocked by Mg++ at resting Vm, may become unblocked for a long time to allow PSP's to propagate through these neurons.
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how can the NMDA receptors become unblocked?
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depolarization by AMPA type receptors receiving input at nearby synapses or from backpropagation of AP's generated in the soma from EPSP's that propagate toward the dendrites (thus NMDA receptors are said to be coincidence receptors by detecting activation of synapses due to the activation of other synapses) this all is thought to deal with accessing conscious memories.
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where does the long term portion of long term potentiation come into play?
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Once the NMDA receptors are activated, Ca++ can now flow through, Ca++ couples with calmodulin and activates the kinases PKC and CamKII. These kinases apparently target AMPA receptors to be inserted or maintained in the same synapse for a long time
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how can previously "silent" synapses be "turned on?"
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long term potentiation, insert those AMPA receptors (this is thought to be seen in development).
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CamKII may also release what that maybe required for some forms of long term potentiation?
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NO (a retrograde messenger in this case)that is released postsynaptically and acts on the presynaptic cell to release more glutamate. Now that there are more AMPA receptors, more GLU can be bound if more is released.
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Why is the hippocampus susceptible to stroke?
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it is a watershed area via fine branches of the anterior choroidal artery
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how do neurons in the hippocampus die from stroke?
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Glutamate reuptake by astrocytes into the presynaptic neuron requires ATP (and thus oxygen from the blood supply). In ischemic stroke, the glutamate remains in the synaptic cleft and the neurons fire themselves to death. Thus the mechanisms of LTP can be excitotoxic.
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