Introductory Neurobiology Week 3 Notes
Introductory Neurobiology Week 3 Notes Biol 3640
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This 6 page Class Notes was uploaded by lucy allen on Wednesday January 20, 2016. The Class Notes belongs to Biol 3640 at University of Denver taught by Dr. John C Kinnamon in Fall 2016. Since its upload, it has received 39 views. For similar materials see Introductory Neurobiology in Biology at University of Denver.
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Date Created: 01/20/16
The Action Potential What We Will Cover Today -origins of neuronal signals -generator and receptor potentials -signal conduction in a wire vs a neuron -electrotonic conduction -the action potential -threshold -voltage-gated ion channels -inward and outward currents -myelination and saltatory conduction -refractory period -neurotoxins -all of the potentials we have studied so far are graded, passive responses to a stimulus -properties of passive spread are determined by the time constant and the length constant Neurons Generate and Conduct Electrical Signals -in addition to passive spread -these signals originate as either generator potentials or receptor potentials -classic generator potentials are Excitatory Post Synaptic Potential (EPSP) and inhibitory post synaptic potential (IPSP) -excitatory drives the neuron towards the threshold, increasing likelihood that neurotransmitter is released -IPSPs hyperpolarize the potential, driving the neuron further from the action potential, decreasing likelihood of neurotransmitter release -muscle spindle generates a graded receptor potential -hard enough will generate an action potential in the sensory nerve, going to the spinal cord and dorsal route ganglion cell -generate an EPSP, sufficient to generate action potential in motor neuron, which synapses onto motor muscle in your leg, and the Characteristics of Generator and Receptor Potentials -graded -passively spread -electrotonic potentials; analog in form -can be distorted by R m C mnd R i -time course determined by R anm C m Signal Conduction in a Wire vs a Neuron -conductance is 10 times less in a neuron -current carried by ions in a nerve (electrons in a wire) -ions have a smaller mobility and fewer numbers -current flow attenuates much more in a nerve cell -membrane of a nerve cell is a poor insulator -membrane of nerve cell is leaky to ions -nerve cells have high internal resistance (R) i -nerve cell membrane has high capacitance Electrotonic Potentials Decrease During Spatial Conduction -signal decrement occurs during the conduction of an electrotonic signal along the processes of a neuron -this decrement is due to the membrane resistance (R ) anm the internal resistance (Ri for each unit of length along a neuronal process Action Potentials Allow A Rapid and Reliable Transfer of Signals over Large Distances -for a given neuron the potential is always the same amplitude -stimulation of a nerve intensely increases the frequency of action potentials but not the magnitude -falling below resting potential creates an 'undershoot' (see slide 14) Action Potentials Are Triggered By Depolarizations That Reach An Action Potential -slide 15 -electrodes injecting positive current into cell body -see a series of action potentials -note identical magnitude of each action potential -slide 16 -resting potential is the dotted line -between dotted line and solid line the dashed line should show an action potential -lines with negative slope (away from threshold) are due to IPSPs -slide 19 -three different levels of stimulation -increased injected current causes more action potentials per unit time (frequency) -no change in amplitude of action potentials -slide 20 shows the same thing Causes of Hyperpolarization/Depolarization -some channels open and shut in a voltage-dependent manner -voltage gated sodium channel -must depolarize to open -sodium rushes in, making the interior of the axon even more positive charged -responsible for rising phase of the action potential -regenerative phenomenon -depolarization of one voltage-gated sodium channel causes the depolarization of subsequent voltage- gated sodium channels -sodium flow into the cell drives this regeneration -rare example of positive feedback -positive feedback: product of the reaction drives further reaction -has two gates in 1st model -at rest, M gate is closed and H gate is open -depolarization of the ion channel opens the M gate and allows an inward rush of sodium -only lasts about a millisecond -then the H gate swings shut -inactivation gate: inactivating voltage-gated potassium channel -second model: patch clamp recording -shows inward currents, downward by convention -depolarization allows opening for a short time -particle comes in an blocks channel to stop flow of sodium during depolarization -after repolarization, particle leaves and ion channel goes back to closed configuration -voltage gated potassium channels -responsible for downward phase of the action potential + Delayed Rectifier K Channel -to repolarize the membrane must get rid of all the positive charge that has come in -this potassium channel accomplishes this -rectifier: brings membrane back to resting potential -first model has one gate: n gate -closed at rest -immediately after depolarization it is closed -about 5 milliseconds after depolarization it opens -***lag time! voltage-gated sodium channel had no lag! -stays open until membrane is repolarized -slide 29 -one y axis shows conductance, the other shows membrane potential -x axis is time -gNA shows sodium conductance -g : shows potassium conductance NA -open up, allow sodium to leave, allowing for the drop of the action potential -sodium-potassium ATPase pump brings the action potential back to the resting potential -slide 30: patch clamp recordings showing how ion channels open at different times -summation of the recordings shows the resulting curve (bell curve) -not all voltage-gated ion channels open simultaneously -sodium currents are inward/down, and potassium currents are outward/up with regards to patch clamp recordings -slide 31 follows the same upward/downward conventions as slide 30 -TTX: tetrodotoxin: poison that comes from puffer fish -blocks voltage-gated sodium channels -does not block leak sodium channels -does not affect resting potential*, only the action potential -fatal, feel tingling in your mouth, causes paralysis and respiratory failure and then you die -Japanese name for Puffer Fish: Fugu -on the slide you only get the outward potassium current, hence only the upward curve -TEA: Tetraethylammonia: not a toxin, a chemical that blocks voltage-gated potassium channels -still get the inward sodium current but no outward potassium current -does not affect resting membrane potential*, just voltage- gated potassium channels -slide 32: about scorpion toxin: affects the inactivation gate of voltage- gated sodium channel so that your neurons remain depolarized -another representation of the conduction of the action potential -entry of positive charge depolarizes the subsequent regions, causing a cascade of regeneration of action potentials -only thing that stops the regeneration of the action potential is the inactivation gate Action Potentials in Myelinated Neurons -you increase the distance between the parallel plates, decreasing the capacitance -decreases the amount of time required to charge the capacitors in the axonal membrane, making Tao shorter (equal to membrane capacitance times membrane resistance) -this increases the conduction velocity -increased diameter also explains this -myelination is discontinuous -breaks in myelination are nodes of Ranvier -where sodium goes in and potassium comes out -in between nodes of Ranvier, in internodal region (myelinated region) there is no movement of sodium in and potassium out, just the passive spread of the potential -passive spread is fast, but ion exchange in and out is slow -saltatory conduction: action potential electrically leaps from Node of Ranvier to Node of Ranvier where it regenerates itself -passive spread from node to node and at each node regeneration occurs -action potential maintains the same amplitude as it leaps Multiple Sclerosis (MS) -demyelination disease -neurons which would normally conduct action potentials over long distances lose their myelin and the action potentials get smaller and eventually stop, not reaching the muscles -results in loss of control of muscles Speed of Impulse Conduction -faster in myelinated than in non-myelinated -in myelinated axons, lipids act as insulation (the myelin sheath) forcing local currents to jump from node to node -in myelinated neurons, speed is affected by -thickness of myelin sheath -diameter of axons -large-diameter conduct more rapidly than small-diameter -large diameter axons have grater surface area and more voltage- gated sodium channels why are Myelinated Fibers so Fast? -time constant -Cm -length constant To Increase Conduction Velocity (Slide 43) -larger the diameter the faster it gets in an unmyelinated axon -'slower' slope than myelinated axon -increasing diameter of myelinated axon drastically increases conduction velocity Refractory Period -when we have an action potential there is a brief period after the AP during which no matter how much you depolarize the neuron you will not get an action potential -voltage-gated sodium channels are shut, not repolarized yet -as more and more sodium channels are repolarized, then the relative refractory period begins -excitability of the neuron goes back up and now can be depolarized for an action potential Nerve Fiber Types -Type A: large diameter (4-20 micrometers), heavily myelinated, conduct at 15-120 m/s (300 mph) -motor neurons supplying skeletal muscles and most sensory neurons carrying info about position, balance, delicate touch -Type B: medium diameter (2-4 micrometers), lightly myelinated, conduct at 3-15 m/s -sensory neurons carrying info about temperature, pain, general touch, pressure sensations -Type C: small diameter (0.5-2 micrometers), unmyelinated, conduct as 2m/s or less -many sensory neurons and most ANS motor neurons to smooth muscle, cardiac muscle, glands -react to wasabi! Coding For Stimulus Intensity -all action potentials are alike (of the same amplitude) and are independent of stimulus intensity -amplitude of the action potential is the same for a weak stimulus as it is for a strong stimulus -so how does one stimulus feel stronger than another? -strong stimuli generate more action potentials than weak stimuli -the CNS determines stimulus intensity by the frequency of impulse/transmission Where Do Action Potentials Typically Start? -spike initiation zone (axon hillock), at the beginning of the axon -large concentration of voltage-gated sodium channels here Lambda -large lambda means passive spread will go far and we will have a larger potential and a larger distance along the axon -small lambda means the membrane potential will go down rapidly and the membrane potential will be below threshold -larger region of suprathreshold excitation
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