Popular in Cellular Neuroscience
Popular in Neuroscience
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This 32 page Study Guide was uploaded by Emma Notetaker on Friday October 9, 2015. The Study Guide belongs to NSCI 3310 at Tulane University taught by Jeffrey Tasker in Summer 2015. Since its upload, it has received 163 views. For similar materials see Cellular Neuroscience in Neuroscience at Tulane University.
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Date Created: 10/09/15
Action Potential Propagation 09/21/2015 conduction of AP: action potential = CHANGE IN PERMEABILITY of membrane generated at axon hillock passive spread of cations through axon depolarization of membrane: o opening of channels create more permeability crosses threshold – voltage gated sodium channels open in initial segment: influx of Na+ - positive charge spreads passively BOTH downstream and upstream (passive depolarization on both sides of initiation side) downstream flow charges next segment of axon: + charge depolarizes this segment to threshold voltage-gated Na+ channels open, passive spread both downstream and upstream AP REGENERATING – all-or-none when charge goes upstream: does not generate AP due to the absolute refractory period those voltage-gated sodium channels are INACTIVATED – WILL NOT flux current cannot cause any more sodium to go in until membrane repolarizes prevents back propagation if you stick electrode into MIDDLE of axon (inject positive charge): sodium will fan out and depolarize membrane BOTH upstream and downstream backpropagation and forward antidromic spikes this is experimental, unknown if can occur naturally no one is ever at equilibrium – steady state at resting potential set up combination of active and passive properties active voltage-gated sodium channels passive fan out of charge propagation of the action potential orthodromic: action potential travels in one direction (down axon to the axon terminal) antidromic o axon: ONLY experimental – antidromic spike o backpropagation CAN happen in dendrites: so much positive charge coming in, some makes it to dendrites this can result in dendritic nt release in certain cells (with nt packaged in vesicles INSIDE dendrites) influences nt release for synapse from presynaptic membrane depends on number of voltage gated channels, leakiness in dendrites typical conduction velocity: o unmyelinated axon: 2m/s o myelinated: 120 m/s duration of AP: around 2ms factors influencing conduction velocity: axonal diameter (bigger=faster) o ex: pain receptors in skin: C fibers – unmyelinated pain and temperatures thin and unmyelinated – SLOWEST other pain fibers – thin but myelinated – faster touch sensors are faster – pain comes later (ex: when touching hot pan) myelin: layers of myelin sheath facilitate current flow o myelinating cells: Schwann (PNS) – take entire body and wrap it around axon (one to one) oligodendrocytes (CNS) – has branches that can wrap around segments of 3 or 4 separate axons saltatory conduction: myelinated axons nodes of Ranvier – unmyelinated segment in between myelin o high voltage-gated Na channel density can generate action potentials full number of potassium channels o increased membrane capacity (C ) m high capacity to store charge (only one lipid bilayer separating inside and outside) o conduction slows lots of charges to interact with, so takes longer to get out internodes - myelin thin layers of cell membrane virtually no charge in the inner layers myelin very little interaction between charges inside and outside charges on inside of cell very separated form charges on outside of myelin fewer Na channels (low density of Na channels) decreased membrane capacity (C ) m low capacity to store charge (because insulated by myelin) charges “jump” to next node rapid conduction – not many charges to interact with so they can rapidly go through demyelinating diseases: multiple sclerosis: multiple CNS sites o “many scars” o one of the most common diseases in CNS o inflammatory demyelinating condition o some of the charge escapes o disrupts conduction of electrical impulses to and from brain o effects speed and efficiency with which impulses are conducted o effects smooth, rapid and coordinated movement o sites where myelin is los plaques or lesions scars in brain and spinal cord Guillain-Barre disease: PNS o sensory and motor nerves Passive vs. Active propagation synaptic potentials = passive propagation o once current reaches o change in shape and decreased amplitude with distance action potentials = active propagation no change in shape or amplitude with distance, all or none because generated and regenerated entire axon length conductance (g) – “acceptance” of current flow inverse of resistance (1/R) more open channels = higher membrane conductance factors that govern passive conduction in neurons 1. membrane capacitance – charge accumulation on membrane o capacitance (C) - capacity to store charge o based on surface area bigger surface = more capacitance o opposite charges “hold” each other in place across membrane o specific membrane capacitance (C ) – measured in Farads charge accumulation per cm of membrane 2. membrane resistance o resistance (R) - resistance to current flow function of number of channels in membrane no channels = infinite resistance many channels = little resistance o inverse of conductance (1/g) o specific membrane resistance (R ) –mmeasured in Ohms resistance of total plasma membrane per cm 2 3. axial resistance – resistance of cytoplasmic axis measured in Ohms o axis = CENTER of whatever you’re looking at resistance on INSIDE of cable membrane is equivalent to an RC circuit has resistance – keeps certain charge in o capacitor = membrane capacitance responsible for membrane voltage capacitative current resistor: membrane resistance leak channels leak current battery: membrane potential potential to generate current separation in charge between two poles – current created when poles are connected introducing (+) charge – fans out some goes to membrane to depolarize positive charges held outside pushed away creates flow of charge – nothing actually crossing membrane capacitative charge some charge leaks out through channel – creates ionic current membrane current = I + c ionic capacitative current + ionic current magnitude of passive membrane potential response is determined by membrane resistance Ohm’s Law: V = IR or ΔV = ΔIR o determines membrane excitability o change in voltage proportional to change in current under resting conditions – membrane resistance is stable membrane potential change (passive) in response to current injection (or membrane current) is function of membrane resistance a neuron will respond to larger current with a greater change in membrane potential (proportional) o passive response will be bigger I-V (current – voltage) curve is linear (current – voltage) – because proportional until you reach threshold (while it stays passive) if you change R (by opening or closing channels), this relationships is changed kinetics of passive membrane response is determined by membrane time constant membrane time constant (τ) – determined kinetics of membrane potential change in response to current injection o speed of membrane charging/discharging function of resistance and capacitance (R anm C ) m funtion of open channels and ability to store charge τ = R input mmeasured in ms) exponential decay TIME to charge 63% of V OR to discharge by 63% (discharge TO max 37% of Vmax) – IN ONE POINT IN SPACE determines rate of passive change in potential if T = 10, will take 10ms (in that point in space) to decay by 63% if T = 1ms, takes 1ms to degrade by 63% in that point in space long τ = slow response short τ = fast response important in terms of cell’s integration over time of received inputs axonal/dendritic membrane = series of RC circuits each segment can be modeled as equivalent of electrical circuit resistor (number of open channels) and capacitor (storage of charge in lipid membrane) in parallel (creates a voltage across membrane) ra = axial resistance over 1cm rm = membrane resistance/unit length of cylinder if current is introduced, o charges membrane capacitance (changes potential) o some charge leaks out through membrane resistance o some continues down through axis of cable to next segment o this repeats – with each successive segment, there is less charge to change capacitance (smaller change in voltage) passive signal transmission: constant velocity signal decreasing is function of time constant (time it takes to decrease by 63% (to 37%) time constant etermines how signal is integrated (how it changes) over time distance travelled by passive membrane response is determined by membrane length constant length constant (λ): distance of passive current spread o INDEPENDENT OF TIME o exponentially decays with distance travelled (graph is inverse exponential) o function of: 1. axial resistance (ra) 2. membrane resistance (r ) m λ = √(r mr a ratio of membrane resistance versus axial resistance distance traveled to decay by 63% or to 37% of original greater λ will travel greater distance (signal going farther) bigger at each successive segment in membrane (starts off larger – each one will be larger because same amount is leaked) cell with larger length constant MUCH more excitable because maintain magnitude and amplitude over longer distance still degenerative signal dendrite is studded with synapses – signals at different times are generated by all those synapses physiological impact of length constant: red neuron: lambda = 1mm (travels 1 mm before decaying by 63%) blue neuron: lambda = .1mm (travels .1 mm before decaying by 63%) SO red much more excitable, more likely to generate AP in response to any given input Test question examples: cell has .1mm length constant with threshold of 5mV above resting potential o start at 10mV, 1 length constant away from axon hillock o will cell generate AP??? o NO – it will be 3.7 mV (smaller by 1 length constant) – does not reach threshold if 2 excitatory synapses, both 1 length constant away (same properties) YES – converge on axon hillock and summate to make 7.4 mV (which reaches threshold) 10 mV EPSP, 1 length constant away from axon hillock (generated at timend) 2 EPSP 1 length constant away BUT generated 1 time constant later (t=10ms) 1 EPSP: 3.7 mV when reaches hillock BUT waits for 1 time cndstant so decays another 63% 1.3 mV 2 : 3.7 mV at hillock 3.7 mV summation: 5mV which is exactly threshold 2 forms of integration temporal: time-dependent function of time constant change over time in one point in space spatial: function of length constant changes over distance travelled 2 types of synaptic transmission 1. electrical synapse: o gap junction: electrotonic coupling (passive spread of charge in living cell) direct current spread between pre and post synaptic ions can flow directly rapid communication passive transfer of charge cytoplasmic bridge between one cell and another provides resistance to charge transfer between cells (more channels = less resistance) half of channel is provided by each cell (hemichannels) hemichannel is connexon (each cell provides ONE connexon – these meet up to form gap junction) 6 protein subunits/connexon each subunit is called connexin gated by pH and intracellular calcium concentration normally open closed by acidity OR high intracellular calcium bidirectional flow of current rectifying/non-rectifying rapid transmission – anything electrical in presynaptic or postsynaptic cell FELT by the other (depends on where signal is being generated tight synchrony – respond instantaneously to what the others are doing (because transmission is so quick) passive signal similar to passive conductance of signal within a neuron (except with non-uniform axial resistance) 2. chemical synapse: (look at picture on slide) chemical transmitters exocytose NOT direct transmission of charge transduction between electrical chemical electrical neurotransmitters go through extracellular space and bind to postsynaptic cell OPENS ion channels ions flow in postsynaptic receptors slower transmission function: presynaptic: AP Ca entry vesicle fusion nt release postsynaptic: binding of neurotransmitter opening of ion channels influx/efflux of ions EPSP or IPSP suprathreshold AP in postsynaptic neuron unidirectional flow of info coupling coefficient efficiency of which charge transfers electrotonic coupling via gap junctions coupling coefficient – measure of strength of coupling magnitude of response in postsynaptic over that of presynaptic will be value less than 1 (if at 1, perfect coupling – almost impossible) ratio of post response to pre response (B:A) function of number of gap junction channels more gap junctions = greater coupling effect fewer gap junctions = lower coupling effect the chemical synapse: synaptic cleft postsynaptic presynaptic active zone (nt release) chemical synaptic function synapses axodendritic: stimulate or inhibit action potential generation upstream from axon hillock influences whether or not AP generated at axon types: dendritic shaft – usually inhibitory GABA in more favorable position to influence postsynaptic cell because closer to axon hillock dendritic spine – usually excitatory glutamate axosomatic – generally inhibitory stimulate or inhibit action potential generation upstream from axon hillock influences whether or not AP generated at axon on soma of postsynaptic cell axoaxonic: increases or decreases nt release mainly at the axon terminal INCAPABLE to influence generation of AP in postsynaptic cell facilitates or depresses nt release probability of release 1. can increase or decrease by influencing the membrane potential 2. influence the synaptic machinery chemical synapses asymmetric synapses: excitatory glutamate bunch of vesicles in presynaptic terminal postsynaptic cell has fuzzy dense material under the membrane proteins that have become electron dense (PSD-95) associated with glutamate receptors/synapses in membrane symmetric synapses: 2 membrane look the same inhibitory GABA EPSP: inward current depolarization increase in positive charge inside membrane IPSP: outward current hyperpolarization EPSP + IPSP : inward current + outward current summed response presynaptic mechanism of nt release experiment: voltage clamp in presynaptic terminal record inward membrane current in presence of TTX (blocks voltage gated sodium channels) NOT sodium dependent record postsynaptic change in voltage EPSP block voltage-gated calcium channels with cadmium this block abolishes EPSP TRANSMITTER release is CALCIUM dependent calcium influx triggers nt release (exocytosis) to get calcium into the cell, we have to activate voltage-gated Ca channels via depolarization NT RELEASE DEPENDENT ON DEPOLARIZATION AP conducted to terminal membrane depolarization opening of voltage-gated calcium channels calcium influx nt release **molecular mechanism of nt release is NOT directly voltage- dependent calcium dependent process voltage-gated calcium channels are responsible for allowing calcium to enter nt release caused by increase in calcium concentration in terminal exocytosis – nt release (calcium dependent) 1. vesicle docking – vesicle and plasma membrane SNARE proteins associate with one another vesicles SNARE: synaptobrevin (in membrane of vesicle) plasma membrane SNARE: syntaxin (on pm) and SNAP-25 (on pm) 2. SNARE complexes form, pulling vesicles close to plasma membrane (vesicle docking/priming) proteins interact in space between vesicle and pm 3. calcium entering interacts with vesicle membrane protein synaptotagamin (Ca sensitive protein) ca binds to synaptotagmin (calcium sensor) synaptotagamin changes conformation- draws vesicle to pm and both membranes fuse 4. vesicle fusion with membrane vesicle folds into membrane, dumps entire contentsneurotransmitter another process – kiss and run (pulls back off membrane instead of folding) synaptic vesicle cycle: multiple pools of vesicles storage pool – not ready for release connected to actin cytoskeleton to immobilize them in presynaptic terminal mobilized in calcium dependent process to go to readily releasable pool readily releasable sits next to plasma membrane (docked and ready to release when calcium enters) synaptic proteins: complex protein-protein interactions in release anchoring to cytoskeleton trafficking to plasma membrane docking at membrane fusion of vesicular membrane with pm formation of fusion pore several protein interactions triggered by calcium surface area increased with every exocytotic event – needs something to fix that membrane capacitance will increase capacitance of membrane is a function of surface area – capacitance increases (more charge on more surface area) can measure exocytosis by seeing storage of charge folding of membrane (for fusion) attracts clathrin proteins to cover an area of the membrane to designate for endocytosis endocytosis: internal budding of vesicles (vesicles coated with clathrin) compensates for exocytosis (maintains SA of the cell) function of exocytosis (more exocytosis more endocytosis) vesicle membrane subtracted from pm dynamin: protein that clips vesicle off after invagination decrease in surface area decrease in capacitance compensatory quantal release: neurotransmitters released in quanta each vesicle is DEFINED QUANTAL UNIT quanta: volume of neurotransmitter contained within a vesicle experiment: stimulate motor axon, record endplate potentials (EPP) of muscle fibers EXCITATORY EPP motor endplate: axon terminal + muscle fiber spontaneous EPP (no stimulation of axon): miniature endplate potentials (MEPP) very small evoked by single vesicle of neurotransmitters being released smallest potential possible unitary event evoked EPP amplitudes integral multiples of mini’s for most, there is a failure to generate an endplate potential function of the probability of release (we reduced this probability by bathing it in chemicals) smallest evoked response is about the same size as the mini EPP quantal analysis: plotting number of events vs. amplitude of that event EPP amplitude histogram: number of events at each amplitude – each event is multiple of smallest event (same size of mini_) due to nature of nt release (QUANTAL) – defined by number of nt in synapse every vesicle that goes through exocytosis binds to about the same number of receptors on postsynaptic membrane, opens about the same number of channels, causes same amplitude polymodal distribution (multiple peaks) – all multiples of smallest event histogram peaks are integral multiples of unitary EPP (mini’s) release is QUANTAL (discreet units) 1 quantum = 1 packet of transmitter = 1 vesicle unitary response (miniature postsynaptic potential) same principles in CNS as in motor endplate EPSP generation: neurotransmitters: Acetylcholine (NMJ) glutamate (CNS) triggers inward current EPSP depolarization receptors are ionotropic double channels for K and Na ionic selectivity: Na+ K+ Ca (only sometimes in CNS) only one subtype IPSP generation: neurotransmitters: GABA (most of NS) outward membrane current glycine (mainly in spinal cord, retina) ionic selectivity: Cl- flows in (outward + current) hyperpolarization ***No inhibitory junctions in NMJ receptors: excitatory synapses o neuromuscular junction Ach receptors central excitatory synapses glutmate inhibitory synapses GABA receptors chemical synapses – receptors 2 types of receptors o 1. ionotropic: ligand-gated channels receptor-channel complex ionotropic – tropic for ions 2. metabotropic: 2 ndmessenger-gated G-protein-coupled receptors (receptors are NOT channels) link up to channels via G intracellular, downstream signal cascade opens or closes target channel types of ion channels 1. leak 2. ligand-gated (IONOTROPIC) o domain in extracellular portion of protein that forms pocket – recognizes specific neurotransmitter causes conformational change in protein to form channel o neurotransmitter-dependent ondon channel=receptor 3. 2 messenger-gated target of metabotropic receptors phosphorylation-dependent once neurotransmitter binds, causes biochemical cascade leads to phosphorylation of target protein (channel) this event causes conformational change in protein opens channel 4. voltage-gated membrane-potential-dependent voltage sensor 5. mechanically gated sensitive to stretch of membrane neurotransmitter receptors often have both ionotropic and metabotropic receptors ( multiple receptor subtypes for each nt o Ach receptors: endogenous agonist nicotinic (ionotropic) in neuromuscular junction muscarinic (metabotropic) glutamate receptors ionotropic metabotropic receptor agonists: activate receptors triggers function (ex: opens channel, starts signal cascade) ex: nicotine (for nicotinic receptors), muscarine (for muscarinic receptors) receptor antagonists: block receptors 2 methods: bind to ligand binding site on receptor (blocks binding of nt) bind to somewhere else on protein to change conformation that prevents nt from binding ex: crurare (for nicotinic receptors), atropine (for muscarinic) neuromuscular junction: specialized synapse – motor endplate o muscles made of multiple muscle fibers – each one gets innervation from motor neuron that makes multiple synapses from ONE axon o can have multiple active zones in each synaptic bouton o nerve-muscle synapse of motor neurons o axon terminals – synaptic boutons on SAME muscle fiber area of neurotransmitter release active zones: synaptic specializations pre and postsynaptic specialization docking and fusion proteins mitochondria (energy stores) synaptic vesicles – Ach (ALL somatic muscles use ACh) ACh is excitatory in all areas ALL nicotinic, ionotropic receptors inward membrane current – influx of positive charge depolarizes membrane calcium channels postsynaptic muscle fiber junctional folds Ach receptors – at lips of folds nicotinic receptors ionotropic basement membrane (under folds) acetylcholinesterase Ach breakdown into choline + acetate choline taken back up into presynaptic terminal to remake ACh motor axon: neural innervation of muscle fibers, 1 axon/fiber muscle fiber: postsynaptic endplate potentials (EPP) miniature EPP – spontaneous release of single vesicles stochastic - random AP – evoked release of multiple vesicles suprathreshold – causes AP in muscle muscle contraction nicotinic Ach receptors CHOLINERGIC requires TWO ACh molecules to bind!!! 5 protein subunits – pentamer (heterooentamer bc different subunits) o 2α, 1β, 1δ, 1γ subunit o Ach binding site on α (requires 2 alpha subunits) 2 Ach molecules required to bind to open channel nicotinic ACH receptors ligand-gated channel MIXED cation channel ligand: ACh selective for Na AND K both go in opposite directions (Na in, K out) due to driving force net INWARD current – Na influx and K efflux Na influx dominates K efflux due to GREATER driving force endplate potential (EPP) = EPSP of NMJ (only time we call it anything other than EPSP) single channel currents each time TWO Ach combine recorded with patch clamp techniques o all or none o inward summation of single channel current = whole cell current = waveform EPP (endplate potential) reversal potential Na= I K I inI out Vrevfor = 0mV membrane potential of muscle fiber at which current zeroes and reverses direction on the other side Vm where EPC (endplate current) reverses direction when we go above reversal potential: more K out than sodium in reverse current direction – outward current at resting potential: -120 mv driving force on sodium, 10 on K more on Na move membrane potential from resting to -30mV activate synapse driving force of -90 mV on sodium, 50 mV on K Na still dominates, but getting closer SMALLER inward current (more potassium going out relative to sodium going in than previous example) move membrane potential to 0 mV driving force -60mV on Na, 80 mV on K K driving force dominates – larger OUTWARD current takes a little more driving force on K because Na can go through channels easier (higher permeability in channel) single channel current parallel whole-cell currents, except they’re square (all or none) membrane will be polarized in direction of the current inward - add positive charge inside – EPP that is excitatory (depolarizes) outward –positive charge goes out – EPP that is inhibitory (hyperpolarizes) look at picture on slide! (EPP reversal potential) whole cell currents produce endplate potentials current flow direction and amplitude sum of constituent ionic currents, which is a function of the driving force on each ion video: ionotropic glutamate receptors (excitatory) when glutamate binds, these receptors open channel different proteins 3 receptors: *AMPA (AMPA required to bind, then AMPA channel opens) *Kainate NMDA AMPA and Kainate mixed cation channel that fluxes sodium and potassium same efficiency as nicotinic receptors (same ions) when glutamate binds, sodium flows in, potassium flows out because sodium dominates in terms of driving force permeable to Na and K similar to ACh, nicotinic receptors purely ligand-sensitive EPSP/EPSC reversal if both ions flux with equal efficiency, reversal potential is halfways between two equilibrium potentials for these it is -10 (sodium is slightly better at coming in than potassium is at going out) reversal potential of AMPA and Kainate is 0 mV current through these receptors almost identical to current through nicotinic and cholinergic receptors recruitment of afferent axons increasing stimulus intensity increasing EPSP amplitude neurotransmitter = glutamate receptors = AMPA receptors reversal potential mixed Na/K current Vreversal0mV similar to ACh nicotinic R NMDA receptors (ionotropic glutamate receptor) Na/K AND Ca permeable Ca will flow inward through NMDA ligand-gated AND voltage sensitive Mg2+ block leads to voltage-sensitivity Mg binding in site within pore depolarizes induces unblock when resting potential – magnesium clogs pore (EVEN if glutamate has binded) to get ion flux through channel, membrane needs to be DEPOLARIZED to remove magnesium block (weakens negative charge inside) more depolarized less magnesium occurs around -40—50 mV once Mg leaves binding site, both Ca and Na in (combination acts like Na alone in AMPA receptor), K out mixed current reversal potential of 0mV requires co-agonist (based on subunit composition) ONLY NMDA receptor needs this some need glycine, some need serine CRITICAL for activation – without it glutamate binding does not open channel requires TWO ligands at different sites to open gate other modulatory sites glycine or serine– co-agonist provided by glia plenty floating around – always available Zn – antagonist PCP – antagonist mixed AMPA/NMDA mixed population of postsynaptic receptors (NMDA and AMPA) under normal conditions, glutamate released and binding to NMDA and AMPA because Mg block, only AMPA receptors flux ions and mediate inward membrane current (in baseline conditions) EPSP backpropagating action potentials have a huge role – depolarizing dendrites to kick Mg out of NMDA receptors permanent changes in terms of plasticity long term potentiation works at glutamate synapse synaptic plasticity (changing postsynaptic signals) triggered by calcium influx through NMDA receptors AMPA/NMDA current generate current voltage relationship Na, K and Ca channels NMDA will only come online when depolarized mixed glutamate receptors APV NMDA receptor antagonist (blocks only NMDA) blocks NMDA current NMDA current slow component takes longer than AMPA doesn’t open until few seconds after initiation of response slow offset though – lasts longer slower than AMPA (activated immediately) also very rapid offset hyperpolarized potential: activate AP synapse EPSP inward current when stimulated 2 ndtime with APV – little to no change in synaptic current (because NMDA was already blocked and there is no ion flux) because only AMPA, high current lasts longer depolarized to -40 activate AP synapse EPSP response duration changes upon addition of APV (because at -40 mV the NMDA was going to influence the EPSP) due to APV, NMDA much larger NMDA receptor component yellow portion on graph is solely due to NMDA voltage sensitivity NMDA current at depolarized membrane potentials only Mg block blocks channel at hyperpolarized potentials 0 current, 0 change in voltage channel unblocked at depolarized potentials (threshold around -60 mV) voltage sensitivity of NMDA current abolished with 0 Mg current-voltage relationships non-linear with Mg, linear without Mg current through Kainic and AMPA receptors doesn’t change with voltage, whereas current for NMDA gets bigger with depolarization NMDA curve NOT linear GABA rAceptors heteropentamer α, β, δ, γ, p subunits Cl- channel modulatory sites 1. GABA – ligand 2. barbiturate – agonist 3. benzodiazepine – agonist 4. steroid – agonist 5. picrotoxin – antagonist 6. ethanol – agonist outward current – composed of outward single channel currents IPSP reversal inhibitory interneuron neurotransmitter =GABA (CNS and spinal cord) =glucine (only spinal cord) receptors GABA GABA recAptors glycine glycine receptors outward current at rest Vreversal = -70 mV Cl- current shunting inhibition shunting of current out of cell via open Cl- channels Ohm’s law V= IR
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