Passive Properties NSCI 3310
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This 13 page Class Notes was uploaded by Emma Notetaker on Thursday October 1, 2015. The Class Notes belongs to NSCI 3310 at Tulane University taught by Jeffrey Tasker in Summer 2015. Since its upload, it has received 60 views. For similar materials see Cellular Neuroscience in Neuroscience at Tulane University.
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Date Created: 10/01/15
Action Potential Propagation 10/1/15 3:37 PM • 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 o 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 o voltage-gated Na+ channels open, passive spread both downstream and upstream o AP REGENERATING – all-or-none • when charge goes upstream: does not generate AP due to the absolute refractory period o those voltage-gated sodium channels are INACTIVATED – WILL NOT flux current o cannot cause any more sodium to go in until membrane repolarizes • if you stick electrode into MIDDLE of axon (inject positive charge): o sodium will fan out and depolarize membrane BOTH upstream and downstream à 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 • refractory membrane upstream • prevents back propagation • propagation of the action potential • orthodromic: action potential travels in one direction (down axon to the axon terminal) • antidromic (experimental ONLY): o only experimental in axon – 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) ú 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 ú 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 o 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 o thin layers of cell membrane § virtually no charge in the inner layers myelin § very little interaction between charges inside and outside o charges on inside of cell very separated form charges on outside of myelin o fewer Na channels (low density of Na channels) o decreased membrane capacity (C ) m § low capacity to store charge (because insulated by myelin) o charges “jump” to next node o 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 à plaques or lesions § scars in brain and spinal cord • Guillain-Barre disease: PNS o sensory and motor nerves Passive Properties (aka Cable Properties) 10/1/15 3:37 PM • 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 o 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 ) – memsured in Farads § charge accumulation per cm of membrane • 2. membrane resistance – resistance to current flow across membrane o resistance (R) - resistance to current flow § function of number of channels in membrane ú no channels = infinite resistance ú many channels = little resistance o inverse of conductance (1/g) o specific membrane resistance (R ) – measured in Ohms m 2 § resistance of total plasma membrane per cm • 3. axial resistance – resistance of cytoplasmic axis o measured in Ohms o axis = CENTER of whatever you’re looking at o 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 o resistor: membrane resistance § leak channels § leak current o battery: membrane potential § potential to generate current § separation in charge between two poles – current created when poles are connected • introducing + charge – fans out o some goes to membrane to depolarize o positive charges held outside pushed away o creates flow of charge – nothing actually crossing membrane à capacitative charge o some charge leaks out through channel – creates ionic current • membrane current = I + Ic ionic o 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 curve is linear (current – voltage) – because proportional o 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 and C ) m m § funtion of open channels and ability to store charge § τ = RinputCm (measured in ms) • exponential decay • TIME to charge 63% of V max OR to discharge by 63% (discharge TO 37% of Vmax) – IN ONE POINT IN SPACE • determines rate of passive change in potential o if T = 10, will take 10ms (in that point in space) to decay by 63% o 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 • physiological impact of membrane τ • 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 (r a § 2. membrane resistance (r ) m ú λ = √(r mr )a ú ratio of membrane resistance versus axial resistance ú distance traveled to decay by 63% or to 37% of original o 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) o cell with larger length constant MUCH more excitable because maintain magnitude and amplitude over longer distance o 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) o 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 time=0) nd o 2 EPSP 1 length constant away BUT generated 1 time constant later (t=10ms) st o 1 EPSP: 3.7 mV when reaches hillock BUT waits for 1 time constant so decays another 63% à 1.3 mV nd o 2 : 3.7 mV at hillock à 3.7 mV o summation: 5mV which is exactly threshold • 2 forms of integration • temporal: time-dependent o function of time constant o change over time in one point in space • spatial: function of length constant o changes over distance travelled Synaptic Transmission 10/1/15 3:37 PM • 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 ú ions can flow directly § rapid communication § passive transfer of charge § cytoplasmic bridge between one cell and another • 2. chemical synapse: o chemical transmitters exocytose § NOT direct transmission of charge o neurotransmitters go through extracellular space and bind to postsynaptic cell § OPENS ion channels à ions flow in o postsynaptic receptors o slower transmission • Gap junctions: • provides resistance to charge transfer between cells (more channels = less resistance) • half of channel is provided by each cell (hemichennales) • hemichannel is connexon (each cell provides ONE connexon – these meet up to form gap junction) o 6 protein subunits/connexon o each subunit is called connexin • gated by pH and intracellular calcium concentration o normally open o closed by acidity OR high intracellular calcium • bidirectional flow of current o rectifying/non-rectifying o rapid transmission – anything electrical in presynaptic or postsynaptic cell FELT by the other (depends on where signal is being generated § cells can be both pre and postsynaptic o 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) coupling coefficient • electrotonic coupling via gap junctions • coupling coefficient – measure of strength of couling o ratio of post response to pre response o function of number of gap junction channels o more gap junctions = greater coupling effect o fewer gap junctions = lower coupling effect the chemical synapse: • synaptic cleft • postsynaptic • presynaptic • active zone (nt release) chemical synaptic function • presynaptic: o AP à Ca entry à vesicle fusion à nt release • postsynaptic: o binding of neurotransmitter à opening of ion channels à influx/efflux of ions à EPSP or IPSP à suprathreshold à AP in postsynaptic neuron o unidirectional flow of info synapses • axodendritic: o dendritic shaft – usually inhibitory o dendritic spine – usually excitatory • axosomatic – generally inhibitory • axoaxonic: o increases or decreases nt release o stimulates or inhibits AP generation o facilitates or depresses nt release chemical synapses • asymmetric synapses: o excitatory § glutamate • symmetric synapses: o inhibitory § GABA EPSP: inward current à depolarization IPSP: outward current à hyperpolarization EPSP + IPSP : inward current + outward current à summed response presynaptic mechanism of nt release • experiment: voltage clamp presynaptic terminal à record membrane current o record postsynaptic change in voltage à EPSP o block voltage-gated calcium channels with cadmium o this block abolishes EPSP § TRANSMITTER release is CALCIUM dependent calcium influx triggers nt release • AP conducted to terminal à membrane depolarization à opening of voltage-gated calcium channels à calcium influx à nt release **molecular mechanism of nt release is NOT directly voltage-dependent • BUT voltage-gated calcium channels are responsible for allowing calcium to enter • nt release caused by increase in calcium concentration in terminal exocytosis – nt release • 1. vesicle docking – vesicle and plasma membrane SNARE proteins associate with one another o vesicles SNARE: synaptobrevin o plasma membrane SNARE: syntaxin and SNAP-25 • 2. SNARE complexes form, pulling vesicles close to plasma membrane (vesicle docking/priming) • 3. calcium entering interats with vesicle membrane protein synaptotagamin (Ca sensitive protein) • 4. vesicle fusion with membrane synaptic vesicle cycle: • synaptic proteins: complex protein-protein interactions in release o anchoring to cytoskeleton o trafficking to plasma membrane o docking at membrane o fusion of vesicular membrane with pm o formation of fusion pore • several protein interactions triggered by calcium exocytosis: vesicle-plasma membrane fusion • transmitter release • vesicle membrane added to plasma membrane • increase in surface area • increase in membrane capacitance endocytosis: internal budding of vesicles (vesicles coated with clathrin) • vesicle membrane subtracted from pm • decrease in surface area • decrease in capacitance à compensatory quantal release: • experiment: o stimulate motor axon, record endplate potentials (EPP) of muscle fibers o spontaneous EPP: miniature endplate potentials o evoked EPP amplitudes integral multiples of mini’s quantal analysis: • EPP amplitude histogram: o number of events at each amplitude o polymodal distribution o histogram peaks are integral multiples of unitary EPP (mini’s) o release is QUANTAL (discreet units) § 1 quantum = 1 packet of transmitter = 1 vesicle ú à unitary response EPSP generation: • neurotransmitters: o Acetylcholine o glutamate • ionic selectivity: o Na o K o Ca IPSP generation: • neurotransmitters: o GABA o glycine • ionic selectivity: o Cl
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