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Unit V ELECTROPHYSIOLOGY

Biology 220 Anatomy & Physiology I. Unit V ELECTROPHYSIOLOGY. Chapter 11 pp. 396-424. E. Gorski/ E. Lathrop-Davis/ S. Kabrhel. Plasma Membrane. Membrane potential = electrical voltage difference across plasma membrane of cell

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Unit V ELECTROPHYSIOLOGY

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  1. Biology 220 Anatomy & Physiology I Unit VELECTROPHYSIOLOGY Chapter 11 pp. 396-424 E. Gorski/ E. Lathrop-Davis/ S. Kabrhel

  2. Plasma Membrane Membrane potential =electrical voltage difference across plasma membrane of cell • caused by differences in ion concentrations maintained by plasma membrane proteins Membrane structure • phospholipids • integral proteins - form channels Review chapter 3 (pp. 68-80): membrane structure, transport Fig. 11.6, p. 397

  3. Membrane Channels Two major classes of channels: 1. Leakagechannels (non-gated or passive channels) • always open • more K+ than Na+ channels • allow influx of Na+, efflux of K+ • found in cell body and dendrites 2. Gated channels • open/close based on environment • found in cell body, dendrites, axon hillock, unmyelinated axons and myelinated axons (nodes of Ranvier)

  4. Types of Gated Channels • chemically gated* -- respond to neurotransmitters, hormones, ions (e.g,. H+, Ca2+) • found in cell bodies and dendrites • voltage gated* -- respond to change in membrane potential • found in axon hillock, axon • mechanically gated -- respond to mechanical change (vibration, pressure, stretch; e.g., stretch or touch receptors) Fig. 11.6, p. 397

  5. Outside: more Na+, Cl- Inside: more K+, protein (anion) Resting Membrane Potential (RMP) Intracellular environment different from extracellular environment in ionic composition Fig. 11.8, p. 398 Negative inside compared to outside; RMP = -70 mV

  6. Resting Membrane Potential (RMP) • cell membrane with a potential (difference in voltage across membrane) is polarized • in neuron, at rest: • inside: more K+, protein (anion) • K+ diffuses out of cell through open K+/ Na+ channels • outside: more Na+, Cl- • Na+ diffuses into cell through open K+/ Na+ channels • ion gradients (necessary for passive moment of ions) maintained by Na+/K+ pump (active transport system) See also Chapter 3, pp. 81-83

  7. Sodium-Potassium (Na+/K+) Pump Active transport (requires ATP) • uses transport protein in membrane (Na+/K+ Pump) • moves 3 Na+out of cell; 2 K+into cell Fig. 3.9, p.76 Diffusion Diffusion • sets up and maintains ion gradients necessary for diffusion

  8. Types of Potentials GradedPotential • magnitude varies with stimulus • more depolarization with stronger stimulus • decays away from point of stimulus Action Potential • magnitude stays the same • once started, passes along axon as nerve impulse

  9. Graded Potential • magnitude varies with stimulus --> allows graded responses • localized • short-lived • membrane may be: • hyperpolarized (more negative than resting potential; caused by influx of Cl- efflux of K+), or • depolarized (less negative than resting; caused by influx of Na+) • at receptor = receptor potential • at synapse = synaptic potential

  10. Depolarization and Hyperpolarization Fig. 11.9, p. 399

  11. Graded Potential • depolarization starts at area of stimulus • spreads by ions moving on either side of membrane (not from outside to inside) • larger stimulus opens more channels • if membrane reaches threshold (~ -50 to -55 mV), action potential (AP) will be initiated Fig. 11.10, p. 400

  12. Action Potential • membrane potential goes from -70 mV to +30 mV then back to -70 mV (after hyperpolarization) • all-or-none principle: • either start and pass AP, or don’t • continues once started • passed through membrane of excitable cells (neurons and muscles) • called nerve impulse when passed through axon

  13. Action Potential (con’t) • long-distance communication • propagation is unidirectional (one direction away from point of stimulation) • includes depolarization, repolarization and undershoot (hyperpolarization) • depolarization: -70 mV to +30 mV • based on influx of Na+ • repolarization: +30 mV to -70 mV • based on efflux of K+ • undershoot (hyperpolarization): -70 mV to -90mV • potassium permeability continues

  14. Events of an Action Potential Fig. 11.12, p. 402

  15. AP: Depolarization stimulus See Fig. 11.12, p. 402 chemically-gated Na+ channels open Na+ influx graded depolarization of dendrite or cell body spreads to axon hillock, if threshold reached voltage-gated Na+ channels open (#2 in figure) Na+ influx (positive feedback) timedgates on Na+ channels close, K+ channels open for repolarization

  16. AP: Repolarization Na+ channels closed, gated K+ channels open K+ leaves cell taking + charge with it  repolarization (#3) goes past normal resting potential (hyperpolarization) (#4) gated K+ channels close Na+/K+ pump returns Na+/K+ levels to resting See Fig. 11.12, p. 402

  17. AP: Refractory Period Time during which neuron membrane does not respond normally to additional stimuli • Absolute refractory period: time in which a new AP cannot be started • Relative refractory period: time in which new AP can only be started by stronger stimulus Fig. 11.15, p. 405

  18. Amplitude Variable Always the same (all-or-none) Duration Variable (depends on stimulus) Rapid membrane change Channels Chemically- or mechanically-gated Voltage-gated Location Dendrites, perikaryon Axon hillock, axon Propagation Localized (short-distance) Transmitted along axon as impulse Refractory period None (allows summation) Absolute (no new APs); Refractory (only with stronger stimulus) Membrane voltage change Depolarization or hyperpolarization Depolarization, followed by repolarization and hyperpolarization Comparison of Graded andAction Potentials Characteristic Graded Potential Action Potential

  19. Impulse Conduction • action potential (AP) passed through the axon as an impulse • “Rapid, transient, self-propagating reversal in membrane potential” Raven & Wood, 1976 • two types of conduction: • continuous • saltatory

  20. Continuous Impulse Conduction • involves passage of AP along entire membrane • occurs in unmyelinated axons and muscle fibers • depolarization/ repolarization occurs in step-wise manner as Na+ and K+ channels open and close in adjacent parts of membrane Fig. 11.13, p. 404 direction is one-way due to absolute refractory period shown in light blue

  21. Saltatory Conduction • AP passed from one node of Ranvier to the next • occurs in myelinated fibers • saves ATP (Na+/K+ pump only used at nodes) • faster Fig. 11.16, p. 406

  22. Stimulus Intensity • affects number of impulses sent per unit time • does not affect velocity of conduction • also affects number of neurons involved Fig. 11.14, p. 405

  23. Factors Influencing Impulse Conduction: Intrinsic Factors 1. Fiber diameter • larger (thicker) is faster (because of lower resistance) 2. Degree of myelination • myelinated fibers are quicker because of saltatory conduction • multiple sclerosis – degenerative autoimmune disease in which myelin sheaths of CNS are destroyed by person’s own antibodies

  24. Factors Influencing Impulse Conduction: Intrinsic Factors 3. Three groups of fibers: • A • B • C • Groups based on: • diameter • degree of myelination

  25. Fiber Types - Group A • Group A (fastest): • largest diameter (thickest) • thick myelin sheath • conduction velocities of 15-150 m/s • include somatic motor and some somatic sensory (from skin, skeletal muscles and joints - touch, pressure, hot/cold, stretch, tension)

  26. Fiber Types - Group B & C • Group B (intermediate): • intermediate diameter • thin myelin sheath • conduction velocities of 3-15 m/s • Group C (slowest): • small diameter • no myelin sheath (continuous conduction) • conduction velocities of 1 m/s, or less • Group B & C include: • autonomic NS motor fibers to viscera • sensory fibers from viscera • small somatic fibers from skin (pain, some pressure and light touch receptors)

  27. Factors Influencing Speed of Conduction: Extrinsic Factors Factors other than axon itself 1. temperature – due to general influence of heat on chemical reactions • warmer goes faster • colder goes slower 2. pH • decreased pH < 7.35 (increased H+)  decreased excitability (depression) • increased pH > 7.45 (decreased H+)  increased excitability

  28. Extrinsic Factors (con’t) 3. excessive or prolonged pressure (interrupts blood flow) 4. inhibitory chemicals reduce membrane permeability to Na+ (harder to depolarize) • alcohol, sedatives, anesthetics 5. excitatory chemicals cause easier depolarization • caffeine, nicotine 6. Ca2+ levels • low Ca2+ - increases excitability • high Ca2+ -decreases excitability

  29. Synapses • junctions between neurons at which information is passed from one neuron (presynaptic neuron) to another (postsynaptic neuron) • junction between neuron and effector (muscle or gland) usually called neuroeffector junction(NEJ) • neuromuscular junction (NMJ) • neuron to muscle • neuroglandular junction (NGJ) • neuron to gland

  30. Structure of Distal End of Axon • telodendria – terminal branches of axon • allow axon to contact more than one cell or one cell in several places • axonal terminals = synaptic end bulbs • contain neurotransmitter (or gap junctions) • synaptic cleft – space between presynaptic and postsynaptic membranes See Fig. 11. 17, p. 408 See Figure 11.18, p. 409

  31. Types of Synapses Defined by: 1. location: where signal comes from (e.g., axon) to where it goes (e.g., dendrite, muscle) 2. how signal is transferred a. based on location: • neuron-neuron • neuron-muscle • neuron-gland b. based on method of information transfer: • electrical synapses • chemical synapses

  32. Synapse Locations Based on locations, most common are: • axodentritic = axon (presynaptic) to dendrite (postsynaptic) • axosomatic = axon (presynaptic) to cell body, or soma (postsynaptic) • axoaxonic = axon (presynaptic) to axon or axon hillock (less common than the other 2) Fig. 11.17, p. 408

  33. Electrical Synapses • less common type of synapse • joined by gap junctions • cells said to be “electrically coupled” • very rapid transmission • excitatory only • allow bi-directional flow • importance: • allow synchronization of neuronal firing (important to stereotypical behavior) • important during development of nervous system (later, most replaced by chemical synapses) • also present in visceral smooth muscle, cardiac muscle

  34. Chemical Synapses • axonal terminal of presynaptic neuron releases neurotransmitter (NT) from synaptic vesicle into synaptic cleft • postsynaptic membrane (of neuron or effector) contains receptors that recognize NT • slower than electrical • unidirectional (one way) • inhibitory or excitatory • found at: • most neuron-neuron synapses • neuroeffector junctions Fig. 11.18, p. 409

  35. Events at Chemical Synapse 1. impulse within presynaptic neuron reaches axon terminal, depolarizes membrane  voltage-gated Na+and Ca2+ channels open in presynaptic membrane --> Ca2+ enters cell 2. entrance of Ca2+ into cell signals synaptic vesicles to fuse with axonal plasma membrane  for release of NT into synaptic cleft (exocytosis) See A.D.A.M. Nervous System II CD Fig. 11.18, p. 409

  36. Events at Chemical Synapse (con’t) 3. NT diffuses across synaptic cleft 4. NT binds to its specific receptor on postsynpatic membrane 5. ion channels open in postsynpatic membrane allowing ion movement See A.D.A.M. Nervous System II CD Fig. 11.18, p. 409

  37. Postsynaptic Potentials and Synaptic Integration • transmission from presynaptic to postsynaptic neuron is excitatory or inhibitory depending on type of NT released • each presynaptic neuron releases eitherexcitatory NT orinhibitory NT • postsynpatic membranes normally dendrite or cell body (soma or perikaryon)

  38. Postsynaptic Potentials and Synaptic Integration • reaction of receptors to NTs is graded, response depends on number of receptors involved (which depends on amount of NT released) • excitatory postsynaptic potentials (EPSPs) • inhibitory postsynaptic potentials (IPSPs)

  39. Excitatory Synapses and EPSPs • binding of NT released by presynaptic membrane to receptor (on postsynaptic membrane) causes opening of membrane channels that allow both Na+ and K+ to diffuse across postsynaptic membrane • because more Na+ enters than K+ leaves • --> net depolarization • local graded excitatory postsynaptic potential (EPSP) • if EPSP is sufficiently large, may spread to axon hillock leading to AP

  40. Excitatory Synapses and EPSPs Fig. 11.19, p. 410

  41. Inhibitory Synapses and IPSPs • binding of NT released by presynaptic membrane to receptor (on postsynaptic membrane) causes opening of membrane channels that allow K+ to diffuse out of post-synaptic cell, or Cl- to diffuse in, or both • causes hyperpolarization Fig. 11.19, p. 410

  42. Modification of Synaptic Events • Temporal summation • 1 or more presynaptic neurons fire before 1st EPSP fades • if summed EPSP is large enough, then get AP Fig. 11.20, p. 412

  43. Modification of Synaptic Events Spatial summation • large number of axonal terminals from different neurons or the same neuron fire at the same time • if EPSP is large enough, then get AP Fig. 11.20, p. 412

  44. Spatial Summation EPSP and IPSP • IPSP and EPSP have opposite effects • if only IPSPs occur, postsynaptic membrane becomes hyperpolarized • effects of IPSP may be temporally or spatially summed • usually IPSPs prevent membrane from becoming as depolarized as it would with only EPSPs Fig. 11.20, p. 412

  45. Synaptic Potentiation and Facilitation • synaptic potentiation:presynaptic axonal terminal that has received repeated (in short period of time) or continuous stimulation contains more intracellular Ca2+ than normal triggers greater release of NT into synaptic cleft --> produces larger EPSP in postsynaptic cell (important in memory and learning processes) • facilitation:postsynaptic neuron that has been partially depolarized is more likely to undergo AP,

  46. Termination of NT Effects • removal from cleft by reuptake into astrocytes or presynaptic membrane (e.g., norepinephrine) • degradation of NT by enzymes present in postsynaptic membrane or synaptic cleft • e.g., acetylcholine [ACh] degraded by the enzyme acetylcholinesterase - [AChE] • diffusion away from cleft

  47. Functional Classification ofNeurotransmitters (NTs) A. Based on effects • excitatory – cause depolarization (glutamate) • inhibitory – cause hyperpolarization (GABA) • effect of some depends on postsynaptic membrane receptors • ACh and NE have different receptor types – some that cause excitation and other types that causes inhibition B. Based on mechanism of action • direct (channel-linked receptors) • indirect (G protein-linked receptors = second messenger system)

  48. Modes of Action: Direct Action • excitatory examples: aspartate, acetylcholine (ACh), glutamate, ATP • open Na+/K+, Ca2+ channels leading to depolarization • inhibitory examples: gamma aminobutyric acid (GABA), glycine • open Cl- or K+ channels leading to hyperpolarization • open ion channels • immediate and localized action • action depends on binding of NT to receptors followed by channel activation, ion influx and membrane potential changes Fig. 11.22, p. 418

  49. Modes of Action: Indirect Action • slower, longer-lasting effects • work through second messengers • binding of NT with receptor activates G protein in membrane which works through cyclic AMP (cAMP = second messenger) to: • regulate ion channels (open or close) • activate kinase enzymes within cytoplasm (activate proteins in cytoplasm)

  50. Modes of Action: Indirect Action • Examples • Biogenic amines (dopamine, norepinephrine, epinephrine) • Peptides (endorphins, dynorphins, substance P) • ACh (at muscarinic receptors) Fig. 11.22, p. 418

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