Unit V: Electrophysiology - CCBC Faculty Web

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 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 Membrane Channels Two major classes of channels: 1. Leakage channels (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) 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 Resting Membrane Potential (RMP) Intracellular environment different from extracellular environment in ionic composition Fig. 11.8, p. 398

Outside: more Na+, Cl- Inside: more K+, protein (anion) Negative inside compared to outside; RMP = -70 mV 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

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

Diffusion Types of Potentials Graded Potential 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 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 Depolarization and Hyperpolarization Fig. 11.9, p. 399 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 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 dont continues once started passed through membrane of excitable cells (neurons and muscles) called nerve impulse when passed through axon Action Potential (cont)

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 Events of an Action Potential

Fig. 11.12, p. 402 stimulus AP: Depolarization 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 voltagegated Na+ channels open (#2 in figure) Na+ influx (positive feedback) timed gates on Na+ channels close, K+ channels open for repolarization

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 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 Comparison of Graded and Action Potentials Characteristic

Amplitude Graded Potential Variable Action Potential Always the same (all-or-none) Duration Variable (depends on stimulus) Rapid membrane change

Channels Chemically- or mechanically-gated Dendrites, perikaryon Voltage-gated Location Propagation Refractory period Membrane voltage change

Axon hillock, axon Localized (short-distance) Transmitted along axon as impulse None (allows summation) Absolute (no new APs); Refractory (only with stronger stimulus) Depolarization or Depolarization, followed by hyperpolarization repolarization and hyperpolarization 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 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 direction is one-way due to absolute refractory period

shown in light blue Fig. 11.13, p. 404 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 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 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 persons own antibodies Factors Influencing Impulse Conduction: Intrinsic Factors 3. Three groups of fibers: A B

C Groups based on: diameter degree of myelination 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)

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) 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 Extrinsic Factors (cont) 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

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

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 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

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 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 Chemical Synapses

Fig. 11.18, p. 409 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 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

Events at Chemical Synapse (cont) 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 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 either excitatory NT or inhibitory NT postsynpatic membranes normally dendrite or cell body (soma or perikaryon) 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) 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 Excitatory Synapses and EPSPs Fig. 11.19, p. 410 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 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

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 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 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, Termination of NT Effects 1. removal from cleft by reuptake into astrocytes

or presynaptic membrane (e.g., norepinephrine) 2. degradation of NT by enzymes present in postsynaptic membrane or synaptic cleft 3. e.g., acetylcholine [ACh] degraded by the enzyme acetylcholinesterase - [AChE] diffusion away from cleft

Functional Classification of Neurotransmitters (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) Modes of Action: Direct Action excitatory examples: aspartate, acetylcholine (ACh), glutamate, ATP *open Na+/K+, Ca2+ channels leading to open ion channels depolarization immediate and localized inhibitory examples: action gamma aminobutyric acid action depends on binding (GABA), glycine of NT to receptors followed *open Cl- or K+ channels

by channel activation, ion leading to influx and membrane hyperpolarization potential changes Fig. 11.22, p. 418 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) 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 Structural Classes of Neurotransmitters

Classified according to chemical structure: Acetylcholine (ACh) Biogenic Amines Amino Acids Peptides Novel Messengers Acetylcholine (ACh)

first NT to be discovered excitatory to skeletal muscles excitatory/inhibitory to viscera found in CNS and PNS (NMJ with skeletal muscle, NEJ for parasympathetic nervous system) formed from acetyl-CoA and choline degraded by acetylcholinesterase (AChE) Myasthenia gravis - autoimmune disorder of skeletal muscle ACh receptors Alzheimers disease - decreased ACh level in brain that ultimately results in mental deterioration

Biogenic Amines synthesized from amino acid tyrosine found in CNS and PNS catecholamines - norepinephrine [NE], epinephrine, dopamine, - excitatory or inhibitory indolamines - seratonin and histamine

- generally inhibitory play role in emotional behavior and help regulate biological clock; norepinephrine is main NT of sympathetic division of ANS schizophrenia - overproduction of dopamine Parkinsons disease - deficient dopamine in basal ganglia Amino Acids & Peptides

Amino Acids GABA = gamma amino butyric acid (principal inhibitory NT in brain), glycine (generally inhibitory NT, in spinal cord), glutamate (CNS, excitatory) Peptides (Neuropeptides) strings of amino acids produced in CNS and PNS: - endorphins and enkephalins (natural opiates) - substance P (mediator of pain signals)

some also produced by nonneural tissues (e.g., cells of GI tract - somatostatin, cholecystokinin, vasoactive intestinal peptide [VIP]) Novel Messengers Neurotransmitters that dont fit other categories NO = nitric oxide involved in long-term synaptic potentiation (learning and memory) relaxation of intestinal smooth muscles responsible for brain damage in stroke patients ATP = adenosine triphosphate promotes synthesis and uptake of other NTs in CNS and PNS CO = carbon monoxide

enhances neurotransmission in some circuits involved in logic regulator of cyclic GMP (second messenger) Organization of Neurons: Types of Circuits Simple series circuit Converging circuit Diverging circuit

Reverberating (oscillatory) circuit Parallel after-discharge circuit Simple Series Circuit one presynaptic neuron goes to one postsynaptic neuron; e.g., simple reflex arc presynaptic synapses Fig. 11.25, p. 421 postsynaptic

Converging Circuits several presynaptic axonal terminals go to single postsynaptic neuron (output) input from several pathways produces single result

e.g., voluntary vs subconscious breathing; happy baby Fig. 11.24, p. 420 Diverging Circuits one presynaptic neuron --> several postsynaptic neurons e.g., single motor neuron from brain may go to several motor neurons in spinal cord (thence to several muscle fibers) e.g., single sensory neuron to CNS may be part of reflex but also send info to brain

Fig. 11.24, p. 420 Reverberating (Oscillatory) Circuits chain of neurons with synapses to neurons earlier in circuit sleep-wake cycle breathing possibly short-term memory some motor activities (arm swinging) Fig. 11.24, p. 420

Parallel After-Discharge Circuit one presynaptic neuron fires to several postsynaptic neurons arranged in parallel that eventually result in common output many different responses occur simultaneously may be involved in problem solving Fig. 11.24, p. 420

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