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Transcript
Nerves and Muscles How a nervous impulse becomes A muscular contraction Anatomy of a Motor Neuron Nerve cell body Nucleolus Nissel Bodies Axon Schwann Cell Synaptic Knob Nucleus Dendrite Axon Hillock Nodes of Ranvier Myelin Sheath Synaptic Vesicle The Nervous ImpulseMembrane potential • Potential difference • -is the difference in charge between 2 points –inside and outside the membrane. • -cells are said to be polarized Resting potential • -the potential difference in a neuron when there is no impulse. • -negative ions build up in the cytosol of the neuron next to the membrane • -positive ions build up in the extracellular fluid next to the membrane Charge distribution inside and outside a nerve cell Out + + + + + + + + + + + + + + + + + + + Na • _____________________________________ • ------------------------------ K • In + - + - + - + - + - + - + - + • ------------------------------ • ------------------------------------------------------------Out + + + + + + + + + + + + + + + + + + + + The Facts • Out side the nerve membrane is positive due to Sodium ions • Inside the membrane has positive potassium ions but also – Negatively charged ions (like phosphate) – Negatively charged amino acids – And the inside of a resting nerve cell is NEGATIVE! Potential Difference • The potential difference of a typical neuron is -70 millivolts. • *The minus sign indicates the inside is relatively negative to the outside. • Most body cells are “polarized” Why there is a resting potential: Unequal distribution of ions across the membrane -Extracellular fluid rich in Na+ and Cl-K+ is the main intracellular cation and phosphates and amino acids are the main anions Relative membrane permeability to Na+ and K+ -permeability of plasma membrane is 50-100 times greater for K+ in a resting neuron or muscle fiber. Potassium ions and resting potentialRemember diffusion? -if the membrane were freely permeable to K+ but impermeable to other cations, then K+ would leave the cell until the electrical gradient (holding K+ inside the cell) was equal to the chemical gradient (pushing K+ out of the cell). The Whole Picture • transmembrane potential of –90+mV is the equilibrium potential for K • The –70 mV membrane potential + reflects the effects of Na • The equilibrium potential for Na+ is + +66 mV (Na would flow inward) Active Forces Maintaining Resting Potential • There is a slow Na+ leak inward • There is also a slow K+ leak outward. • These are countered by the action of Na/K pumps and ATPase • Sodium pumps are electrogenic – contribute to electronegativity – pump 3 Na+ out for each 2 K+ in Graded Potentials excitable tissue responds to environmental stimuli • response is a small change in membrane potential • -results from opening or closing of membrane channels • membrane can become more polarized -hyperpolarization • membrane can become less polarized -hypopolarization • -60 -60 • ******** • ****** • -70 **** -70 • ****** • ** • -80 ******* -80 ____________________________________________ _ time (msec)10 time (msec) 10 • • Hyperpolarization Hypopolarization Important points: • Graded membrane potentials are localized • Only spread a short distance down the membrane ACTION POTENTIALS • A sequence of events that will result in a • • • • reversal of membrane potential and then restore resting potential. Result from the opening of 2 types of voltage gated channels -1st lets Na+ rush into the cell = depolarization -2nd lets K+ flow out of the cell = repolarization -whole process takes 1 msec GENERATION OF AN ACTION POTENTIAL Definitions: • Leakage channels: always open • Voltage gated channel: opens in response to a change in membrane potential -has 2 separate gates: • Inactivation gate= open during resting potential • Activation gate= closed during resting, opens when the threshold is reached 1. Depolarization to Threshold • Depolarizing graded potential (local currents) • Potential difference reaches threshold (-55mV) Activation of Sodium Channels, Rapid Depolarization • Voltage gated Na+ channels rapidly start to open • -Inactivation channels stay open in resting potential • -Activation channels open, membrane becomes more permeable to Na+ Next……… • Inrush of Na+ results in depolarization • Depolarization causes inflow of Na+, which causes further depolarization, which increases Na+ inflow -a positive feedback system. • Membrane potential goes from – 55mV to +30 mV in one millisec. Sodium Channel Inactivation and Potassium Channel Activation. -Repolarizing Phase • Positive potential results in a closing of Na inactivation channels • Threshold depolarization opens voltage gated K+ channels • K+ gated channels open slowly • Na+ channels close- Na+ inflow slows • Both electrical and chemical gradients favor the movement of K+ out • Loss of positive charges restores the membrane potential to the resting levels • Na+ Channels remain inactivated until membrane reaches the threshold • Remain closed but can open at this time And…… • When membrane reaches normal resting potential, K+ channels begin to close • Membrane reaches –90 mV before K+ channels are closed. Refractory Period • Absolute refractory period • Period where the membrane cannot respond to stimulation • Period begins from the point that all the Na voltage gated channels open at the threshold –(cannot open more!) • Period ends when sodium channels regain their normal resting condition. More.. • Relative refractory period is the period of hyperpolarization before resting potential is restored that requires a higher stimulation. And….. • Local anesthetics work by blocking the opening of the voltage gated sodium channels. • Propagation of the impulse: spreads to adjacent regions along the neuron. SIGNAL TRANSMISSION AT SYNAPSES • Important terms…. • Presynaptic neurons • Postsynaptic neurons • Synaptic cleft Types: • Electrical synapses: • Gap junctions -Tubular proteins called connexons -100 / gap junction -Connect cytosol of 2 cells -Provides a path for ions (current) • Visceral smooth muscle • Cardiac muscle Advantages • -faster -direct • -synchronization of the activity of a group of neurons or muscle fibers • -produce coordinated contractions • -2 way transmission Chemical Synapses • Action potential arrives at synaptic bulb • • • • (knob) Depolarization opens voltage gated Ca2+ channels Increase in Ca2+ concentration triggers exocytosis of synaptic vesicles Neurotransmitters are released into the synaptic cleft Diffuse across cleft and bind to neurotransmitter receptor sites Jump! • Binding of neurotransmitter to receptor is part of a ligand gated channel, these will open • Open channels allow the flow of ions across the membrane. • Change in the polarization of the membrane will result. • One way transfer. • Acetylcholine is the neurotransmitter of skeletal muscle Questions you need to be able to answer: • • • • • • • 1. What is potential difference? 2. What is resting potential in a neuron? 3. What is a graded potential? 4. What is an action potential? 5. What is the sequence of events in an action potential? 6. What is the role of neurotransmitters? 7. What is the sequence of events in the release of neurotransmitters? NEUROMUSCULAR JUNCTIONS: Chapter 10, p315 • Definition: the synapse between a motor neuron and a skeletal muscle fiber. NMJ are usually at the middle of long skeletal muscle fibers. • Motor neuron divides into many synaptic “bulbs” • Motor end plate is the region of the sarcolemma that is adjacent to the synaptic bulb. Important structures in “Jump”! • Motor Unit: Muscle fibers controlled by a motor neuron • Motor Unit • Motor Neuron • Neuromuscular Junction • Motor End Plate • Sarcolemma GENERATION OF A MUSCLE ACTION POTENTIAL • Motor Neuron releases acetylcholine (Ach) from the synaptic bulbs • ACh binds receptors on the sarcolemma • Gated ion channels open letting in Na+ • Na makes the inside of the muscle fiber more + • Triggers muscle action potential And then….. • -travels along the sarcolemma • -into the T tubules • One nerve impulse triggers one muscle action potential • ACh is broken down by acetylcholinesterase (AChE) – attached to collagen fibers in the synaptic cleft • Muscle action potentials cease Clinical Correlations: • Botulinum Toxin: blocks the exocytosis of synaptic vesicles at NMJ. ACh is not released and contractions do not occur. Paralysis • Curare: binds the ACh receptor so the gated channel does not open. Paralysis • Anticholinesterase agents: slow the activity of cholinesterase. Prolongs the time ACh is in the synaptic cleft.