Neurons: Cellular and Network Properties HUMAN PHYSIOLOGY POWERPOINT

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POWERPOINT LECTURE SLIDE PRESENTATION by LYNN CIALDELLA, MA, MBA, The University of Texas at Austin Additional text by J Padilla exclusively for physiology at ECC UNIT 2 8 Neurons: PART A Cellular and Network Properties HUMAN PHYSIOLOGY AN INTEGRATED APPROACH FOURTH EDITION DEE UNGLAUB SILVERTHORN

About this Chapter Organization of the nervous system Electrical signals in neurons Cell-to-cell communication in the nervous system Integration of neural information transfer

Nervous System Subdivisions

Organization of the Nervous System Figure 8-1

Model Neuron Dendrites receive incoming signals; axons carry outgoing information Figure 8-2

Cells of Nervous System (NS): Axons Transport Slow axonal transport Moves material by axoplasmic flow at 0.2 2.5 mm/day Fast axonal transport Moves organelles at rates of up to 400 mm/day Forward transport: from cell body to axon terminal Backward transport: from axon terminal to cell body

Cells of NS: Glial Cells and Their Function Glial cells maintain an environment suitable for proper neuron function Figure 8-5 (1 of 2)

Graded Potential The cell body receives stimulus The strength is determined by how much charge enters the cell The strength of the graded potential diminishes over distance due to current leak and cytoplasmic resistance The amplitude increases as more sodium enters, the higher the amplitude, the further the spread of the signal

Electrical Signals: Graded Potentials Subthreshold and suprathreshold graded potentials in a neuron If a graded potential does not go beyond the treshold at the trigger zone an action potential will not be generated Figure 8-8a

Electrical Signals: Graded Potentials Depolarizing grading potential are excitatory Hyperpolarizing graded potentials are inhibitory Graded potential= short distance, lose strength as they travel, can initate an action potential Figure 8-8b

Electrical Signals: Trigger Zone Graded potential enters trigger zone- summation brings it to a level above threshold Voltage-gated Na + channels open and Na + enters axon a segment of the membrane depolarizes Positive charge spreads along adjacent sections of axon by local current flow as the signal moves away the currently stimulated area returns to its resting potential Local current flow causes new section of the membrane to depolarize this new section is creating a new set of action potentials that will trigger the next area to be depolarized The refractory period prevents backward conduction; loss of K + repolarizes the membrane Once the Na+ close they will not open in response to backward conduction until they have reset to their resting position- ensures only one action potential is initiated at time.

Electrical Signals: Voltage-Gated Na + Channels Na+ channels have two gates: activation and inactivation gates Figure 8-10c

Changes in Membrane Potential Terminology associated with changes in membrane potential (chpt 5 figure) PLAY Animation: Nervous I: The Membrane Potential Figure 5-37

Electrical Signals: Action Potentials Cell is more positive outside than inside Rising phase Figure 8-9 (1 of 9)

Electrical Signals: Action Potentials Rising phase As ions move across the membrane the potential increases Figure 8-9 (2 of 9)

Electrical Signals: Action Potentials Rising phase Graded potentials have brought the membrane potential up to threshold Figure 8-9 (3 of 9)

Electrical Signals: Action Potentials Rising phase Beyond threshold potential the sodium gated channels allow the ion to move in, making the inside of the cell more positive Figure 8-9 (4 of 9)

Electrical Signals: Action Potentials Na+ continues to move into the cell until it reaches electrical equilibrium. At that point Na+ movement stops Figure 8-9 (5 of 9)

Electrical Signals: Action Potentials Falling phase K+ moves out of the cell along its gradient and the inside of the cell becomes more and more negative Figure 8-9 (6 of 9)

Electrical Signals: Action Potentials Hyperpolarization (undershoot) occurs when the potential drops below resting; caused by the continuing movement of K+ out of the cell Figure 8-9 (7 of 9)

Electrical Signals: Action Potentials Leaked Na+ & K+ in cell increases potential toward resting voltage Figure 8-9 (8 of 9)

Electrical Signals: Action Potentials Returns to its original state where the outside is more positive than the inside and the membrane potential is -70mv Figure 8-9 (9 of 9)

Electrical Signals: Ion Movement During an Action Potential Figure 8-11

Electrical Signals: Action Potentials Figure 8-9

Electrical Signals: Refractory Period Action potentials will not fire during an absolute refractory period Figure 8-12

Action Potential Travel Down Axon Each region of the axon experiences a different phase of the action potential

Electrical Signals: Myelinated Axons Saltatory conduction- signal seems to jump from node to node moving swiftly- compensates for smaller diameter. Demyelination slows down signal conduction because the current leaks. Sometimes conduction does not reach the next node and dies out.

Electrical Signals: Speed of action potential Speed of action potential in neurons is influenced by: Diameter of axon Larger axons are faster- less resistance to ion flow due to the larger diameter. Large diameter axons are only found in animals with small less complex nervous systems. Resistance of axon membrane to ion leakage out of the cell Myelinated axons are faster the myelin sheath insulates the membrane allowing the action potential to pass along myelinated are sustaining conduction without slowing down by ion channels opening.

Electrical Signals: Coding for Stimulus Intensity Since all action potentials are identical, the strength of a stimulus is indicated by the defrequency of action potentials. Neurotransmitter amounts released are directly propertional to frequency as long as a sufficient supply is available Figure 8-13b

POWERPOINT LECTURE SLIDE PRESENTATION by LYNN CIALDELLA, MA, MBA, The University of Texas at Austin Additional text by J Padilla exclusively for physiology at ECC UNIT 2 5PART A Membrane Dynamics HUMAN PHYSIOLOGY AN INTEGRATED APPROACH FOURTH EDITION DEE UNGLAUB SILVERTHORN

Electricity Review Law of conservation of electrical charges- the net amount of electrical charge produced in any process is zero. Opposite charges attract; like charges repel each other- happens with protons & electrons Separating positive charges from negative charges requires energy membrane pumps use active transport so separate ions Conductor versus insulator a conductor allows the charges to move towards each other and an insulator keeps them separate- does not carry current.

Separation of Electrical Charges Resting membrane potential is the electrical gradient between ECF and ICF Inside of the cell is more negative than the outside Electrical gradient create the ability to do work just like concentration gradients Figure 5-32b

Separation of Electrical Charges Resting membrane potential is the electrical gradient between ECF and ICF. Resting membrane potential is due mostly to potassium- it is the equilibrium potential of K+ A relative scale shifts the charge to a -2 Figure 5-32c

Potassium Equilibrium Potential

Sodium Equilibrium Potential Can be calculated using the Nernst Equation Concentration gradient is opposed by membrane potential Figure 5-35

Electrical Signals: Nernst Equation Predicts membrane potential for single ionmembrane potentials result from an uneven distribution of ions across a membrane. Membrane potential is influenced by : Concentration gradient of ions Na+, Cl-, & Ca2+ have higher [extracellular] and K+ has a higher [intracellular] Membrane permeability to those ions - only K+ is allowed to move in so this ion contributes to the resting potential

Electrical Signals: GHK Equation Predicts membrane potential using multiple ionsresting membrane potential= the contribution of all ions that cross the membrane X membrane permeability values. Ion contribution is proportional to membrane permeability for that ion. Potentials will be affected if ion concentrations change. P=permeability value

Electrical Signals: Ion Movement Resting membrane potential determined by K + concentration gradient Cell s resting permeability to K +, Na +, and Cl Gated channels control ion permeability Mechanically gated respond to physical forces (pressure) Chemical gated - respond to ligands (neurotransmitter) Voltage gated - respond to membrane potential changes Threshold voltage varies from one channel type to another the minimum stimulus required and the response speed varies for each type

Cell-to-Cell: Postsynaptic Response Fast and slow responses in postsynaptic cells involve ion channels and G-protein receptor Presynaptic axon terminal Rapid, short-acting fast synaptic potential Chemically gated ion channel Neurotransmitter Slow synaptic potentials and long-term effects G protein coupled receptor G R Postsynaptic cell Alters open state of ion channels Inactiv e pathw ay Activ ated second messenger pathw ay Ion channels open More Na + in EPSP = excitatory depolarization More K + out or Cl in Less Na + in IPSP = inhibitory hyperpolarization Ion channels close Less K + out EPSP = excitatory depolarization Modifies existing proteins or regulates synthesis of new proteins Coordinated intracellular response Figure 8-23

Cell-to-Cell: Chemical Synapse Chemical synapses use neurotransmitters; electrical synapses pass electrical signals. Chemical synapses are most common. Electrical synapses are found in the CNS and other cells that use electrical signals (heart) Figure 8-20

Cell-to-Cell: Calcium Events at the synapse Action potential 1 An action potential depolarizes the axon term inal. Axon term inal Synaptic vesicle 2 3 The depolarization opens voltagegated Ca 2+ channels and Ca 2+ enters the cell. Calcium entry triggers exocytosis of synaptic vesicle contents. 1 Voltage-gated Ca 2+ channel 2 Ca 2+ Ca 2+ Docking protein 3 4 4 5 Receptor Neurotransmitter diffuses across the synaptic cleft and binds with receptors on the postsynaptic cell. Neurotransmitter binding initiates a response in the postsynaptic cell. Postsynaptic cell Cell response Exocytosis: Classic versus kiss-and-run 5 Figure 8-21

Cell-to-Cell: Acetylcholine Synthesis and recycling of acetylcholine at a synapse Figure 8-22

Integration: Long-Term Potentiation Long-term potentiation- mechanism used in learning and memory using Glutaminergic Receptors. Figure 8-30

Cell-to-Cell: Inactivation of Neurotransmitters Figure 8-24

Cell-to-Cell: Neurocrines Seven classes by structure - Acetylcholine (Ach) neurotransmitter composed of choline and coenzyme A (acetyl CoA), binds to cholinergic receptors Amines neurotransmitter, derived from a single amino acid: Dopamine, Norepinephrine, Epinephrine, Serotonin, Histamine Amino acids an amino acid that functions as a neurotransmitter: Glutamate, Aspartate, Gamma-aminobutyric, Glycine Purines made from adenine Gases act as neurotransmitter, half-life of 2-30 sec. Peptides -neurohoromones, neurotransmitters, and neuromodulator, Lipids eicosanoids

Cell-to-Cell: Amine Derived from single amino acid Tyrosine Dopamine -neurotransmitter/neurhormone Norepinephrine -tyrosine, neurotransmitter/neurhormone, secreted by noradrenogenic neurons, Epinephrine - neurotransmitter/neurhormone, also called adrenaline, secreted by adrenogenic neurons Others Serotonin neurotransmitter, is made from tryptophan Histamine neurotransmitter, is made from histadine

Cell-to-Cell: Amino Acids Glutamate: primary excitatory CNS Aspartate: primary excitatory brain (select regions) Gamma-aminobutyric(GABA): Inhibitory brain Glycine Inhibitory spinal cord May also be excitatory

Cell-to-Cell: Neurocrines Peptides -involved in pain and pain relieve pathways Substance P and opioid peptides Purines- bind purinergic receptors AMP and ATP Gases- produced inside the body, function and mechanisms not totally understood NO and CO Lipids -bind cannabinoid receptors in brain and immune system cells Eicosanoids

Cell-to-Cell: Receptors Cholinergic receptors Nicotinic on skeletal muscle, in PNS and CNS Monovalent cation channels Na + and K + Muscarinic in CNS and PNS Linked to G proteins Adrenergic Receptors α and β- two classes Linked to G proteins- initiate second messenger

Integration: Injury to Neurons If the cell body is not damaged the neuron will most likely survive. Axon healing is similar to growth cone of a developing axon. Figure 8-32