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Chapter 5b Nerve Cells

Chapter 5b Nerve Cells. Chris Rorden University of South Carolina Norman J. Arnold School of Public Health Department of Communication Sciences and Disorders University of South Carolina. MCQ. Visual problem after superficial damage to this region of left hemisphere… Blind

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Chapter 5b Nerve Cells

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  1. Chapter 5b Nerve Cells • Chris Rorden University of South Carolina Norman J. Arnold School of Public Health Department of Communication Sciences and Disorders University of South Carolina

  2. MCQ • Visual problem after superficial damage to this region of left hemisphere… • Blind • Blind left of fixation • Blind right of fixation • These regions not responsible for vision.

  3. MCQ • Movement problem after superficial damage to this region of left hemisphere… • Paralyzed on both sides • Weak on left • Weak on right • These regions not responsible for movement.

  4. MCQ • Somatosensory problem after superficial damage to this region of left hemisphere… • Unable to feel on either side • Numb on left • Num on right • These regions not responsible for touch.

  5. MCQ • Language problem after superficial damage to this region of left hemisphere… • Poor speech comprehension • Poor language comprehension • Poor speech production • Poor writen language production

  6. Hierarchy of Organism Structures • Organism • Organ Systems • Organs • Tissues • Cells • Organelles • Organic Molecules

  7. Cell components • Channels • Structural Proteins • Sodium-Potasium Pump (Na-K) • Extracellular fluid • Intracellular fluid • Membranes – lipids attached to proteins. • Lipids (fats) do not dissolve in water • Separates extra and intra-cellular fluids.

  8. Cell membranes • Lipoproteins line up in double layer with protein (head) to outside and lipid tail to inside of membrane

  9. Resting Potentials • All Cells have General Characteristic of Irritability. • Need Irritability to Respond to Outside Influences. • Well Developed in Neurons. • Intracellular Fluid is -70 mvolts as Compared to Extracellular Fluid.

  10. Why? • Uneven distribution of • Positively charged sodium • Positively charged potassium • Negatively charged chloride ions • Other negatively charged proteins. • Channels Open to Selectively Allow Movement of Ions. • Na-K Pump Helps to Keep Resting Potential.

  11. Intra vs Extracellular fluid

  12. MCQ • What is hyperkalemia • Not enough potassium • Not enough sodium • Too much patassium • Too much sodium

  13. hyperkalemia • hyper- means high (contrast with hypo-, meaning low). • kalium, which is neo-Latin for potassium. • -emia, means "in the blood". • Death by lethal injection, kidney failure • If neurons can not maintain a K gradient, they will not generate an action potential.

  14. Graded local potentials • Mechanical or Chemical Event Affects Neuronal Membrane • Neuron Becomes Perturbed (Perturbation) • Channels Open Causing Negative Ions to Flow Out or Positive Ions to Flow in

  15. Changes in resting potential • Resting Potential Becomes Less than -70 mvolts = Depolarization • Resting Potential Becomes More than -70 mvolts = Hyperpolarization • If voltage exceeds threshold (~-55mV) the neuron fires.

  16. Movement of Graded Potentials • Potential changes can occur in soma, along dendrite or initial portions of axon • Spreads along membrane, effect becomes smaller. • If depolatrization is at least 10mv at axon hillock, action potential is triggered • Smaller changes in potential will not influence neuron.

  17. Action potential • During an action potential • Membrane is Depolarized, then Sodium (Positive Charge) Flows into Cell Causing Interior Potential to Become Positive. • Impulse Occurs – travels down axon to terminals • Absolute Refractory Period • After Impulse Fires, Over Reaction Drives Interior Charge to -80 or -90 mV • Any Additional Charge Would be Hard to Activate Until Cell Returned to Normal Resting State of -70mV

  18. Impulse conduction • Neighboring Areas of the Cell Undergo Positive Charge Changes • The Impulse is Carried Through Continuous Short Distance Action Potentials • Myelin Speeds up the Impulse Through Saltatory Conduction • Unmyelinated: .5 to 2 meters/sec • Myelinated: 5 to 120 meters/sec

  19. An action potential

  20. Impulses Between Cells • Synapse • When a neuron fires, it pours neurotransmitters into the synaptic clefts of its terminals. • These neurotransmitters influence the post-synaptic membrane, either polarizing (inhibiting) or depolarizing (exciting) the target neuron.

  21. Conduction Velocities • Dependent on Size of Axon and Whether it is Myelinated or Not • Myelinated Fibers Conduct at 6m/sec Times Size of Fiber • ( 3um x 6m/sec=18m/sec) • Unmyelinated Fiber Diameter of 1 um Conducts Impulse at <1m/sec

  22. Neuronal Response to Injury • Two Types • Axonal (Retrograde) Reaction: Occurs When Sectioning of Axon Interrupts Information that returns to Cell Body and Interferes with Support Reprogramming • Wallerian Degeneration: Occurs When Axon Degenerates in Region Detached from cell Body

  23. Axonal Reaction • Chromatolysis: degenerative process of a neuron as a result of injury, fatigue, or exhaustion. • Begins between axon hillock and cell nucleus • Nissl bodies disintegrate • Displacement of nucleus from center of soma • If RNA Production and Protein Synthesis Increase, Cell May Survive and Return to Normal Size

  24. Wallerian Degeneration • Axon Dependent on Cytoplasm from Cell Body • Without Nourishment, Distal Portion of Axon Becomes Swollen and Begins Degenerating in 12-20 Hours • After 7 Days, Macrophagic Process (Cleanup) Begins and Takes 3-6 Months

  25. Neuroglial Responses • Glial cells multiply in Number: Hyperplasia • Increase in Size: Hypertrophy • Neurophils (Scavenger White Blood Cells) Arrive at Injury • Astrocytes Form a Glial Scar • Microglia Cells Ingest Debris • Cells May Return to Function

  26. Axonal Regeneration • PNS: • Ends of Axon are Cleaned • Sheath of Schwan Cell Guides Axon to Reconnect • Grows 4 mm/day • May Have Mismatch of Axons • CNS: • Minimal restoration after injury • Growth occurs, but not significant enough to be functional

  27. Neuro-transmitters • Two Types • Small molecules: transient effects • Acetylcholine, Norepinephrine, Dopamine, Serotonin, Glutamate, Y-aminobutyric acid (GABA) • Large Molecules - Longer Effects • Peptides : Table 5.4

  28. Neurotransmitter: Acetylcholine • Major Player in the PNS • Released in Synapses Where it is Released to Facilitate Stimulation of Synapse • Needed for Continuous Nerve Impulses • Most Studied Neurotransmitter • After Use, Picked Up By Acetylcholinesterase • Regulates Forebrain and Inhibits Basal Ganglia • Example: Scopolamine used for motion sickness. Blocks acetylcholine receptors

  29. Related Diseases • Myasthenia Gravis • Affects Acetylcholine receptors • Behavioral Example: Fatigue in Speaking • Alzheimer's Disease • Implication of Deficient Projections in Cortex, Hippocampus, and Orbito-frontal Cortex

  30. Dopamine • Cells are Located in Upper Midbrain and Project Ipsilaterally • Mesostriatal - Midbrain and Striatum • Substantia Nigra to Basal Ganglia • Results in Parkinson’s Disease • Mesocortical - Midbrain and Cortex • Can Result in Problems of Cognition and Motivation • Can be Affected by Drug Abuse to Gain Pleasurable Feelings

  31. Dopamine • Parkinson's disease: loss of dopamine in the neostriatum • Treatment: increase dopamine • Schizophrenia: Too much dopamine • Treatment: Block some (D2) dopamine receptors. • Problem: Overdose or prolonged dose leads to Parkinson's disease-like tremors (tardive dyskinesia) Not enough DA Parkinsons ‘Normal’ Too much DA Schizophrenia

  32. Norepinephrine • Pons and Medulla • Reticular Formation and Locus Ceruleus • Project to Diencephalon, Limbic Structures and Cerebral Cortex, Brainstem, Cerebellar Cortex and Spinal Cord • Maintain Attention and Vigilance • May be Related to Handedness Due to Asymmetry in Thalamus

  33. Serotonin • Found Primarily in Brain. Blood Platelets and GI Tract • Terminals at Most Levels of Brainstem and in Cerebrum • Involved in General Activity of CNS and in Sleep Patterns • Increased Concentration of Serotonin in Synaptic Cleft, Decreases Depression and Pain (Prozac)

  34. Y-Aminobutyric Acid (GABA) • Major Player in the CNS • Pyramidal (Motor Cortex) Cells Rich in GABA • Present in Hippocampus, Cortex of Cerebrum and Cerebellum • Suppress Firing of Projection Neurons • Implicated in Huntington’s Disease • Reduced GABA Causes High Amount of Dopamine and Acetylcholine and Uncontrolled Movements

  35. Peptides • Important in Pain Management • Examples • Enkephalin • Endorphins • Substance P

  36. Drug Treatments • Blocking Enzymatic Breakdown of Neurotransmitter • Allows for Increased Neurotransmitter to Continue Function • e.g. Myasthenia Gravis • Regulating Activity of Postsynaptic Membrane • Blocking Effects of Released Neurotransmitter Causing Problem

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