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1 Chapter 5b Nerve Cells Chris Rorden University of South Carolina Norman J. Arnold School of Public...
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Transcript of 1 Chapter 5b Nerve Cells Chris Rorden University of South Carolina Norman J. Arnold School of Public...
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Chapter 5b Nerve Cells
Chris RordenUniversity of South CarolinaNorman J. Arnold School of Public HealthDepartment of Communication Sciences and DisordersUniversity of South Carolina
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MCQ
Visual problem after superficial damage to this region of left hemisphere…
A. Blind
B. Blind left of fixation
C. Blind right of fixation
D. These regions not responsible for vision.
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MCQ
Movement problem after superficial damage to this region of left hemisphere…
A. Paralyzed on both sides
B. Weak on left
C. Weak on right
D. These regions not responsible for movement.
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MCQ
Somatosensory problem after superficial damage to this region of left hemisphere…
A. Unable to feel on either side
B. Numb on left
C. Num on right
D. These regions not responsible for touch.
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MCQ
Language problem after superficial damage to this region of left hemisphere…
A. Poor speech comprehension
B. Poor language comprehension
C. Poor speech production
D. Poor writen language production
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Hierarchy of Organism Structures
Organism– Organ Systems
Organs– Tissues
Cells Organelles Organic Molecules
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Cell components
ChannelsStructural ProteinsSodium-Potasium Pump (Na-K)Extracellular fluid Intracellular fluidMembranes – lipids attached to proteins.
– Lipids (fats) do not dissolve in water– Separates extra and intra-cellular fluids.
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Cell membranes
Lipoproteins line up in double layer with protein (head) to outside and lipid tail to inside of membrane
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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.
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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.
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MCQ
What is hyperkalemia
A. Not enough potassium
B. Not enough sodium
C. Too much patassium
D. Too much sodium
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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.
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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
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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.
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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.
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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
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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
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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.
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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
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Neuronal Response to Injury
Two Types1. Axonal (Retrograde) Reaction: Occurs When
Sectioning of Axon Interrupts Information that returns to Cell Body and Interferes with Support Reprogramming
2. Wallerian Degeneration: Occurs When Axon Degenerates in Region Detached from cell Body
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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
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Wallerian Degeneration
Axon Dependent on Cytoplasm from Cell BodyWithout 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
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Neuroglial Responses
Glial cells multiply in Number: Hyperplasia Increase in Size: HypertrophyNeurophils (Scavenger White Blood Cells)
Arrive at InjuryAstrocytes Form a Glial ScarMicroglia Cells Ingest DebrisCells May Return to Function
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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
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Neuro-transmitters
Two TypesSmall molecules: transient effects
– Acetylcholine, Norepinephrine, Dopamine, Serotonin, Glutamate, Y-aminobutyric acid (GABA)
Large Molecules - Longer Effects– Peptides : Table 5.4
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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
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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
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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
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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 DAParkinsons
Too much DASchizophrenia
‘Normal’
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Norepinephrine
Pons and MedullaReticular Formation and Locus CeruleusProject to Diencephalon, Limbic Structures and
Cerebral Cortex, Brainstem, Cerebellar Cortex and Spinal Cord
Maintain Attention and VigilanceMay be Related to Handedness Due to
Asymmetry in Thalamus
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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)
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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