Transcript Temporal Aspects of Visual Extinction

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
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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
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.
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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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Intra vs Extracellular fluid
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MCQ

A.
B.
C.
D.
What is hyperkalemia
Not enough potassium
Not enough sodium
Too much patassium
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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An action potential
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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 postsynaptic 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 Types
1. 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 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
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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
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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 Types
Small 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 DA
Parkinsons
‘Normal’
Too much DA
Schizophrenia
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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
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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
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Peptides
Important in Pain Management
Examples
– Enkephalin
– Endorphins
– Substance P
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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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