Lecture #5 Plasticity, Healing, Aging Flashcards

1
Q

Plasticity

A
  • Experience can influence neural activity
  • Maximal during critical periods
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2
Q

Critical Period

A
  • Time which a behavior requires specific environmental influences to develop normally
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3
Q

Significance of Plasticity

A
  • Provide individuality
  • Recovery of function following brain trauma
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4
Q

Functional alterations of neural circuitry

A
  • Changes in the existing synaptic connections
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5
Q

Anatomical alterations of neural circuitry

A
  • longer term
  • Growth of new synaptic connections
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6
Q

Short-Term

A
  • Facilitation
  • Depression
  • Last a few minutes or less
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7
Q

*Facilitation

A
  • Elevation of presynaptic Calcium levels
  • Increase in neurotransmitter release
  • Bigger Postsynaptic potential
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8
Q

*Depression

A
  • Decrease in neurotransmitter release in response to high-frequency stimulation
  • Progressive depletion of synaptic vesicles
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9
Q

Long-Term

A
  • Anatomical Change
  • Long term Potentiation (Cerebellum)
  • Long term depression
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10
Q

State-Dependent

A

The state of the membrane potential of the postsynaptic cell determines whether or not LTP occurs

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11
Q

Input Specificity

A
  • LTP induced by activation at one synapse does not occur in other
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12
Q

Associativity

A
  • If one synapse is weakly activated while adjacent synapse onto the same cell is strongly activated, both synapses undergo LTP
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13
Q

Steps of Long-Term Potentiation

A
  • High-frequency stimulation with release of glutamate
  • Simultaneous depolarization through non-NMDA receptors & activation of NMDA receptors
  • Large and fast increase of Calcium

-Activation of Calcium dependent enzymes (intracellular signaling pathways)

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14
Q

Effects of Long-Term Potentiation

A
  • Increase in sensitivity to the neurotransmitter
  • Increase in excitatory postsynaptic potential size
  • Change in gene expression and synthesis of proteins
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15
Q

Potential cellular and molecular mechanisms of Hebb’s Postulate

A

Cells that fire together, wire together

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16
Q

Steps of Long-Term Depression

A
  • Low frequency stimulation with release of glutamate
  • Simultaneous depolarization through non-NMDA receptors & activation of NMDA receptors
  • Small and slow increase of Calcium
  • Activation of Calcium dependent enzymes (intracellular signaling pathways)
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17
Q

Effects of Long-Term Depression

A
  • Decrease in sensitivity to the neurotransmitter
  • Decrease in excitatory postsynaptic potential size
  • Changes in gene expression and synthesis of proteins
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18
Q

Growth of New Synaptic Connections

A
  • Long lasting effects of long term potentiation
  • Pruning of preexisting synapse and production of new ones
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19
Q

Memory

A

Long-term potentiation in the hippocampus can help with consolidating memories of events and facts

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20
Q

Primary Somatosensory Cortex

A

The area previously dedicated to the amputated digit becomes dedicated to the adjacent digits

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21
Q

Primary Motor Cortex

A

Areas previously dedicated to the hands become dedicated to the feet

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22
Q

Intermodal

A

Blind humans reading Braille have increased blood flow In both primary visual and visual association areas

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23
Q

What is important about Cortical Maps?

A

Activation of previously inactive connections is thought to play an important role

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24
Q

Tissue healing involves?

A
  • Regeneration
  • Repair
  • Combination of both
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25
Q

What is Regeneration?

A

Regrowth of original tissue

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26
Q

Regeneration occurs only if?

A
  • Parenchymal cells can undergo cell mitosis
  • Surrounding connective tissue is intact
27
Q

Regeneration must have cells that can?

A

Divide

28
Q

What is Repair?

A
  • Replacement of non regenerated parenchymal cells with connective tissue
  • Formation of a connective tissue scar
29
Q

Repair occurs with?

A
  • Necrosis of permanent parenchymal cells
  • excessive necrosis of tissues
30
Q

Neurons

A
  • Majority are not capable of regeneration
  • Neurogenesis requires a population of neural stem cells
  • Neural stem cells only give rise to interneurons in the olfactory bulb and hippocampus
31
Q

Neuron axons and dendrites can regenerate if?

A
  • Their cell bodies, basement membranes, and endoneurium are intact
  • Cell body intact, scaffolding present
32
Q

Glial Cells

A
  • Capable of regeneration
  • Responsible for repair
33
Q

Damage to the PNS and CNS can occur from?

A
  • Physical Trauma
  • Hypoxia
  • Degenerative disease
34
Q

CNS Repair occurs in response to?

A

Neuronal cell death through necrosis/apoptosis

35
Q

Necrosis

A
  • sequence of morphologic changes that occur in irreversibly injured cells
36
Q

Apoptosis

A

Programmed cell death

37
Q

Breakdown and Removal of Necrotic Tissue

A

Formation of an Empty Cavity

38
Q

Microglia & Macrophages

A

Phagocytosis and produce and secrete chemical mediators and growth factors

39
Q

Endothelial Cells

A

Involved in angiogenesis

40
Q

Fibroblasts

A
  • Only present if blood-brain barriers are broken / Menings are penetrated
41
Q

Astrocytes

A
  • Involved in gliosis and produce and secrete many molecules that serve structural functions
42
Q

Gliosis

A

Astrocytes form a dense aggregate with their cytoplasmic processes within the empty cavity

43
Q

Purpose of CNS Repair

A
  • Reestablish the physical and chemical integrity in the CNS
44
Q

Axonal Regeneration occurs in response to?

A

Damage to axons

45
Q

Axotomy

A
  • Transaction of an axon more slowly by crushing
  • Axon Regeneration more likely to occur
46
Q

Axon Degeneration

A
  • Proximal Segment: undergo reversible ultrastructural changes
  • Distal Segment: Undergoes Wallerian degeneration, nerve terminals fail rapidly
47
Q

Migration and Proliferation of Cells

A
  • PNS: Schwann, promote axon regeneration
  • CNS: Astrocytes, form glial scars that prevent axon growth and secrete molecules that inhibit axon regeneration
  • Oligodendrocytes: inhibit axon regeneration
48
Q

Axonal Sprouting - PNS

A
  • Axonal sprouts grow from the proximal segment, enter the connective tissue of the distal segment
  • Process largely directed by Schwann Cells
49
Q

Axonal Sprouting - CNS

A
  • Axonal sprouts approach glial scars
  • Axonal growth cones develop bulbous abnormalities and unable to migrate through glial scar
50
Q

Significance of Axon regeneration

A
  • Restore normal tissue structure and function
  • Axonal regeneration is greater in the PNS
51
Q

What in the PNS are critical to successful regeneration?

A

Schwann cells

52
Q

What prevents neuronal regrowth in the CNS?

A

Formation of glial scars

53
Q

Damage in the CNS

A

Neuronal cell death

54
Q

Greater life expectancy increases?

A

the risk of dementia - impaired memory and cognitive capacities

55
Q

What is the most common cause of senile dementia?

A

Alzheimer disease

56
Q

Similarities of the Mechanisms of Aging

A
  • May result from changes in informational macromolecules (DNA, RNA, and proteins)
57
Q

What are the 3 mechanisms of Aging

A
  1. Errors in the duplication of DNA increase with age
  2. There is a specific genetic program for aging
  3. A cell can only divide a limited number of times
58
Q

Structural Alterations for CNS (5)

A
  1. Decrease in Brain Volume and Weight - loss of tissue and neuron shrinkage
  2. Decrease in Nerve Conduction Velocity - fragmentation and loss of myelin
  3. Decrease in receptors and neurotransmitters
  4. Decrease in and alterations of synapses
  5. Increase in concentration of Plaques and Tangles
59
Q

Senile Plaques

A
  • Extracellular deposits of beta-amyloid protein
60
Q

Neurofibrillary Tangles

A
  • Filamentous inclusions
  • Lesions are abundant in Alzheimer disease
61
Q

Structure Alterations for PNS (4)

A
  1. Decrease in Number of Unmyelinated and Myelinated Nerve Fibers - loss of motor units
  2. Decrease in Nerve Conduction Velocity - fragmentation and loss of myelin
  3. Alterations of Density and Morphology of Sensory Receptors - vestibular, visual, and somatosensory systems
  4. Decrease in and Alterations of Synapses
62
Q

Age-related structural alterations can cause

A
  • Diminished blood supply occurs in the CNS and PNS
63
Q

Motor functional alterations

A
  • Posture less erect,
  • Postural reflexes are slowed
  • Slow Gait
  • Stride length shorter
    Increase in risk of falls
64
Q

Cognitive functional alterations

A
  • Decrease in speed of learning, problem-solving, and general intelligence