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Neuroscience > Lecture #5 Plasticity, Healing, Aging > Flashcards

Lecture #5 Plasticity, Healing, Aging Flashcards

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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
What is Regeneration?
Regrowth of original tissue
26
Regeneration occurs only if?
- Parenchymal cells can undergo cell mitosis - Surrounding connective tissue is intact
27
Regeneration must have cells that can?
Divide
28
What is Repair?
- Replacement of non regenerated parenchymal cells with connective tissue - Formation of a connective tissue scar
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Repair occurs with?
- Necrosis of permanent parenchymal cells - excessive necrosis of tissues
30
Neurons
- 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
Neuron axons and dendrites can regenerate if?
- Their cell bodies, basement membranes, and endoneurium are intact - Cell body intact, scaffolding present
32
Glial Cells
- Capable of regeneration - Responsible for repair
33
Damage to the PNS and CNS can occur from?
- Physical Trauma - Hypoxia - Degenerative disease
34
CNS Repair occurs in response to?
Neuronal cell death through necrosis/apoptosis
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Necrosis
- sequence of morphologic changes that occur in irreversibly injured cells
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Apoptosis
Programmed cell death
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Breakdown and Removal of Necrotic Tissue
Formation of an Empty Cavity
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Microglia & Macrophages
Phagocytosis and produce and secrete chemical mediators and growth factors
39
Endothelial Cells
Involved in angiogenesis
40
Fibroblasts
- Only present if blood-brain barriers are broken / Menings are penetrated
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Astrocytes
- Involved in gliosis and produce and secrete many molecules that serve structural functions
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Gliosis
Astrocytes form a dense aggregate with their cytoplasmic processes within the empty cavity
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Purpose of CNS Repair
- Reestablish the physical and chemical integrity in the CNS
44
Axonal Regeneration occurs in response to?
Damage to axons
45
Axotomy
- Transaction of an axon more slowly by crushing - Axon Regeneration more likely to occur
46
Axon Degeneration
- Proximal Segment: undergo reversible ultrastructural changes - Distal Segment: Undergoes Wallerian degeneration, nerve terminals fail rapidly
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Migration and Proliferation of Cells
- 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
Axonal Sprouting - PNS
- Axonal sprouts grow from the proximal segment, enter the connective tissue of the distal segment - Process largely directed by Schwann Cells
49
Axonal Sprouting - CNS
- Axonal sprouts approach glial scars - Axonal growth cones develop bulbous abnormalities and unable to migrate through glial scar
50
Significance of Axon regeneration
- Restore normal tissue structure and function - Axonal regeneration is greater in the PNS
51
What in the PNS are critical to successful regeneration?
Schwann cells
52
What prevents neuronal regrowth in the CNS?
Formation of glial scars
53
Damage in the CNS
Neuronal cell death
54
Greater life expectancy increases?
the risk of dementia - impaired memory and cognitive capacities
55
What is the most common cause of senile dementia?
Alzheimer disease
56
Similarities of the Mechanisms of Aging
- May result from changes in informational macromolecules (DNA, RNA, and proteins)
57
What are the 3 mechanisms of Aging
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
Structural Alterations for CNS (5)
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
Senile Plaques
- Extracellular deposits of beta-amyloid protein
60
Neurofibrillary Tangles
- Filamentous inclusions - Lesions are abundant in Alzheimer disease
61
Structure Alterations for PNS (4)
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
Age-related structural alterations can cause
- Diminished blood supply occurs in the CNS and PNS
63
Motor functional alterations
- Posture less erect, - Postural reflexes are slowed - Slow Gait - Stride length shorter Increase in risk of falls
64
Cognitive functional alterations
- Decrease in speed of learning, problem-solving, and general intelligence

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