Mcb 80 - Lecture 22

Front 1

Describe the small-scale cellular changes that lead to plasticity in the adult nervous system

Back 1

- Changes in synaptic efficacy
- Changes in synaptic size
- Gain or loss of synaptic boutons

Front 2

Describe large-scale cellular changes that lead to plasticity in the adult nervous system.

Back 2

- Growth of new axon branches
- Formation of new synaptic connections
- "Pruning" of axon branches
- Elimination of synaptic connections
- Formation of new neurons

Front 3

How do owls localize sounds?

Back 3

Interaural time difference (ITD) and interaural intensity difference; coordinates visual and auditory space maps

Front 4

Describe how owls coordinate visual and auditory space maps.

Back 4

The visual and auditory receptive fields are in corresponding locations; input from the ears passes through the ICX (auditory space map) which evaluates the time it took to reach the ears and coordinates that in the optic tectum with visual input from the eyes which encode the angle of visual input

Front 5

Who did the experiment that showed owls "require" to match the two receptive fields created by goggles?

Back 5

Eric Knudsen

Front 6

What are 3 ways to extend the critical period for owls with the goggles?

Back 6

1. If first fit young owl with prisms during the critical period, then re-fit during adulthood, there is much greater remapping than if the prisms are first fit in adulthood
2. There is much more remapping if prisms of increasing strength are fit successively than if full-strength ones fit all at once.
3. Increased motivation/attention

Front 7

What did M. Merzenich show?

Back 7

When middle digit removed, its field was taken over by digits 2 and 4 (so even spread to cover absence)

Front 8

WHat happened when 3 fingers stimulated so that the brain thought they were one finger/

Back 8

Greater field given to those three fingers.

Front 9

Describe the difference in regeneration between peripheral and central axons.

Back 9

Peripheral axons in mammals (sensory, motor, autonomic) regenerate well following injury and function is sometimes completely restored; central axons (brain and spinal cord) regenerate very poorly and there is little recovery following central injury

Front 10

What happens when the axon is cut?

Back 10

Myelin degrades slowly, glial cells proliferate, and connective tissue builds up, so the nerve and tract persists even after the axon has degenerated

Front 11

Describe the experiment done to evaluate whether egenerative failure is due to the neuron or its environment.

Back 11

Take two nerves: one a motor nerve between spinal cord and muscle that normally would not regenerate, and optic nerve between retina and brain that normally would regenerate; cut both and all w it to regenerate; cut and swap; optic nerve between the spinal cord and muscle does not generate; motor neuron between retina and brain does regenerate ~ environment not the neuron itself

Front 12

Who did the regenerative experiment in which the neurons were cut and swapped?

Back 12

Aguayo

Front 13

What are 4 reasons the environment of the central nervous system does not allow regeneration.

Back 13

1. Neurons don't grow on myelin left behind after injury, because components of myelin inhibit axon growth
2. Neurons don't grow, because growth-promoting substances present during development are absent from the adult pathway
3. Astrocytes at sites of injury proliferate after injury and deposit scar tissue that blocks axon growth
4. There may also be problems with the neuron itself: decreased ability to re-enter "growth state."

Front 14

What are therapies to treat the factors that make the central nervous system unable to regenerate new neurons?

Back 14

1. Neurons don't grow on myelin left behind after injury, because components of myelin inhibit axon growth --- Therapy: Neutralize the inhibitor with antibodies or drugs or block their receptors on neurons
2. Neurons don't grow, because growth-promoting substances present during development are absent from the adult pathway --- Therapy: Add growth promoting substances or implant cells that make them
3. Astrocytes at sites of injury proliferate after injury and deposit scar tissue that blocks axon growth ---Therapy: Inject enzymes that dissolve the scars
4. There may also be problems with the neuron itself: decreased ability to re-enter "growth state." ---Therapy: Manipulate second messenger pathways in neurons to promote growth

Front 15

What are 3 ways that we might save injured neurons that would otherwise die or replace neurons that die?

Back 15

1. Interfering with apoptotic pathway after a potentially lethal insult but before the time of "commitment to die."
2. Stimulate neural stem cells in adults to generate additional neurons
3. Implant neurons or neural stem cells obtained from donors or other parts of the brain.

Front 16

For the trend of cognitive decline, what are the variables?

Back 16

Variation among individuals and among tasks

Front 17

Brings shrink with age. Is it because neurons are lost?

Back 17

No. Surprisingly few neurons are lost. Rather, caused by synapses, myelin, and dendrite degradation

Front 18

What are 8 characteristics of aged NMJs?

Back 18

1. Fragmentation: receptors are broken up into individual junctions rather than continuous
2. Dim AChRs
3. Partial Occupancy: axon begins to retract from synapse
4. Denervation
5. Sprouts: as if to migrate to another territory
6. Multiple Innervation
7. Axonal Dystrophy
8. Preterminal distension

Front 19

What percentage of adults over 85 are affected by dimentia?

Back 19

30-50%

Front 20

What shrinks during Alzheimer's disease?

Back 20

The hippocampus; You can actually see the ventrical shrinking

Front 21

What are 2 cellular hallmarks of alzheimers?

Back 21

1. Amyloid plaques: aggregates of peptide called "Abeta"
2. Tangles: Aggregates of a hyperphosphorylated form of "tau," a protein associated with microtubules

Front 22

What are amyloid plaques aggregates of?

Back 22

A peptide called "Abeta"

Front 23

What are tangles made of?

Back 23

Tau

Front 24

What scanning method provided the first way to see amyloid int he living brain?

Back 24

PET scan

Front 25

Do most cases of Alzheimer's have genetic components?

Back 25

No; most are "sporadic;" a subset, however, are clearly genetic

Front 26

What are 3 of the genes encode that are involved in the rare subset of genetically-transmitted Alzheimer's disease?

Back 26

1. APP
2. Presenilin-1
3. Presenilin-2

Front 27

What is APP?

Back 27

Protein from which the Abeta peptide, from which amyloid is derived; APP is cut into Abeat by enzymes called secretases

Front 28

What is Presenilin-1?

Back 28

A secretase that takesp art in cutting APP into Abeta

Front 29

What is Presenilin-2?

Back 29

Another APP-cutting secretase