6/9- Neuroplasticity II Flashcards Preview

Term 5: Neuro > 6/9- Neuroplasticity II > Flashcards

Flashcards in 6/9- Neuroplasticity II Deck (48):

What does this show? What theory does it prove? 

CT scan of 44 yo man with normal IQ and only mild leg pain but very little brain matter

- Due to remarkable flexibility in programs of neural development, this did not prevent normal cognition and behavior; NEUROPLASTICITY!


T/F: Neural rewiring is an ongoing process



What accounts for brain's tremendous flexibility?

- Forming/eliminating neurons and their synapses

- Modifying the properties of existing synapses


How are experience-dependent changes stored?


- Synapses that get good feedback for performance stay strong and remain while others go away


How do neuromuscular junctions exemplify the theme of competition?

- Each muscle fiber is innervated by axons from several motor neurons, but by adulthood it is innervated by the axon of only 1 motor neuron

- This comes about through Darwinian competition; neurons have to find an open niche and chronically defend it 


What are neurons competing for?


- Life preserving chemicals that promote growth/survival, guide axons, and stimulate synaptogenesis

- Ex) Nerve Growth Factor (NGF)


How do ocular dominance columns display competition?

- At 15 days, layer 4 has uniform input from L and R eyes

- Labeling in this layer becomes patchy, reflecting alternating input if one eye is active and the other is inactive; shrunken columns result from occlusion of one eye (reduced effort -> reduced real estate)

- Depends on activity! 


What is this? 

Ocular dominance columns that are normal (left) and shrunken (occluded R eye)


What is strabismus? Impact?

- Unequal refraction, or an unclear media (cataract, vitreous hemorrhage, corneal blood staining)

- Input from that eye is taken over by the dominant eye, causing the weak eye to become blind (amblyopia)


Solution to strabismus?

Dominant eye must be suppressed, allowing weak eye to recapture territory

- Fix problem in weak eye

- Patch the strong eye


What is the critical period for the sensory alterations/clinical interventions for the visual cortex?

Before 7 yrs old (fairly early; visual world information doesn't really change over time)


What is the critical period for the sensory alterations/clinical interventions for the motor system?

Plasticity is lifelong (since you grow, get injured...)


Examples of motor plasticity?

- Cortical reorganization from motor output such as between a keyboard player and string player with an omega sign either bilaterally or unilaterally (respectively), indicating great fine motor movements in the hand(s)

- Gained function in other hand following a break

- Recovered function after a stroke from binding the other (strong) arm


What is Rasmussen's encephalitis? Treatment?

Rare, chronic inflammatory disease that usually affects only one hemisphere of the brain (in this case, causing increasingly frequent seizures)

Neurosurgeons did hemispherectomy (only resulted in slight limp) 


Can someone retain complete function after a hemispherectomy?

As long as the surgery is performed before the age of 8, the child does remarkably well (although would kill an adult)


How does the brain develop/get wired with so few genes?

Mother Nature builds a sloppy brain and then pushes it out into the rest of the world for experience to wire up the rest

- Ex) Circadian rhythm not initially 24 hrs

- Ex) Learning culture/societal norms of one's environment

- The gamble is the possibility of an impoverished environment


What was the result of early visual deprivation vs. enriched environment in analyzing the environmental alterations to the brain?

Early visual deprivation:

- Fewer synapses and dendritic spines in primary visual cortex

- Deficits in depth and pattern vision

Enriched environment:

- Thicker cortices

- Greater dendritic development - More synapses per neuron 


The case of Genie reveals the impact of what?

The impact of severe deprivation on development


What impact did Genie's environment have on her?

- Genie had been beaten, starved, restrained, kept in a dark room, denial of normal human interactions

- Discovered at age 13: 59 pounds, 54" tall

- Had almost no language

- Could not chew solid food and could hardly swallow

- Not toilet trained and could not focus her eyes beyond 12 feet


What is the critical period for the sensory alterations/clinical interventions for language?

The ability to learn language is limited to the years before puberty- after which the ability is lost


Could the damage be undone in Genie's case?

- Her vocabulary improved a bit, but she never understood the rules of grammar

- Critical period: the ability to learn language is limited to the years before puberty- after which the ability is lost


Why are young brains more plastic?

- Overproduction of synapses- prune back synapses based on use

- Cell death: 50% more neurons than are needed are produced; cell death is normal, due to failure to compete for chemicals


What is responsible for the growth of the brain after birth?

- New synapses

- Myelination

- Increased dendritic branching


T/F: Development of the prefrontal cortex is relatively fast due to its importance in executive control


Development of the prefrontal cortex is SLOW; it continues to develop until age 20


What is the effect of the relative rate of development (fast or slow) of the prefrontal cortex? What is the PFC responsible for?

Development of the prefrontal cortex is SLOW; it continues to develop until age 20

- This is what underlies age-related changes in cognitive function

- Plays a role in decision making, impulse control, working memory, and planning and carrying out sequences of actions


T/F: Cortex looks the same everywhere

T/F: Cortex is the same everywhere



Cortex looks the same everywhere because it is the same


If cortex is all the same, what determines its different fates?

Its fate depends largely on the input it receives

- If visual fibers rerouted to auditory cortex, then auditory cortex can see


T/F: Unused cortex is always taken over by competing neighborhoods



Examples of cortical reorganization following lack of use of parts of the cortex

- Ex) In the congenitally blind, verbal tasks activate the otherwise unused visual cortex; sound can activate the "visual" cortex

- Ex) distal arm/hand region in somatosensory cortex taken over by face and proximal arm/trunk/leg following amputation (or peripheral nerve damage or primary cortical area damage) 


T/F: Cortical reorganization/takeover is relatively slow

False; cortical takeovers are rapid!


How does cortical reorganization occur/territory become encroached so rapidly?

Short term: unmasking of already-existing connections

Long term: growth of new axons


What does cortical reorganization following disuse allow therapeutically? Examples?

Sensory substitution!

The brain is so plastic it will figure out any signal you plug into it

- Retinal implants

- Video converted into audioscape (seeing through your ears)

- VEST (versatile extra-sensory transducer) converting auditory vibrations into vibrations felt on chest

- Future will be plugging input directly into the brain


There is constant reorganization with sensory cortex maps by neural activity. What are some examples of this?

- Tinnitus produces major reorganization of 1' auditory cortex

- Adult musicians who play instruments fingered by left hand develop an enlarged representation of the hand

- Skill training (e.g.) juggling leads to reorganization of motor cortex


Neuroplastic responses to nervous system damage?

- Degeneration: deterioration

- Regeneration : regrowth of damaged nuerons

- Reorganization

- Recovery


What are the different types of neuronal degeneration? Characteristics?

Anterograde- degeneration of the distal segment, between the damage and synaptic terminal

- Cut off from the cell's metabolic center

- Swells and breaks off within a few days

Retrograde- degeneration of the proximal segment, between the damage and cell body

- Progresses slowly

- If regenerating axon makes new synaptic contact, the neuron may survive


T/F: Neural regeneration is common in the CNS? PNS?


- Regeneration is virtually nonexistent in the CNS of adult mammals

- Regeneration is unlikely, but possible, in the PNS


___ (CNS/PNS) neurons regenerate when transplanted into the ___ (CNS/PNS), but not vice versa

CNS neurons regenerate when transplanted into the PNS, but not vice versa


What cells promote neural regeneration? How?

Schwann cells (PNS)

- Neurotrophic factors stimulate growth

- Cell adhesion molecules provide a pathway


What cells block neural regeneration?

Oligondendroglia (CNS)


What are the outcomes for the following situation (neural regeneration in the PNS):

- Nerve is damaged without severing Schwann cell sheaths (e.g. by crushing)

Individual axons regenerate to their correct targets


What are the outcomes for the following situation (neural regeneration in the PNS):

- Nerve is damaged and the severed ends of the Schwann cell sheaths are slightly separated

Individual axons often regenerate up incorrect sheaths and reach incorrect targets


What are the outcomes for the following situation (neural regeneration in the PNS):

- Nerve is damaged and the severed ends of the Schwann cell sheaths are widely separated

There is typically no functional regeneration


What factors play a role in the recovery of function after brain damage?

- Some true recovery, some compensatory changes

- Cognitive reserve (education and intelligence)- important role in recovery of function; may permit cognitive tasks to be accomplished in new ways

- Adult neurogenesis may play a role in recovery


What are the principles for treating nervous system damage?

- Reducing brain damage by blocking neurodegeneration

- Promoting recovery by promoting regeneration

- Promoting recovery by transplantation

- Promoting recovery by rehabilitative training


What neurochemicals can be used to block or limit neurodegeneration?

- Apoptosis inhibitor potein- induced via a virus

- Nerve growth factor- blocks degeneration of damaged neurons

- Estrogens- limit or delay neuron death

- Neuroprotective molecules- tend to also promote regeneration


What can be used to induce regeneration experimentally (recall, regen typically doesn't normally occur in the CNS)?

- Eliminate inhibition of oligodendroglia and regeneration can occur

- Provide Schwann cells to direct growth


How can recovery be promoted by neurotransplantation?

Fetal tissue

- Fetal substantia nigra cells used to treat monkey models of Parkinson's Disease

- Limited success with humans

Stem cells

- Rats with spinal damage "cured", but much more research is needed



How can recovery be promoted by rehabilitative training?

Constrain-induced therapy

- Restrain functioning limb while training the impaired one

- This creates a competitive situation to foster recovery