Lecture 14 Neuroplasticity Flashcards
(39 cards)
What is neuropraxia?
- local myelin damage
- axon remains intact
- results in slow AP (mild weakness, tingling)
- symptoms are mild or transient (short time)
What is axonotemesis?
- continuity of axon is lost
- loss of continuity leads to Wallerian degeneration (degeneration distal to injury)
What is neurotmesis?
complete transection of nerve
What axonal injury is the least severe?
neuropraxia
What axonal injury is the most severe?
neurotmesis
Describe the steps that occur after a peripheral nerve is injured that has the potential to regrow
1) Wallerian degeneration (degeneration distal to injury)
2) macrophages clear debris AND Schwann cells become phagocytic to degenerating axon and myelin
3) central end of axon tunnels into endoneurial sheaths left behind
4) Schwann cells increase as axon regrows - help produce new myelin and guide axon regrowth
5) axon re-establishes postsynaptic target
6) axon diameter increases, more myelin created
What is Wallerian degeneration?
degeneration of axon distal to injury
What are the two different types of axonal sprouting?
- collateral
- regenerative
What is collateral axonal sprouting?
start with 2 neurons, 1 dies and doesn’t regrow, but neighboring neurons help hit postsynaptic receptors
What is regenerative axonal sprouting?
start with 2 neurons, 1 degenerates, then regrows back to postsynaptic receptor
Why can’t the CNS regenerate?
- CNS damage triggers necrosis and apoptotic (release neurotoxins) cell death down whole neuron
- clean up is slow due to lack of schwann cells (oligodendrocytes in CNS) and macrophages
- astrocytes causes glial scarring
- microglial activation - can’t tell what is good and bad
What HAS been shown to have neurogenesis capabilities? Where in the CNS can these structures be found?
- glial cells (support cells)
- found in Olfactory bulb and Hippocampus
Define neuroplasticity. In general, how does it work?
- Ability of CNS to change its chemical profiles, structure, and function in response to a given stimuli or situation
- Activated by environmental, behavioral, or neural processes
What is chemical neuroplasticity?
- see when we start to use a pathway repetitively
- immediate to short-term changes to chemical synapses
- increase neurotransmitters released into synaptic cleft
What is structural neuroplasticity?
- long-term changes to neuronal structure
- modify existing postsynaptic receptors
- create new postsynaptic receptors
- increase dendritic growth
- increased terminal axons
What is functional neuroplasticity?
- long-term changes to the neuronal function
- Neurons change roles, function, and information being relayed
What is cortical remapping? What are some examples?
- Process in which the existing cortical “map” is affected, and ultimately changed, by a stimulus
- blindness (other senses are stronger)
- phantom limb
What is habituation?
- simplest form of neuroplasticity
- When our brain decides to decrease its sensitivity or response to repeated and benign stimulus
- lets us pay attention to what is important and what is not
ex: young vs old snoring couple
What is short-term habituation?
< 30 minutes
- changes pre-synaptic (decrease release of excitatory neurotransmitters)
- effects are transient (short term and no structural changes)
What is long-term habituation?
> 30 minutes
- changes post-synaptic (decrease receptors on postsynaptic)
What drives our ability to learn and remember? Through what processes is this manifested?
past experience
Long-term potentiation and depression
What is long-term potentiation? What is required to see this process occur?
- major way for the brain to increase sensitivity
- synaptic connections between neurons become stronger by frequent activation
- Requires high intensity stimulation
What receptors are involved in long-term potentiation?
AMPA
NMDA
What are AMPA receptors permeable to and how do they respond?
- permeable to Na+
- glutamate binds to ligand receptor causing them to open and let Na+ through
