Neuroplasticity Flashcards
(23 cards)
What is neuroplasticity?
- Ability of the NS to CHANGE in function, chemical profile, and structure
- Occurs secondary to experience and changes in our state of health (healthy AND impaired CNS)
- Continuous creation/modification of neuronal networks
Neurons the fire together, wire together <3
What is short term synaptic plasticity?
Modifies synaptic transmission over a timespan of a few minutes or less
-> Short-lived changes in brain function (changes to what you need in the moment)
- Affects the amount of neurotransmitter released in response to a presynaptic AP
What is Augmentation and Potentiation? (Short term)
Both work to enhance calcium’s ability to trigger fusion of the synaptic vesicles to the presynaptic membrane
Augmentation: lasts seconds (building up)
Potentiation: Lasts seconds to minutes (has the potential to go)
-> during depression state, vesicles need time to refill
-> Results in post-titanic potentiation (delay/ depression causes a bunch of neurotransmitters to release w/ one single AP once vesicles are refilled)
What is Habituation (Behavioral Plasticity)?
- Learned suppression of a non-noxious stimulus
- Decrease in response with repetitive stimulation (sensitization is an increased responsiveness to repeated stimulation)
-> Can be reversed with delay stimulation
Basically becoming desensitized to a certain stimulus and not thinking about it
What is Long Term Synaptic Plasticity ?
Experience-Dependent Plasticity: something routinely done
-> how we learn and memory
Involves persistent, long-lasting changes of synaptic strength
-> Observed at the excitatory glutamatergic synapses
-> Occurs in the cerebellum and the motor, somatosensory, visual and auditory cortices
What is Long Term Potentiation (LTP) and how does it work?
- INCREASE in synaptic strength
- Vesicles bind to presynaptic membrane
- Glutamate is release and binds to AMPA and NMDA
- AMPA is LIGAND gated, so sodium is able to pass through the channel
NMDA is VOLTAGE gated, Mg is blocking the channel - Depolarization occurs and Mg gets kicked out, which allows ions to pass through such as Ca and Na
- Calcium causes a cascade of other reactions in the postsynaptic terminal., stored AMPAs are released and allow to depolarization to happen quicker
What is Long Term Depression and how does it occur?
- Permits new information to be processed and stored (we only have enough stores, so sometimes we have to let things go to make more room)
- Necessary to allow for other synapses to strengthen
- Result of low Ca levels
Basically, AMPA receptors go back in and internalize because the are not needed as much
How does Transcranial Magnetic Stimulation work with neuroplasticity?
- Stimulates nerve cells in the brain -> cortical excitability
-> Magnetic pulses depolarize neurons and create an AP - Can induce LTP OR LTD
- Can be used for depression and OCD
Why is there limited ability for the brain to produce new neurons?
Barriers to CNS REGENERATION
- Local injury to brain tissue often results in neuronal death (direct cell damage or via excitotoxicity)
- Non-neuronal cells actively limit axonal growth (glial cells get in the way )
- Immune responses of the brain further limit extensive regrowth
- Neural stem cells are constrained in their ability to divide, migrate and differentiate
Brain REORGANIZES rather than regrows
What are the different types of Neuronal Repair?
- Regrowth of Axons
- Most successful form of repair (PRIMARILY PNS) - Regrowth of damaged neurons
- “Sprouting” of intact nerve cells
- Limited secondary to overgrowth of glial cells (glial cells can clog the area) - Genesis of new neurons
- Limited secondary to the constraints of neural stem cells
What cells influence PNS Regeneration in response to injury?
Schwann cells: support axon stump, provide a substrate for regrowth, and provide adhesion molecules/trophic factors (myelin sheath)
Macrophages: clear debris and stimulate immune response
Fibroblasts: create bridge for regrowth
Endothelial cells: physical guide for growth
Outcomes maximized when axon stumps are surgically realigned following injury
What is BDNF?
Brain Derived Neurotrophic Factor
- Contribute to neuron growth
- Protein found in CNS and PNS
- Activity dependent regulation of expression and secretion
- Mediator of neuronal plasticity/neuronal survival
- Expression of BDNF decreases in the presence of inflammation
NGF (neuro growth factor) promotes and supports area for neuron regeneration
How does BDNF contribute to Exercise?
- BDNF INCREASES following a single session of exercise
- Regular exercise intensifies effect of a single session of exercise on BDNF levels
- Small effect of increased resting BDNF after regular exercise
- Smaller effect on women than men
How does the CNS respond to injury?
- Apoptosis (cell death) of brain tissue
-> Result of direct cell death and excitotoxicity
Glial growth/proliferation and microglial activity (immune response; inflammation) actively inhibit growth
-> Clog area
-> Increase in growth-inhibiting molecules
Glial cells are like cockroaches and are not affected by apoptosis and out-live neurons
What is glial scarring?
-Local overgrowth of astrocytes and Oligodendrocytes
- Inhibit axonal extension and dendritic growth
What happens during CNS Immune responses and inflammation?
-Response activated before, during, and after glial scar formation
-> Local damage to brain tissue
-> Damage to the BBB
- Molecules and immune cells now able to pass through compromised tight junctions
-> Neuroinflammation
What is a Stroke (Cerebrovascular Accident; CVA)?
- Disruption of blood flow within cerebral blood vessels
-> Ischemic (blockage of the vessel)
-> Hemorrhagic (rupture of the vessel) - Central portion of insult results in necrosis (core) with surrounding cellular dysfunction (penumbra)
Where does Neurogenesis Occur?
Neurogenesis: genesis of new neurons
2 locations
1. Olfactory bulb (sub ventricular zone)
2. Hippocampus (subgranular zone)
New nerve cells are interneurons
-> Potential to integrate into functional synaptic connections
-> Most die prior to integration within brain circuitry (not able to migrate beyond)
What happens then if the brain has limited capability to repair itself or generate new neurons?
- Alters specific synapses
-
Functionally Reorganizes
-> Changes as individual synapses reorganize the brain and alter how the brain functions
-> Cortical regions routinely adjust how it processes information and has the ability to develop new functions
-> Cortical plasticity is the premise for neurorehabilitation
Primary motor cortex: pre central gyrus (frontal)
Somatosensory cortex: post central gyrus (partietal)
What are genetic mutations?
- Uncommon variation in DNA that results in functional changes and often disease causing
Ex: Huntington’s
What are genetic Polymorphisms?
- Relatively frequent variations in DNA
- Not disease causing but impact different systems especially when interacting with different genetic variants and environmental conditions
What is Single Nucleotide polymorphism (SNP)
- Polymorphism variation where one nucleotide is exchanged for another
- May lead to biological variations that may have functional consequences
Individuals may respond differently to interventions that would engage neuroplastic processes
How does SNP affect BDNF, Dopamine, and Apoliprotein (ApoE)?
BDNF: activity dependent, plays crucial role in enhancing synaptic transmission and supports learning
- may show decreased response to neuroplasticity-based interventions (can’t learn as well)
Dopamine: Involved w/ mood, movement, addiction, learning, reward, and impulse control
- linked to both increased and decreased dopamine levels
Apoliprotein (ApoE): plays a role in neuronal processes related to repair and recovery
- can result in both positive and negative effects
