Lesson 4: Neuronal plasticity

when does the gill withdrawal reflex of Aplysia happen?

after their syphon is touched

can the gill withdrawal reflex of Aplysia be only observed in live animals?

no, it can also be observed in semi-intact preparation

what is semi-intact preparation

most body dissected apart from siphon, gills and tails + neurons responsible for them

What is the relationship between serotonin and the gill withdrawal reflex?

serotonin is necessary and sufficient for the sensitization of the reflex

what does tail shock release?

consequent amounts of serotonin

what does blocking serotonin receptors lead to?

the reflex cannot be sensitized

How does serotonin change the sensory neurons of the siphon of Aplysiait p?

leads to the phosphorylation of voltage-gated potassium channels

what does blocking CREB lead to?

the possibility of short-term but not long-term sensitization

hebbian synapse

is strengthened only if it was active when the postsynaptic cell was depolarized enough to fire an action potential

What do we mean when we say that the NMDA receptor is a coincidence detector?

detect the coincidence of presynaptic glutamate release and postsynaptic depolarization

proximate cause of LTP induction

calcium entry through NMDA receptors

how can we block the stabilization of LTP, but not its induction?

block protein synthesis

what are special in the brains of skilled pianists and violonists?

greater representation of the hands in motor cortex

How does environmental deprivation affect the brains of rats and humans?

environmentally deprived individuals have smaller brains

role of PKA in sensitization

it is activated by serotonin and phosphorylates voltage-gated potassium channels in the neuronal membrane which decreases the probability that they will open (decreases the membrane’s depolarization rate) so the AP will last for longer

how is PKA activated?

increased cAMP levels as a result of serotonin release

how long does Aplysia remember a single tail shock?

a few minutes or hours

how long will Aplysia remember 5 shocks over the span of 4 days?

several weeks

experiment that proves the involvement of CREB in long-term sensitization

by injecting oligonucleotides then inflecting several serotonin pulses, short-term sensitization is observed if the oligonucleotides contain CRE segments but both short and long term potentiation is observed if they don’t contain CRE segments because then CREB cannot be prevented to bind to the DNA

how does ubiquitin hydrolase modify the activity of PKA?

it degrades the regulatory subunit of PKA which means that PKA can stay active long after the release of serotonin

what are some differences between LTP and the gill withdrawal reflex in Aplysia?

* homosynaptic for LTP vs heterosynaptic for GWR
* postsynaptic influence in LTP vs only presynaptic in GWR

two stages of LTP

* induction
* stabilization

how would blocking calcium channels impair LTP?

LTP wouldn’t occur because it is triggered by the entrance of calcium and sodium in the postsynaptic cell

how does CaMKII affect AMPA receptors?

* creates more AMPA receptors on post-synaptic cells
* phosphorylates some of them which improves ion flow rate

tonotopic map

spatial arrangement of where sounds of different frequencies are processed in the brain. Tones close to each other are represented in topologically neighboring regions

at rest, is potassium moving in or out of the cell?

both directions, because it is moving out down of its concentration gradient and it is moving in to satisfy the electrical potential (more negative inside the cell)

is the cell potentiated if PKA is inactived?

no

is the cell potentiated if ubiquitin ligase is injected without serotonin beforehand?

yes

what type of ion channel is involved with reaching the action potential threshold?

ligand-gated cation channels

what type of ion channel is involved with the rising phase?

voltage-gated sodium channels

what type of ion channel is involved with the falling phase?

voltage-gated potassium channels

what would happen if voltage-gated potassium channels were blocked during an action potential?

the neuron would stay depolarized

benefit of increasing axon diameter

lowers internal resistance in the axon which allows electrical current to flow more easily

disadvantage of increasing axon diameter

takes up more space in the brain than using myelin sheaths (to allow the same speed as myelinated axons by increasing axon diameter, we would need 10 times our brain volume).

advantage of myelination

blocks potassium leak channels which reduces the length constant of the neuron because the decay of the current is lessened for similar distances. It lowers the effect of the ‘capacitor’ which allows easier flow through the membrane of sodium ions which causes faster depolarization.

why is myelination not used everywhere?

it is costly (hard to create and maintain) and bulky (can’t exist in tightly packed neurons)