Special Lecture: Protein Synthesis Versus Neural Activity Flashcards
What is the psych model of memory?
event –> STM –> LTM
What is the neuro model of memory?
event –> STP (short-term plasticity) –> LTP (long-term plasticity)
What is long-term potentiation (LTP)?
activity dependent, associative mechanism for increasing synaptic efficacy
What is E-LTP?
early phase LTP
does not depend on the synthesis of proteins
What is L-LTP?
late phase LTP
protein synthesis dependent
In what way does memory maintenance require new proteins?
decrease in memory performance after injection of protein synthesis inhibitors
to transfer memories to LTM need activation of nucleus to perform protein synthesis
critical window after training where protein synthesis occurs (consolidation); if don’t give PSI within interval, no deficits will be seen (4 hour window)
What is the De Novo protein synthesis hypothesis?
acquisition and short term retention –> protein synthesis independent
long-term memory –> protein synthesis dependent
amnesia is due to lack of new proteins –> not to side effects
What was the experiment to determine if PSIs affect ongoing hippocampal neural activity?
inject Ani. to one side of hippocampus
huge drop in neural activity in the side with injection
effect was still there four hours later
the more we inhibit protein synthesis, do we decrease the neural activity more?
correlation between level of neural activity and level of PSI (decreased activity, increased PSI)
Do PSIs affect ongoing hippocampal neural activity?
yes!
ANI and CHX cause profound suppression of neural activity
the level of protein synthesis inhibition is correlated to the suppression level of neural activity
What was the experiment to determine how PSIs (ANI) disrupt neural activity?
method: suction off part of membrane so pipette becomes part of the membrane and the cytoplasm
after ANI was injected, there was a rise in membrane potential, which stayed even after ANI was stopped injecting; increases depolarization so can’t respond to other stimuli
input resistance of a neuron reflects the extent to which membrane channels are open
membrane time constant: the amount of time it takes for the change in potential to reach 63% of its final value
ANI impairs mitochondrial activity; impacts the sodium potassium pump
ANI acts rapidly; neurons are shut off by disruption of their potential through disruption of the sodium-potassium pump
How do PSIs (ANI) disrupt neural activity?
loss of RMP without changes in input resistance
dysfunction of cellular energetics –> impairment in mitochondrial function
Does emetine affect ongoing hippocampal neural activity?
inter-hippocampal emetine infusion suppresses protein synthesis and disrupts theta activity
injection of emetine was able to inhibit protein synthesis in a specific area
drop in activity post-infusion
inhibition of protein synthesis is correlated with the suppression of neural activity
Does protein synthesis inhibition disrupts neural activity regardless of the drug being used?
yes!
emetine (same as other PSIs) disrupts neural activity
pretty much the same as the first experiment discussed
What was the experiment to determine if ANI affects hippocampal function?
unconditioned fear/anxiety: no training, protein synthesis should not be involved
rats tend to go to arms that are closed, not the open ones; if rats are less anxious, they’ll stay in the open arms
ventral, not dorsal, hippocampal infusions of ANI induce anxiolytic behavior
spatial navigation: ability to navigate a new space, does not need training, should be no PSI
intra-hippocampal ANI, like TTX, disrupts spatial navigation in the Morris water maze
Does ANI affect hippocampal function?
yes!
ANI disrupts the hippocampal involvement in both: unconditioned unlearned behavior, spatial navigation
