Chapter 11a: Emotional Memory & Engrams Flashcards
What is the pathway of fear conditioning?
conditioning stimuli –> sensory thalamus –> lateral amygdala central –> conditioned and unconditioned fear responses
What is the engram?
refers to the enduring offline physical and/or chemical changes that were elicited by learning and underlie the newly formed memory associations
What is the association and influence of CREB to fear memories?
CREB is activated in the lateral amygdala after a cued fear-memory-inducing protocol; increase of CREB in fear response cells, but not others
CREB deficient mice don’t show fear memory
need CREB activation to remember; CREB deficient rats did not learn the task
CREB viral infections target about 20% of lateral amygdala neurons
CREB viral infections only ameliorate memory in CREB-deficient mice; when injected with more CREB there were no change; when CREB deficient mice are injected with CREB the memory was restored
What were the experimental and control groups in the experiment about imaging and influencing the engram?
Overall Arc: group of genes activated at the beginning of a cell’s life; allow us to know what cells were active at a specific time
GFP+: virus injected in amygdala, neurons carry extra CREB and glow green
control: did not inject CREB, just green dye
CREB-infected neurons are more likely to be incorporated into cue-induced fear memories
GFP-infected neurons are not more likely to be incorporated into cue-induced fear memories
What were the results of the study in weak pairing protocols?
CREB-infected lateral amygdala neurons make regular mice more likely to show cued-fear conditioning when trained with weak pairing protocol
infected neurons still more likely to be incorporated in memory trace
more CREB = more response to weaker stimulus
What were the results of the study in CREB injection by itself?
CREB-infection procedure by itself doesn’t do anything anatomically
CREB itself doesn’t do anything
What were the results of the study when super CREB was injected?
super CREB-infection (self phosphorylating version) procedure by itself doesn’t do anything anatomically
doesn’t do anything on its own
What were the results of the study when crappy CREB was injected?
crappy CREB-infection neither improves memory nor labels cells incorporated in memory trace
Does the size of the memory engram change during CREB activation?
memory trace does not change size but the proportion of neurons incorporated increases with good CREB-infections in the lateral amygdala
no change in the number of cells responding; did not change overall number of cells activated
all tasks recruited some number of cells; what changed were what types of neurons were recruited
What were the four main results of the experiment imaging and influencing the engram?
- CREB activation in lateral amygdala is correlated with auditory fear conditioning; ~20% of lateral amygdala cells in wild type (WT) mice show activated CREB following training, increasing CREB function in a similar proportion of lateral amygdala neurons in CREB-deficient mice rescues a fear memory deficit
- neurons with increased CREB function are more likely than their neighbors to be recruited to the fear memory trace
- relative CREB function influences the recruitment of neurons into the memory trace
- constant size of memory trace suggests competitive selection process that is biased by CREB activity
What were the experiments involved in the procedure for erasing the engram?
surgery: inject animal with CREB; green strain, CREB, toxin receptor
train: tone and shock
test 1 and test 2: comparison before and after killing the cells
results: before toxin, big response; after toxin, not as much memory, deletion of engram
What was the major finding of the experiments for erasing the engram?
by targeted killing of lateral amygdala neurons that have been biased into fear memory trace, one can erase the cued fear memory
How did they target and activate specific neurons when inducing memory recall?
chemo-genetic expression of a receptor that does not usually exist in neurons allows for activation (or inactivation) of those same neurons when the ligand is exogenously presented
ligand is present but not in the brain or the amygdala
inject receptor and CREB, then inject ligand to induce activation
Did the chemo-genetic expression of a receptor change the firing of the neurons in the lateral amygdala?
chemo-genetic expression does not change waveform properties of spiking lateral amygdala neurons but does increase their firing rates when the ligand is present
when I inject ligand in cell with receptor the cell will fire
What was the training and experimental design of the experiment for inducing memory recall?
combined CREB and TRP-V expression conducted prior to or after training
implication: CREB infected cells will be biased into memory trace only when infected prior to training; thus, the memory trace can be reactivated using the ligand, capsaicin