Background

Two Views of Amygdala’s Role in Emotional Memory

1. The amygdala has a time-limited involvement in determining the strength of memories formed elsewhere

2. The emotional memory of fear is stored in the amygdala itself

(especially basolateral amygdala--BLA)

View 1

Amygdala as a memory modulator

(Cahill, McGaugh and others)

-animal studies

-human studies

View 2: Amygdala as the structure that stores emotional memories (Fanselow, LeDoux et al)

Lesions or disruption of amygdala before or shortly after fear conditioning disrupt memory

Fear conditioning induces behavioral LTP in amygdala

Fear conditioning induces LTP of auditory thalamic input into amygdala

THIS STUDY

1. The amygdala has a time-limited involvement in determining the strength of memories formed elsewhere

If View 1 is correct then amygdala lesions made long after the memory is stored should not disrupt the memory

THIS STUDY

2. The emotional memory of fear is stored in the amygdala itself

If view 2 is correct, then lesions of the amygdala should impair remote and recent emotional memories equally

A second issue addressed:

Are BLA lesions are truly interfering with the memories or with the behavioral expression of the memory?

I.e., maybe the rats with lesions have normal fear memories but are unable to express them (in this study, unable to freeze).

Methods Overview• 10 tone-shock pairings in 1 context (remote memory)

< wait 16 months >

• 10 tone-shock pairings using a novel tone in a novel context (recent memory)

< wait 24 hrs >

• Excitotoxic lesions of BLA or sham operations

<wait 14-15 days>

• Testing of the memories of tone-shock and context-shock associations

• Open field testing to see if group differences in hyperactivity

• Over-training to see if freezing can be elicited in the BLA lesion group

Counterbalanced: A8->B2B2->A8B8->A2

Context C

No tone

Sham Lesion

Remote and Recent Memory TestsContext

remote recent

Remote and Recent Memory TestsTone

remote recent

Interim Discussion

BLA lesions impaired both recent and remote fear memories (as assessed by freezing behavior)

This is inconsistent with a time-limited role of amygdala in the consolidation of memories.

Maybe it is not the memory, but the expression of the memory that is disrupted by BLA lesions.

Are rats with BLA lesions hyperactive so that they have a more difficult time freezing?

Methods Overview• 10 tone-shock pairings in 1 context (remote memory)

< wait 16 months >

• 10 tone-shock pairings using a novel tone in a novel context (recent memory)

< wait 24 hrs >

• Excitotoxic lesions of BLA or sham operations

<wait 14-15 days>

• Testing of the memories of tone-shock and context-shock associations

• Open field testing to see if group differences in hyperactivity

• Over-training to see if freezing can be elicited in the BLA lesion group

Freezing = “absence of any visible movement (including vibrissae), except that required for respiration”

“BLA lesions produced no significant effects on activity (F(1, 20) = 3.07; p > 0.09).”

(pg. 3813) “ Both groups showed identical levels of activity…”

Discussion (cont.)

“The reaquisition of context-specific freezing is somewhat surprising…”

“Rather than undermining the importance of the BLA as a site of memory storage, this finding suggests that other regions can, under a limited set of circumstances, compensate for BLA damage.”

Discussion

Issue of “savings” in rats with BLA lesions

If the BLA involved in memory storage, and it is taken away, rats should show no savings (no acceleration of learning) on subsequent conditioning

“Although the current results favor a storage interpretation of BLA function, they do not rule out a contribution to the storage of memory for certain aspects of the fear conditioning in other regions or a time-limited role in these processes.”

“…the BLA plays a specialized role in encoding the emotional aspects of the fear conditioning situation rather than coordinating the consolidation of declarative memory in extra-amygdala regions.”