Embedded within contemporary views of emotional learning is a well-founded
agreement that the amygdala plays a pivotal role in the formation and conso
lidation of aversive memories formed during fear conditioning. However, it
is important to determine whether observed deficits are reflective of a mem
ory impairment or whether they are simply attributable to a deficit in the
performance of unconditioned fear responses such as freezing. Within the ne
urobiology of learning and memory literature, there is an ongoing debate co
ncerning the potential role of the amygdala in the performance of unconditi
oned fear responses. A view put forth by Vazdarjanova and McGaugh (1998) su
ggests that the amygdala is not required for the formation and consolidatio
n of the aversive memories formed during fear conditioning, but is essentia
l in the performance of unconditioned fear responses. Data provided by Mare
n (1999) counter this view by positing that the amygdala is not required fo
r the performance of fear responses, but its role is of a mnemonic nature i
n the conditioning of fear to neutral cues. To clarify the amygdala's parti
cipation in these two processes, a useful approach would involve a situatio
n where animals with amygdala damage were examined for their unconditioned
fear responses in reaction to footshock as well as the conditioning of thes
e reactions to previously neutral cues paired with the aversive event. We h
ave previously reported that rats with amygdala or hippocampal damage are i
mpaired in discriminative fear conditioning to context. In the present expe
riment, we report the initial unconditioned fear responses to footshock by
these same animals as well as the conditioned responses during testing. In
both groups, the fear responses assessed (freezing, urination, defecation,
and locomotion) were not impaired and did not differ from those expressed b
y the sham animals. The impairment of discriminative fear conditioning to c
ontext, in combination with the present experiment, represents a dissociati
on where damage to specific memory structures (amygdala or hippocampus) deb
ilitates the mnemonic processes involved in fear conditioning, but not the
performance of the fear responses per se.