Abstract
Two competing theories predict different effects on memory consolidation when the amygdala is inactivated after fear conditioning. One theory, based on studies using inhibitory avoidance training, proposes that the amygdala modulates the strength of fear learning, and post-training amygdala manipulations interfere with memory consolidation. The other, based on studies using Pavlovian fear conditioning, hypothesizes that fear learning occurs in the amygdala, and post-training manipulations after acquisition will not affect memory consolidation. We infused the GABAA agonist muscimol (4.4 nmol/side) or vehicle into lateral and basal amygdala (LBA) of rats either before or immediately after tone-foot shock Pavlovian fear conditioning. Pre-training infusions eliminated acquisition, whereas post-training infusions had no effect. These findings indicate that synaptic activity in LBA is necessary during learning, but that amygdala inactivation directly after training does not affect memory consolidation. Results suggest that essential aspects of plasticity underlying auditory fear conditioning take place within LBA during learning.
| Original language | English (US) |
|---|---|
| Journal | Journal of Neuroscience |
| Volume | 19 |
| Issue number | 24 |
| State | Published - 1999 |
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Functional inactivation of the amygdala before but not after auditory fear conditioning prevents memory formation. / Wilensky, A. E.; Schafe, G. E.; Ledoux, Joseph.
In: Journal of Neuroscience, Vol. 19, No. 24, 1999.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Functional inactivation of the amygdala before but not after auditory fear conditioning prevents memory formation.
AU - Wilensky, A. E.
AU - Schafe, G. E.
AU - Ledoux, Joseph
PY - 1999
Y1 - 1999
N2 - Two competing theories predict different effects on memory consolidation when the amygdala is inactivated after fear conditioning. One theory, based on studies using inhibitory avoidance training, proposes that the amygdala modulates the strength of fear learning, and post-training amygdala manipulations interfere with memory consolidation. The other, based on studies using Pavlovian fear conditioning, hypothesizes that fear learning occurs in the amygdala, and post-training manipulations after acquisition will not affect memory consolidation. We infused the GABAA agonist muscimol (4.4 nmol/side) or vehicle into lateral and basal amygdala (LBA) of rats either before or immediately after tone-foot shock Pavlovian fear conditioning. Pre-training infusions eliminated acquisition, whereas post-training infusions had no effect. These findings indicate that synaptic activity in LBA is necessary during learning, but that amygdala inactivation directly after training does not affect memory consolidation. Results suggest that essential aspects of plasticity underlying auditory fear conditioning take place within LBA during learning.
AB - Two competing theories predict different effects on memory consolidation when the amygdala is inactivated after fear conditioning. One theory, based on studies using inhibitory avoidance training, proposes that the amygdala modulates the strength of fear learning, and post-training amygdala manipulations interfere with memory consolidation. The other, based on studies using Pavlovian fear conditioning, hypothesizes that fear learning occurs in the amygdala, and post-training manipulations after acquisition will not affect memory consolidation. We infused the GABAA agonist muscimol (4.4 nmol/side) or vehicle into lateral and basal amygdala (LBA) of rats either before or immediately after tone-foot shock Pavlovian fear conditioning. Pre-training infusions eliminated acquisition, whereas post-training infusions had no effect. These findings indicate that synaptic activity in LBA is necessary during learning, but that amygdala inactivation directly after training does not affect memory consolidation. Results suggest that essential aspects of plasticity underlying auditory fear conditioning take place within LBA during learning.
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UR - http://www.scopus.com/inward/citedby.url?scp=0033572131&partnerID=8YFLogxK
M3 - Article
C2 - 10594092
AN - SCOPUS:0033572131
VL - 19
JO - Journal of Neuroscience
JF - Journal of Neuroscience
SN - 0270-6474
IS - 24
ER -