Recent evidence suggests that consolidated auditory fear memories,
when reactivated through retrieval, undergo reconsolidation in the lateral
amygdala (LA). Previous studies indicate the involvement of noradrenergic
system in the amygdala in memory consolidation. We therefore asked whether
the noradrenergic system is involved in the consolidation (study 1) and
reconsolidation (study 2) of auditory fear conditioning. Study 1 (consolidation):
Rats were placed in a chamber and given a 30 s 5 kHZ tone (CS) that terminated
with 1, 1.0 mA, 1 s shock. Immediately after, rats received intra-peritoneal
(i.p.) injections of either the beta-adrenergic receptor antagonist propranolol
or saline. Two days later when freezing responses to the CS were assessed
the two groups did not differ. Similar results were found when conditioning
was immediately followed by bilateral infusion of propranolol or cerebro-spinal
fluid in the LA. Study 2 (reconsolidation): On the day following auditory
fear conditioning, rats were presented with a single CS to reactivate the
memory. Immediately after, they received i.p. injections of propranolol
or saline. Propranolol injected rats, tested 48 hrs later, showed impaired
freezing to the CS as compared to the saline controls. Propranolol injections
without memory reactivation did not produce the deficit. Similar findings
were obtained when propranolol was infused directly in the LA immediately
after reactivation. Infusions of propranolol 2mm above the LA following
memory reactivation did not produce a freezing deficit. Our results suggest
that blockade of beta-adrenergic receptors in the lateral amygdala has different
effects on consolidation and reconsolidation of fear conditioning. Because
propranolol is safe for human use, our results pave the way for using propranolol
as a means of blocking reconsolidation in studies of humans, including patients
with PTSD.
Support Contributed By: MH38774, MH58911, MH067048, I/77376, HSF-RGP0094
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