Ge. Schafe et al., Memory consolidation for contextual and auditory fear conditioning is dependent on protein synthesis, PKA, and MAP kinase, LEARN MEM, 6(2), 1999, pp. 97-110
Fear conditioning has received extensive experimental attention. However, L
ittle is known about the molecular mechanisms that underlie fear memory con
solidation. Previous studies have shown that long-term potentiation (LTP) e
xists in pathways known to be relevant to fear conditioning and that fear c
onditioning modifies neural processing in these pathways in a manner simila
r to LTP induction. The present experiments examined whether inhibition of
protein synthesis, PKA, and MAP kinase activity, treatments that block LTP,
also interfere with the consolidation of fear conditioning. Rats were inje
cted intraventricularly with Anisomycin (100 or 300 mu g), Rp-cAMPS (90 or
180 mu g), or PD098059 (1 or 3 mu g) prior to conditioning and assessed for
retention of contextual and auditory fear memory both within an hour and 2
4 hr later. Results indicated that injection of these compounds selectively
interfered with long-term memory for contextual and auditory fear, while l
eaving short-term memory intact. Additional control groups indicated that t
his effect was Likely due to impaired memory consolidation rather than to n
onspecific effects of the drugs on fear expression. Results suggest that fe
ar conditioning and LTP may share common molecular mechanisms.