Double Resonance Sub-Doppler Study of the Allowed and DeltaK = -3 Forbidden Q(3, 3) Transitions to the nu2 Vibrational State of 14NH3

Whereas much is now known about the behavioral importance of the lateral nucleus of the amygdala for the storage of implicit memories of fear, little is known in molecular terms about the signal transduction pathways required for long-term potentiation (LTP) in this nucleus. Using brain slices containing the amygdala, we have studied LTP in the pathway from external capsule to the lateral nucleus, a pathway that mediates information from the auditory cortex important for fear conditioning. We found the induction of LTP is postsynaptic; it is dependent on postsynaptic depolarization, on the influx of Ca2+ into the postsynaptic cell and, at least in part, on the activation of N-methyl-D-aspartate (NMDA) receptors. The LTP is associated with a decrease of paired-pulse facilitation (PPF) and is blocked by bath application but not blocked by postsynaptic injection of inhibitors of the cyclic adenosine monophosphate-dependent (cAMP-dependent) protein kinase (PKA). Consistent with the possibility that the expression might involve PKA presynaptically, the adenylyl cyclase activator forskolin induced synaptic potentiation of this pathway that also was associated with a decrease of PPF, and this potentiation occluded the tetanus-induced LTP.