| 1. Ctr Neural Sci, NYU, NY, NY, USA |
| 2. Dept of Psychol, Yale Univ, New Haven, CT, USA |
retrograde messenger
that contributes to pre-synaptic aspects of LTP expression. We have previously
reported that neuronal nitric oxide synthase (NOS) is localized in the lateral
nucleus of the amygdala (LA) and that a NOS inhibitor impairs amygdala LTP
and memory formation of fear conditioning. In present set of experiments,
we examined the role of NO specifically using a water-soluble NO scavenger,
carboxy-PTIO (c-PTIO). We first examined effect of c-PTIO on induction of
LTP at thalamic inputs to LA. Bath application of 25 
M c-PTIO significantly impaired LTP at thalamic inputs,
but had no effect on synaptic transmission in same pathway. To evaluate
the role of NO in fear conditioning, we gave rats intra-amygdala infusions
of c-PTIO (1g/side) or vehicle
30 min prior to conditioning, and tested for retention of auditory fear
conditioning at 1, 3, 6, and 24 hr after training. Relative to vehicle controls,
c-PTIO produced a significant disruption of long-term fear memory (at 24
hr). Short-term memory (at 1 and 3 hr) was not affected. Finally, we examined
the role of NO in reconsolidation of fear conditioning. Rats were trained
drug-free. The next day they received intra-amygdala infusion of either
c-PTIO (1g/side) or vehicle
30 min prior to a single reactivation trial and were re-tested for memory
retention 3 and 24 hr later. Findings showed no effect of c-PTIO on reactivation
or subsequent retention of auditory fear conditioning at either time point.
Together, these findings suggest that NO is an important component of new,
but not reactivated, fear memories, possibly as a retrograde signal that
participates in presynaptic aspects of plasticity in LA.Support Contributed By: MH38774, MH62519, R01 MH46516, F32 MH070150, K05 MH067048
Poster presentation:Sunday, Oct. 24, 11:00 AM - 12:00 PM
Location: OO1
