[Abstract Title]. - Society for Neuroscience

does not reach the level of overt fear, and that the hippocampus processes novel spatial
information regardless of its emotional content. Current experiments are examining the response
of egr-1 in the medial prefrontal cortex during high and low states of anxiety.
Disclosures: M. Donley , None; J.B. Rosen, None.
Poster
294. Gene Expression and Fear Learning
Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm
Program#/Poster#: 294.9/SS49
Topic: F.02.f. Fear and aversive learning and memory
Support: NARSAD
NRSA
VA Merit Review
Title: Expressing ASIC1a in the BLA of ASIC1a-null mice rescues deficits in fear memory but
not fear learning
Authors: *M. W. CORYELL 1 , A. M. WUNSCH 2 , J. HAENFLER 3 , J. E. ALLEN 3 , M. J.
WELSH 4,5 , J. A. WEMMIE 3,6 ;
1 Neurosci. Prog, 2 Psychiatry, Univ. Iowa, Iowa City, IA; 3 Psychiatry, 4 Intrnl. Med., Univ. of
Iowa, Iowa City, IA; 5 Howard Hughes Med. Inst., Iowa City, IA; 6 Vetrans Affairs Med. Ctr.,
Iowa City, IA
Abstract: The acid-sensing ion channel-1a (ASIC1a) contributes to fear-related behavior
including conditioned fear and unconditioned fear. ASIC1a is expressed widely in the brain, but
is most abundant in the basolateral amygdala (BLA) and other fear circuit structures. However,
where in the brain ASIC1a acts to increase fear is not known. Here, we tested the effects of
restricting ASIC1a expression to the BLA. We used an adeno-associated virus 1 (AAV1)
encoding ASIC1a to restore ASIC1a expression to the BLA of ASIC1a-null mice. We then tested
the behavioral effects in response to the predator odor TMT, a model of unconditioned fear. We
also tested the acquisition of context fear conditioning and conditioned fear memory. We found
that restoring ASIC1a expression to the BLA did not affect TMT-evoked freezing, suggesting
that ASIC1a in the BLA is not sufficient to affect this behavior. In addition, ASIC1a expression
in the BLA did not affect the acquisition of freezing during context fear conditioning; the AAV1-
ASIC1a-injected mice remained impaired and froze no more than AAV1-GFP-injected controls.