| Program#/Poster#: |
914.22/MMM38 |
| Title: |
Prefrontal dopamine D1 receptor
expression predicts estrogen-enhanced memory for fear extinction |
| Location: |
Halls B-H |
| Presentation Time: |
Wednesday, Nov 17, 2010, 2:00 PM - 3:00
PM |
| Authors: |
*R. SHANSKY1,
J. H. MORRISON1, J. E. LEDOUX2,3;
1Dept Neurosci, Mount Sinai Sch. Med., NEW YORK, NY; 2Ctr. for Neural Sci.,
New York Univ., New York, NY; 3Emotional Brain Inst. and the Nathan Kline
Inst., Orangeburg, NY |
| Abstract: |
Women are twice as likely as men to
develop stress-related mental illnesses like Major Depressive Disorder (MDD)
and Post-Traumatic Stress Disorder (PTSD), the symptoms of which may reflect
a disruption of the neural circuitry linking the medial prefrontal cortex
(mPFC) and amygdala. We have recently reported that neurons projecting from
the mPFC to the amygdala are uniquely sensitive to stress-induced morphological
changes in estrogen-treated ovariectomized rats (OVX + E), while resistant
to these effects in males and OVX females without estrogen replacement (OVX
+ veh). The present study investigated the effects of estrogen treatment
on a behavioral task known to be mediated by this pathway--retrieval of
fear extinction. Male, OVX + veh, and OVX + E rats underwent fear conditioning
and extinction training, followed by testing for extinction retrieval. OVX
+ E females displayed less freezing behavior than males and OVX + veh females
during the first two trials of extinction retrieval, suggesting better memory
for extinction. We further asked whether performance of this task correlated
with dopamine D1 receptor expression in the mPFC, as measured by immunofluorescence.
D1 puncta number was positively correlated with extinction retrieval performance
in OVX + E only, suggesting that estrogen may render females uniquely responsive
to dopaminergic actions in the mPFC. Together, these data provide evidence
that estrogen may enhance the function of the mPFC-amygdala pathway, possibly
through interactions with the D1 receptor. |
| Support: |
NIMH grant MH58911
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