Program#/Poster#: |
38.14/B85 |
Title: |
Short-term plasticity as a homeostatic mechanism in the lateral amygdala |
Location: |
Hall A |
Presentation Time: |
Saturday, Oct 17, 2015, 1:00 PM - 5:00 PM |
Presenter at Poster |
Sat, Oct. 17, 2015, 2:00 PM - 3:00 PM |
Topics: |
++B.08.a. Short-term plasticity |
Authors: |
*A. E. FINK, T. J. MADARASZ, J. E. LEDOUX;
Ctr. for Neural Sci., New York Univ., New York, NY |
Abstract: |
The lateral amygdala (LA) is an area that combines sensory information to produce both aversive and appetitive associative learning. Normally a quiet brain region, activity in the LA is thought to be dysregulated in disorders such as anxiety and PTSD. Short-term plasticity (STP) in the normally functioning LA might therefore be a crucial physiological mechanism for maintaining amygdala homeostasis. STP (plasticity lasting from milliseconds to tens of seconds) modulates online processing in neuronal networks, and could also determine both the type of information that is passed through the circuit, as well as whether or not synaptic inputs can be incorporated into a memory engram. Nevertheless, little is known about short-term plasticity in the LA, whether it differs by input, and how it differs by frequency. These questions are important for understanding the LA microcircuit in health and disease, and we have conducted patch-clamp recordings in acute brain slices from adult male mice to identify properties of STP in the LA. We show that during trains of synaptic stimulation at theta (5 Hz), beta (30 Hz), or gamma (100 Hz) frequencies, synaptic inputs onto LA cells undergo a rapid, transient depression that varies both by frequency and by input. This depression is increasingly pronounced at higher frequencies of stimulation. Most importantly, our data suggest that these forms of STP arise from a combined modulation of excitatory input, inhibitory input, and biophysical properties of LA principal cells. We furthermore demonstrate that STP is robust to noradrenergic modulation. Specifically, we find that alpha1 and beta1-adrenergic agonists act primarily through changing excitatory-inhibitory balance, without interfering with frequency-dependent forms of STP. |
Disclosures: |
A.E. Fink: None. T.J. Madarasz: None. J.E. LeDoux: None. |
Keyword
(s): |
AMYGDALA |
|
PLASTICITY |
|
NOREPINEPHRINE |
Support: |
NIH Grant MH046516 |
|
NIDA Grant DA007254-18 |
|
NIMH Grant F32MH100856-01 |
|
|
|
|