Presenter: Harrison Fontaine
Mentors: Leah Deblande and Clifford Kentros, Institute of Neuroscience
Poster: 22
Major: Biology and Human Physiology
The amygdala is a brain structure that is required for the acquisition and storage of fearful memories. In humans, abnormal amygdalar activity has been associated with post-traumatic stress disorder, anxiety, and depression.
One component of simple fear memory formation is the association of a fearful stimulus and an otherwise neutral predictive stimulus. This association occurs in the basolateral amygdala (BLA). While the main inputs to the BLA
are well characterized, the specific coding strategies these inputs use to convey information has not been detailed. We used transgenic mice in conjunction with a modified viral tracer to determine how the inputs to recently active BLA neurons varied after exposure to fear-inducing and non-fear-inducing situations, with the reasoning that if different inputs were labeled after different treatments, inputs must be employing a neuron-specific coding strategy. In addition, we examined the differential activity of neurons in the BLA that may be gating the formation of fear memories. We reasoned that if these neurons were differentially active between fear-inducing and non-fear-inducing situations, these neurons might indeed be gating fear memory formation. Our results supported the use of a neuron- specific coding strategy in BLA input regions, as well as the model of a subset of BLA neurons gating fear memory formation. These results elucidate aspects of fear memory circuitry, and thus have implications in treating fear circuit pathologies.