The Role of Valence in the Selective Activation of the Amygdala by Norephinephrine

Research conducted over the past few decades suggest that the valence of stimuli experienced in an environment elicits unique asymmetric activity in the amygdala. Exposure to unpleasant laboratory stimuli results in more robust activation of the amygdala in the right hemisphere compared to the opposite hemisphere (Lanteaume et. al., 2007; Etkin et. al., 2004; Morris, Ohman & Dolan, 1999). The converse is also noted in that positively arousing situations, such as viewing pleasant images or being informed of winning a fictitious competitive tournament, elicit a disproportionate level of amygdala activity in the left hemisphere (Hamann, Ely, Hoffman & Kilts, 2002; Zalla et. al., 2000). Even though several findings report that the human amygdala is highly responsive to presentation of negative or positive events, there is currently no consensus in the human lateralization literature validating which aspects of a given experience predicts the hemisphere in which the event will be preferentially encoded (Adamec, Blundell & Collins, 2001; Baas, Aleman & Kahn, 2004; Zald, 2003). In addition to the problems encountered in the human literature, few animal studies have approached the lateralization question by identifying neural substrates responsible for selectively activating individual hemispheres after exposure to learning conditions with rewarding or aversive stimuli. The proposed studies will address these shortcomings by examining whether exposure to conditions motivated by stimuli with either positive or negative emotional valence differentially influences neurotransmitter release during initial learning that subsequently impacts the strength these events are encoded into memory. An additional objective of this project is to determine the possible origins of asymmetric norepinephrine release into the basolateral amygdala. Understanding how asymmetric activation of the amygdala is integrated into overall limbic activation during encoding and memory formation is vital given the findings that individuals with anxiety disorders have altered patterns of asymmetric amygdala activation compared to individuals without anxiety disorders (Etkin et. al. 2004, Pissiota et. al., 2002; van der Heuvel et. al., 2004). Consequently, greater comprehension of asymmetric amygdala activation and its origins may help to explain and understand the etiology of anxiety disorders and lead to better treatments.