Name
Dr. Naomi Eisenberger
Article
Brief Biography
Dr. Naomi Eisenberger graduated from UCLA with a B.S. in Psychobiology and then received a Ph.D. in Social Psychology from UCLA in 2005. She is currently a postdoctoral scholar at the UCLA Cousins Center for Psychoneuroimmunology investigating the influence of immune system activity on neural function. Her primary interests are in understanding how the need for social connection has left its mark on the mind, brain, and body. She asks questions such as: “Why does social rejection hurt?” or “Why does social support bolster health and well-being?” and then uses cognitive neuroscience techniques to elucidate the neural systems involved to better understand the computational and experiential substrates of these complex processes.
Abstract:
Recent research has demonstrated a relationship between depression and immune system activity, specifically proinflammatory cytokine activity. Although experimentally-induced immune activation leads to increases in depressed and anxious mood, the neural correlates associated with these changes have remained largely unexplored. Based on relationships between proinflammatory cytokine activity, depression, and heightened physical and social pain sensitivity, this study will investigate the effect of proinflammatory cytokine activation on the neural correlates of socially painful experience that may contribute to depression.
Participants will be randomly assigned to receive either endotoxin (which increases proinflammatory cytokine activity in a safe manner) or placebo. Subsequently, participants will complete a neuroimaging study in which they will be rejected during an online ball-tossing game. We will examine whether individuals exposed to endotoxin report more social distress, endorse more depressive symptoms, and show more dACC activity and more limbic system activity more generally (e.g., amygdala, insula) in response to social rejection. We will also investigate whether, for individuals exposed to endotoxin, greater dACC and general limbic system activity during social rejection mediates the relationship between increased proinflammatory cytokine activity and greater depressive symptoms at the end of the study. This study will be the first to investigate the effect of systemic inflammation on neural reactivity related to social and affective processes that may increase the risk of depression.