Abstract

<b>Abstract ID 14239</b> <b>Poster Board 360</b> Consuming excess salt (NaCl), the primary source of dietary sodium (Na), has become prevalent in modern society. Across species, most research on salt consumption has focused on physiology - in particular, cardiovascular function. As a result, current health guidelines advise reduced sodium intake to attenuate cardiovascular disease risk. In contrast, less research has examined how salt consumption affects brain health and function, and consequently, behavior. Much remains to be learned about how this prevalent, non-caloric component of diet impacts neurophysiology to shift basic behaviors, including responses to stressors/environmental threats. Given the challenges and ethics of manipulating salt intake in humans, we use mice to facilitate rigorous control of salt intake, environment, and stressor exposure. I hypothesized mice consuming excess salt would exhibit increased active coping strategies (e.g., more swimming/climbing, less immobility) relative to controls. Group housed adult (10-week old) male and female C57BL/6J mice had access to one or two diets for 4- or 8- weeks, with cages assigned to: 1) control (0.4% NaCl w/w) diet only; 2) high salt (4.0% NaCl) diet only; or 3) both control and high salt diets (mixed); this last allowed analyses of diet preference over time. Diet consumption, water intake, and body weight were recorded twice a week. During the final diet manipulation day, environmental threat response was assessed using a brief swim stressor. In both males and females on either a 4- and 8-week diet manipulation, swim test results indicated no significant stress responsivity differences in latency to first immobility, nor in time spent immobile, swimming, or climbing between diet conditions. Contrary to our hypothesis, our findings suggest excess salt consumption for 4-8-weeks does not augment behavioral responses to environmental stressors. Mice (8-week females and 4- and 8-week males) in the mixed diet condition initially preferred control diet, but consumed significantly more of the high salt diet after ∼2 weeks. We are presently analyzing microglial activation in brain regions associated with homeostatic control, stress responses, and behavioral inhibition (medial prefrontal cortex, paraventricular nucleus of the hypothalamus, and basolateral amygdala). Overall, our behavioral findings indicate that high salt intake does not influence behaviors in either sex in response to an acute stress.

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