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[Abstract Title]. - Society for Neuroscience

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y cresyl violet staining. Both vehicle and GC-treated animals had mild to substantial CA3<br />

neuron loss; however, GC-treatments dramatically exacerbated CA1 neuron death. These<br />

findings suggest that chronic stress levels of GCs can worsen excitotoxic injury in C57Bl/6 mice<br />

just as they can in rats.<br />

Disclosures: S.F. Sorrells, None; C.D. Munhoz, None; R.M. Sapolsky, None.<br />

Poster<br />

280. Stress and the Brain: Stress and Neuroimmunology I<br />

Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm<br />

Program#/Poster#: 280.9/NN9<br />

Topic: E.06.c. Stress and neuroimmunology<br />

Support: ACS fellowship PF-08-086-01-TBE<br />

Brain Research Foundation Grant<br />

<strong>Title</strong>: Tumors induce depression and alter neuroimmune and neuroendocrine systems<br />

Authors: *L. M. PYTER, V. M. PINEROS, J. A. GALANG, M. K. MCCLINTOCK, B. J.<br />

PRENDERGAST;<br />

Psychology, Univ. of Chicago, Chicago, IL<br />

<strong>Abstract</strong>: The relationship between peripheral health and mental health is reciprocal. A striking<br />

example of this interaction is the high incidence of depression and anxiety disorders in cancer<br />

patients. A number of factors may contribute to this comorbidity, however, the extent to which<br />

tumor-derived chemical messengers (i.e., cytokines) contribute to the central states of depression<br />

and anxiety has never been investigated. We tested the hypothesis that tumors produce cytokines<br />

and dysregulate the HPA axis, which in turn, affect the brain and behavioral measures of<br />

affective state. Female Wistar rats received an injection of nitrosomethylurea (NMU, chemical<br />

carcinogen) to induce mammary tumors. Within 2 weeks of tumor palpation, depression and<br />

anxiety-like behaviors were examined in NMU-treated, tumor-bearing and saline-treated control<br />

rats. In a separate cohort of similarly treated rats, pro- and anti-inflammatory cytokines were<br />

measured in blood, tumors, and limbic brain regions. In a second study, the effects of tumors on<br />

the HPA axis were assessed by measuring corticosterone responses to a stressor and<br />

dexamethasone, and by quantifying glucocorticoid receptor expression in the brain. Preliminary<br />

findings suggest that tumors increase depressive-like behaviors and cytokine production and<br />

increase HPA negative feedback sensitivity. These results suggest that the mechanism by which

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