Rostral Posterior Hypothalamus Modulation of Stress Habituation

Decker, Isa

Undergraduate Honors Thesis

Rostral Posterior Hypothalamus Modulation of Stress Habituation Public Deposited

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Citeable URL: https://scholar.colorado.edu/concern/undergraduate_honors_theses/bc386k576

Abstract

Adaptation to stress is an important mechanism to reduce overall strain and injury to organisms, especially under repeated or chronic challenging conditions. One form of adaptation to repeated stress is habituation, a condition that reduces possibly damaging or energetically expensive stress-induced responses when the same (homotypic) situation is repeatedly encountered over time. Importantly, deficits in stress response habituation are strongly associated with multiple psychiatric and psychological disorders, but the brain regions and mechanisms underlying these deficits are poorly understood. The present study investigated the role of the rostral posterior hypothalamic (rPH) region in acute and repeated stress responses because of its relatively unique position in the brain to modulate multiple responses elicited by stress exposure. Two experiments were conducted, the first using adult female Sprague Dawley (SD) rats that were surgically injected with a chemogenetic receptor (hM4D(G_i)) to functionally inhibit neural activity in the rPH while measuring corticosterone and behavioral stress responses. The immediate-early gene protein Fos and infectivity rate (via detection of the fluorescent protein mCherry expressed with the hM4D(G_i) receptor) were also measured in the rPH region following acute restraint stress and loud noise stress. The second study used adult male SD rats, who were also injected with the hM4D(G_i) viral construct in rPH and analyzed with similar metrics but subjected to six days of repeated loud noise stress under rPH inhibitory conditions and tested for response habituation under drug free conditions on the seventh and last loud noise presentation. While acute rPH neural inhibition failed to modify changes in corticosterone release or behavioral responses to the stressors, repeated rPH inhibition disrupted the repeated stress corticosterone response habituation, as compared to the control groups. These responses were accompanied by rPH activity (Fos) that varied with the stress-induced corticosterone responses and showed moderate correlations with the levels of infectivity achieved by viral injections. These findings suggest that the rPH is necessary for regulation of stress habituation but is not necessary for the neuroendocrine or behavioral responses to acute stressors.

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