Wednesday, December 5, 2018

The Role of the Posterior Hypothalamus in Understanding Stress Pathology

Previous data suggests that interactions between the posterior hypothalamus (PH) and limbic forebrain could represent a neurocircuit critical for stress adaptation and, perhaps, stress pathology. 

This study tests the hypothesis that the PH is an important integrative node that translates forebrain inputs into behavioral and neuroendocrine reactivity. The researchers test the hypothesis that GABAergic signaling within the PH is a critical link between forebrain behavior-regulatory nuclei and the neuroendocrine hypothalamus, integrating social and anxiety-related behaviors with physiological stress reactivity. The researchers identify input to specific endocrine cell groups to elucidate mechanisms by which the PH may regulate physiological reactivity. Based on this connectivity, they also explore the role of the PH in neuroendocrine stress responses, with the goal of determining the neural substrates integrating affective behavior with stress reactivity.

This information establishes an important role for the PH incoordination of behavioral and neuroendocrine responses, likely mediated through interactions with key limbic forebrain circuitry. The studies conducted for this research demonstrate that GABAergic signaling within the PH is critical for reducing anxiety-like behavior, social withdrawal, and HPA axis stress responses.

This study demonstrates that the PH represents an important integrative center linking the stress-regulatory influence of the limbic forebrain with anxiety-like avoidance behavior and neuroendocrine systems. The vast interconnectedness of the PH with cell groups mediating behavioral and physiological processes suggests that the PH may be uniquely positioned to play a role in stress pathologies associated with altered limbic functional connectivity.

Myers, Brent, et al. GABAergic Signaling within a Limbic-Hypothalamic Circuit Integrates Social and Anxiety-Like Behavior with Stress Reactivity. Neuropsychopharmacology, vol. 41, no. 6, 2015, pp. 1530–1539., doi:10.1038/npp.2015.311.

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