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Boris B. Gorzalka

Researcher at University of British Columbia

Publications -  189
Citations -  11451

Boris B. Gorzalka is an academic researcher from University of British Columbia. The author has contributed to research in topics: Endocannabinoid system & Cannabinoid receptor. The author has an hindex of 58, co-authored 189 publications receiving 10531 citations. Previous affiliations of Boris B. Gorzalka include Kalamazoo College.

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Neurobiology of chronic mild stress: parallels to major depression.

TL;DR: The chronic mild stress paradigm evokes an array of neurobiological changes that mirror those seen in depressive disorders and may be a suitable tool to investigate novel systems that could be disturbed in depression, and thus aid in the development of novel targets for the treatment of depression.
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Downregulation of Endocannabinoid Signaling in the Hippocampus Following Chronic Unpredictable Stress

TL;DR: The data suggest that stress-induced downregulation of hippocampal eCB signaling contributes to problems in behavioral flexibility and could play a role in the development of perseveratory and ruminatory behaviors in stress-related neuropsychiatric disorders.
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Recruitment of prefrontal cortical endocannabinoid signaling by glucocorticoids contributes to termination of the stress response.

TL;DR: The ability of stress-induced glucocorticoid signaling within mPFC to terminate HPA axis activity is mediated by a local recruitment of endocannabinoid signaling, which supports a model in which endoc cannabinoidoid receptor engagement to activation of corticolimbic relays that inhibit corticosterone secretion.
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Endogenous cannabinoid signaling is essential for stress adaptation

TL;DR: An important role for endocannabinoid signaling is demonstrated in the process of stress HPA habituation, and it is suggested that AEA and 2-AG modulate different components of the adrenocortical response to repeated stressor exposure.
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Suppression of Amygdalar Endocannabinoid Signaling by Stress Contributes to Activation of the Hypothalamic–Pituitary–Adrenal Axis

TL;DR: Findings suggest that the degree to which stressful stimuli reduce amygdalar AEA/CB1 receptor signaling contributes to the magnitude of the HPA response.