What Got Us Here Won't Get Us There: Critical History in Radical Black Re-imaginations of Canadian Nursing Histories.

As a "foursome" of nursing history students and scholars, upcoming, junior, and seasoned, we presented a panel on new work and possibilities related to histories of Blackness and Black nurses in Canadian nursing history. Our presentation was the 2023 keynote Hannah Panel Presentation for the joint Canadian Society for the History of Medicine (CSHM-SCHM) and the Canadian Association for the History of Nursing (CAHN-ACHN) conference. Reflecting and expanding our perspectives, we share the relevance and significance of engaging with histories of Canadian Blackness and (in)visibility of Blackness in nursing history. This paper considers the overarching question of how does engaging with histories of Canadian Blackness serve as an anti-racist strategy when examining, analyzing and understanding the history of nursing and health care? A core tenant of this work aims at acknowledging how institutional relationships of power are reproduced within scholarship unless there is space for radical re-imaginations. The disruption to power is achieved by exploring the connections between nursing and history from the perspective of Black nurses' history or Black feminist thought. We also disrupt power by our form, in challenging expectations of scientific inquiry as the only format of valid knowledge production within the discipline. Possibilities of arts-based methodology as a site for democratization in nursing knowledge are evoked through the metaphoric language (water, fire, air and earth) interwoven within the text. We highlight how each of us engages with nursing history, further complicating previous narratives of our collective Canadian past. In publishing our thoughts on historical inquiry in a nursing journal, we hope to provoke more curiosity and interest in history within our discipline as a site for liberation!

The CRF1 receptor antagonist SSR125543 prevents stress-induced cognitive deficit associated with hippocampal dysfunction: comparison with paroxetine and D-cycloserine.

RATIONALE: The selective CRF1 (corticotropin releasing factor type 1) receptor antagonist SSR125543 has been previously shown to attenuate the long-term cognitive deficit produced by traumatic stress exposure. Memory disturbances described in post-traumatic stress disorder (PTSD) patients are believed to be associated with changes in neuronal activity, in particular at the level of the hippocampus. OBJECTIVES: The present study aims at investigating whether the effects of SSR125543 (10 mg/kg/day for 2 weeks) on cognitive impairment induced by traumatic stress exposure are associated with changes in hippocampal excitability. Effects of SSR125543 were compared to those of the 5-HT reuptake inhibitor, paroxetine (10 mg/kg/day), and the partial N-methyl-D-aspartate (NMDA) receptor agonist, D-cycloserine (10 mg/kg/day), two compounds which have demonstrated clinical efficacy against PTSD. METHODS: Mice received two unavoidable electric foot-shocks. Then, 1 or 16 days after stress, they were tested for their memory performance using the object recognition test. Neuronal excitability was recorded during the third week post-stress in the CA1 area of the hippocampus. Drugs were administered from day 1 post-stress to the day preceding the electrophysiological study. RESULTS: Application of electric shocks produced cognitive impairment 16, but not 1 day after stress, an effect which was associated with a decrease in hippocampal neuronal excitability. Both stress-induced effects were prevented by repeated administration of SSR125543, paroxetine and D-cycloserine. CONCLUSIONS: These findings confirm that the CRF1 receptor antagonist SSR125543 is able to attenuate the behavioral effects of traumatic stress exposure and indicate that these effects are associated with a normalization of hippocampal neuronal excitability impaired by stress.

The CRF1 receptor antagonist SSR125543 attenuates long-term cognitive deficit induced by acute inescapable stress in mice, independently from the hypothalamic pituitary adrenal axis.

The selective antagonist at the CRF1 receptor, SSR125543, has been shown to produce anxiolytic-like effects in a number of animal models. The aim of the present study was to verify whether these effects are mediated by an action on the hypothalamic pituitary adrenal (HPA) axis. SSR125543 effects were evaluated in a mouse model of post-traumatic stress disorder. Animals received two unavoidable electric foot-shocks (1.5 mA/2 s). Two weeks later they were placed in the shock context and fecal and plasma corticosterone levels were measured by enzyme-immunoassay. Their cognitive performances were evaluated using the object recognition task following administration of SSR125543 at 3, 10 and 30 mg/kg or paroxetine at 20 mg/kg (i.p.), used as positive control. To assess the involvement of the HPA axis in the drug effects, a separate group of animals was subjected to the same procedure and drug regimen, but was treated with dexamethasone to blunt the HPA axis. Stressed mice had higher levels of corticosterone following re-exposure to the context and displayed impaired cognitive performance as compared to control animals. Corticosterone levels were normalized in stressed mice by SSR125543 and the cognitive deficit was significantly attenuated by SSR125543 and paroxetine, whether the HPA axis was blunted or not. These findings confirm that SSR125543 is able to attenuate the deleterious effects of stressful exposure. Importantly, the observation that these effects were still present in dexamethasone-treated mice indicates that this action does not necessarily involve pituitary-adrenal axis blockade, thereby suggesting that extra-pituitary CRF1 receptors may play a role in these effects.

Acute inescapable stress exposure induces long-term sleep disturbances and avoidance behavior: a mouse model of post-traumatic stress disorder (PTSD).

The experience of traumatic stress often leads to long-lasting alteration in sleep quality and behavior. The objective of the present experiment was to investigate the short- and long-term effects of acute inescapable stress (i.e. two electric foot-shocks of 1.5 mA; 2s) on sleep/wakefulness parameters and behavior in Swiss mice using electroencephalographic (EEG) analysis. Baseline EEG recording was performed in the home cage for 6h prior to the application of the foot-shocks in the presence of an object (i.e. a plastic prism). One, 7, 14 or 21 days later, a second 6h EEG recording session was performed after mice had been exposed or not to the same object for 5 min in their home cage. Results showed that at day 1, 7, 14 and 21 post-stress, shocked mice displayed sleep fragmentation as shown by an increase in the number of sleep episodes, regardless the presence of the object or not. In animals exposed to the object, the total duration of wakefulness over 6h was significantly increased at days 7, 14 and 21 post-stress, and rapid eye movement (REM) sleep was significantly decreased at day 14 post-shock. Moreover, in the behavioral experiment, conditioned avoidance to a shock-paired object, which appeared as soon as 24h after shock application, turned into generalized avoidance towards an unknown object 21 days after stress. These findings demonstrate that an acute inescapable stress exposure may cause long-lasting alterations in sleep patterns and behavior. Such modifications may be reminiscent of the profound changes observed in patients suffering from post-traumatic stress disorder.