Increased cannabis intake during the COVID-19 pandemic is associated with worsening of depression symptoms in people with PTSD.

BACKGROUND: Some evidence suggests substance use affects clinical outcomes in people with posttraumatic stress disorder (PTSD). However, more work is required to examine links between mental health and cannabis use in PTSD during exposure to external stressors such as the COVID-19 pandemic. This study assessed mental health factors in individuals with self-reported PTSD to: (a) determine whether stress, anxiety, and depression symptoms were associated with changes in cannabis consumption across the pandemic, and (b) to contrast the degree to which clinically significant perceived symptom worsening was associated with changes in cannabis intake. METHOD: Data were obtained as part of a larger web-based population survey from April 3rd to June 24th 2020 (i.e., first wave of the pandemic in Canada). Participants (N = 462) with self-reported PTSD completed questionnaires to assess mental health symptoms and answered questions pertaining to their cannabis intake. Participants were categorized according to whether they were using cannabis or not, and if using, whether their use frequency increased, decreased, or remained unchanged during the pandemic. RESULTS: Findings indicated an overall perceived worsening of stress, anxiety, and depression symptoms across all groups. A higher-than-expected proportion of individuals who increased their cannabis consumption reached threshold for minimal clinically important worsening of depression, X2(3) = 10.795, p = 0.013 (Cramer's V = 0.166). CONCLUSION: Overall, those who increased cannabis use during the pandemic were more prone to undergo meaningful perceived worsening of depression symptoms. Prospective investigations will be critical next steps to determine the directionality of the relationship between cannabis and depressive symptoms.

Gastrin-releasing peptide attenuates fear memory reconsolidation.

BACKGROUND: Gastrin Releasing Peptide (GRP) may play a role in fear learning. The GRP Receptor is expressed in the basolateral amygdala and hippocampus, and central administration of GRP mediates fear learning. The effects of GRP on reconsolidation, however, have been minimally explored. Reconsolidation, the process by which formed memories are rendered labile following recall, provides a window of opportunity for pharmacological intervention. Although evidence suggests the window of opportunity to alter reactivated consolidation memory can be as long as 6 h, shorter intervals have not been extensively investigated. METHOD: Male Sprague-Dawley rats received six 1.0 mA continuous footshocks. 24 h later, were re-exposed to the context (shock chamber). Immediately following memory retrieval rats received i.p. injection of GRP (10 nmol/kg), Flumazenil (1 mg/kg), GRP + Flumazenil (10 nmol/kg GRP with 1 mg/kg Flumazenil), or Vehicle. Other groups received GRP or Vehicle at 0, 10, 30, or 60 min post-reactivation. 24 h and 5 days later rats were assessed for fear expression upon re-exposure to the fearful stimulus. RESULTS: GRP significantly attenuated the reconsolidation of learned fear when administered immediately (but not 10 min or longer) following recall. Some of the variability in the impact of treatments aimed at disrupting fear memories may be governed, in part, by the time-frame of the reconsolidation window. Our results indicate that the effect of immediate administration persisted for at least 5 days. Co-administration of benzodiazepine-receptor antagonist Flumazenil blocked this effect, suggesting the effect is mediated via a GABAergic mechanism.