Highlights Highlights Parkinson’s disease is characterized by the loss of dopaminergic neurons in the substantia nigra. Glial-glial crosstalk is essential for maintaining the regional milieu, and appears to be particularly important in modulating neuroinflammation and many aspects of neurodegeneration. In particular, astrocytes are critical for maintaining dopamine neuronal integrity and survival, and astroglial dysfunction is prominent in Parkinson’s disease. As such, astrocytes represent a potentially critical therapeutic target in neurodegeneration. In this study, in vivo optogenetics were used to selectively stimulate astrocytes in the substantia nigra following a striatal 6-OHDA lesion. Remarkably, a single bout of optogenetic stimulation was sufficient to attenuate motor deficits and dopamine neuron loss induced by the neurotoxin. Furthermore, bulk RNA-seq and snRNA-seq analysis of the substantia nigra revealed extensive changes in both microglia and oligodendrocytes, suggesting that the neuroprotective effects of stimulating astrocytes may be mediated through alterations in glia-glia crosstalk. Altogether, this work demonstrates the importance of understanding glia-glia interactions in neurodegeneration. ### Competing Interest Statement The authors have declared no competing interest.

Parkinson's disease (PD) is a prevalent neurodegenerative disorder that shows considerable heterogeneity of risk factors however, the degree to which race/ethnicity has been actively pursued in PD risk research is unknown. We examined PD literature from 2000-24 and found that less than half accounted for race/ethnicity and only 4.8% of n = 1142 articles included ethno-racial factors as an integral part of the analysis. This demonstrates that race/ethnicity has been critically understudied in PD and further studies that examine ethno-racial contributions to risk for PD are warranted.

Aims: This paper aims at exploring the subjective experience, particularly in terms of accept-ability and feasibility, of a mindfulness-based intervention for people with a psychotic disorder and social anxiety. Mindfulness interventions benefit from empirical support for decreasing anxiety in people with psychotic disorders, yet the effects on specific anxiety disorders, namely social anxiety, have scarcely been studied.Methods: Three different studies were conducted in order to determine the feasibility and acceptability of the mindfulness intervention and of the use of homework and VR exposure for people with psychotic disorder and social anxiety: two single case studies (one with virtual reality) and a pilot study (n = 6).Results: The intervention proposed was generally well-accepted and appreciated by the participants, but the meditation homework stood out as rather difficult for some participants. The virtual reality addition appeared to have a positive impact on the therapy, being also well-accepted and appreciated by the participant, but also considered stressfull.Conclusions: This paper shows that the mindfulness-based intervention presented is feasible, appreciated by the participants and has potential to be useful and therapeutic in the context of social anxiety in people with a psychotic disorder, even though efficacy cannot be established in these exploratory studies. The added value of encouraging at-home practice and of using VR exposure to the treatment merits further investigation. Future studies are needed to determine the efficacy of the treatment, especially with the virtual reality exposure and homework encouragements.(c) 2023 Association Franc,aise de Therapie Comportementale et Cognitive. Published by Elsevier Masson SAS. All rights reserved.

Astroglial cells are key players in the development and maintenance of neurons and neuronal networks. Astroglia express steroid hormone receptors and show rapid responses to hormonal manipulations. However, despite important sex differences in the cortex and hippocampus, few studies have examined sex differences in astroglial cells in telencephalic development. To characterize the cortical astroglial translatome in male and female mice across postnatal development, we use translating ribosome affinity purification together with RNA sequencing and immunohistochemistry to phenotype astroglia at six developmental time points. Overall, we find two distinct astroglial phenotypes between early (P1-P7) and late development (P14-adult), independent of sex. We also find sex differences in gene expression patterns across development that peak at P7 and appear to result from males reaching a mature astroglial phenotype earlier than females. These developmental sex differences could have an impact on the construction of neuronal networks and windows of vulnerability to perturbations and disease.

| 10:30 am | Opening of Meeting | || | 10:45 am | Opening Remarks – Dr. Jeff Daskalakis, CCNP

OVERVIEW OF EVENTS 10:30 am Opening of Meeting 10:45 am Opening Remarks - Dr. Jeff Daskalakis, CCNP President 10:50 am Introduction - Dr. Cecilia Flores, CCNP Vice-President 11:00 am CCNP 2020 Young Investigator Award Presentation Caroline Ménard, PhD, Department of Psychiatry & Neuroscience, Université Laval: "Sex-specific vascular alterations and biomarkers underlie stress responses in mice mirrored in human depression" 11:50 am CCNP Next Generation Awardee Andrea H. Pantoja Urban, MSc, Integrated Program in Neuroscience, McGill University: "Short and long-term effects of social defeat stress in adolescent female mice" 12:05 pm CCNP Next Generation Awardee Orna Issler, PhD, Department of Neuroscience, Mount Sinai:"The sex-specific role for long noncoding RNAs in depression: from genome-wide patterns to behavioral readout" 12:20 pm Lunch/Break 12:50 pm CCNP 2020 Heinz Lehmann Award Presentation Martin Alda, MD, FRCPC, Department of Psychiatry, Dalhousie University: "Personalized long-term treatment of bipolar disorder" 1:40 pm CCNP Next Generation Awardee Mikaela K Dimick, BA, Centre for Youth Bipolar Disorder, Centre for Addiction and Mental Health: "Cerebral blood flow and core mood symptoms in youth bipolar disorder: evidence for region-symptom specificity" 1:55 pm CCNP Next Generation Awardee Sneha Chenji, PhD, Department of Psychiatry & Pediatrics, University of Calgary: "The effect of rTMS treatment on cortico-striatal-thalamo-cortical (CSTC) circuit connectivity in Tourette's syndrome: a pilot study" 2:10 pm Break 2:20 pm CCNP 2020 Innovations in Neuropsychopharmacology Award Presentation Jeffrey Meyer, MD, PhD, FRCPC, Department of Psychiatry, University of Toronto: "Imaging markers of gliosis and monoamine oxidase in major depressive disorder: implications for personalized prevention and treatment" 3:10 pm CCNP Next Generation Awardee Jasmine D. Cakmak, MSc, Neuroscience, Western University: "The functional and structural consequences of aberrant microglial activity in major depressive disorder" 3:25 pm CCNP Next Generation Awardee Kayla D. Stone, PhD, Department of Psychiatry, University of Calgary: "Dorsolateral prefrontal cortex neurometabolite concentrations in pediatric mild traumatic brain injury" 3:40 pm Break 3:50 pm Keynote Speaker Rémi Quirion, OC, CQ, PhD, FRSC, Chief Scientist of Quebec, Ministry of Economy & Innovation: "A less well travelled road: from neuroscientist to chief scientist and then came COVID-19" 4:50 pm Closing Remarks - Dr. Cecilia Flores, CCNP Vice President Acknowledgments: In keeping with CMA guidelines, program content and selection of speakers are the responsibility of the planning committee. Methods: Here, we characterized the enduring changes in histone modifications in the NAcc of mice exposed to chronic social defeat stress (CSDS), a validated model for the study of depression-like behaviours that separates mouse populations into susceptible (SUS) and resilient (RES) based on a social interaction test (SIT). Tissue from the NAcc of control, SUS, and RES mice was collected either 24 hours or 4 weeks after the SIT and processed for histone profiling via mass spectrometry. From the Department of Psychiatry, University of Alberta, Edmonton, AB, Canada (Yap, Luki, S. Hanstock, Lirette, Zhaoa, Aitchison, Le Melledo);the Department of Medical Genetics, University of Alberta, Edmonton, AB, Canada (Aitchison);the Neuroscience and Mental Health Institute, University of Alberta, Edmonton, AB, Canada (Aitchison);the Edmonton Mood and Anxiety Disorders Program, University of Alberta Hospital, Edmonton, AB, Canada (Aitchison);the Department of Biomedical Engineering, University of Alberta, Edmonton, AB, Canada (C. Hanstock, Seres);and the Royal Alexandra Hospital, Edmonton, AB, Canada (Shandro).

Environmental enrichment has been shown to increase cognitive abilities and accelerate recovery from a number of disease states. Typically, enrichment protocols last from four to eight weeks, however, it has previously been shown that two weeks of environmental enrichment is sufficient to increase cognitive abilities and the proliferation of the astroglial stem cell pool in juvenile mice. The current study examines whether a short-term enrichment protocol can induce similar effects in adults as compared to juveniles. Using juvenile and adult wild-type mice, we examined the effects of short-term environmental enrichment (including a running wheel) on cognitive abilities, anxiety-like behaviour, and the stem cell potential of sub-ventricular neural stem cells (NSC's) in vitro using neurosphere assays. We found that short-term environmental enrichment decreased anxiety behaviour and increased overall memory abilities similarly in juveniles and adults. However, the rate of acquisition on the Morris water maze, hippocampal Sox2 and Ki67 expression, and neurosphere potential increased in response to enrichment only in juveniles, suggesting that the effects of enrichment on these measures are age dependant. Together, these data suggest that the potential beneficial effects of environmental manipulations decrease with age.

Effective pharmacotherapy for major depressive disorder remains a major challenge, as more than 30% of patients are resistant to the first line of treatment (selective serotonin reuptake inhibitors)1. Sub-anaesthetic doses of ketamine, a non-competitive N-methyl-d-aspartate receptor antagonist2,3, provide rapid and long-lasting antidepressant effects in these patients4–6, but the molecular mechanism of these effects remains unclear7,8. Ketamine has been proposed to exert its antidepressant effects through its metabolite (2R,6R)-hydroxynorketamine ((2R,6R)-HNK)9. The antidepressant effects of ketamine and (2R,6R)-HNK in rodents require activation of the mTORC1 kinase10,11. mTORC1 controls various neuronal functions12, particularly through cap-dependent initiation of mRNA translation via the phosphorylation and inactivation of eukaryotic initiation factor 4E-binding proteins (4E-BPs)13. Here we show that 4E-BP1 and 4E-BP2 are key effectors of the antidepressant activity of ketamine and (2R,6R)-HNK, and that ketamine-induced hippocampal synaptic plasticity depends on 4E-BP2 and, to a lesser extent, 4E-BP1. It has been hypothesized that ketamine activates mTORC1–4E-BP signalling in pyramidal excitatory cells of the cortex8,14. To test this hypothesis, we studied the behavioural response to ketamine and (2R,6R)-HNK in mice lacking 4E-BPs in either excitatory or inhibitory neurons. The antidepressant activity of the drugs is mediated by 4E-BP2 in excitatory neurons, and 4E-BP1 and 4E-BP2 in inhibitory neurons. Notably, genetic deletion of 4E-BP2 in inhibitory neurons induced a reduction in baseline immobility in the forced swim test, mimicking an antidepressant effect. Deletion of 4E-BP2 specifically in inhibitory neurons also prevented the ketamine-induced increase in hippocampal excitatory neurotransmission, and this effect concurred with the inability of ketamine to induce a long-lasting decrease in inhibitory neurotransmission. Overall, our data show that 4E-BPs are central to the antidepressant activity of ketamine. The antidepressant-like effects of ketamine in mice depend on the expression of specific eIF4E-binding proteins in excitatory and inhibitory neurons.

Team sports may represent an arena in which adolescent girls can develop skills and abilities to gain control over their lives. The aim of this retrospective study was to explore how participation in a psychosocial programme using sport as an intervention tool could foster the process of empowerment in young women at risk of delinquency and school dropout. Interviews were conducted with seven young women who were involved in the programme during high school. A descriptive content analysis suggests that involvement in the programme may contribute to the participants’ empowerment process through better academic persistency, capacity to resist negative external influences and the development of life skills. Results, however, indicate that the empowerment process is moderated by the participants’ differential social environment and life trajectory after high school.

The neuroplasticity hypothesis of depression proposes that major depressive disorders are related to decreased hippocampal and cortical neural plasticity, which is reversed by antidepressant treatment. Astroglial cells have emerged as key mediators of neural plasticity and are involved in the cause and treatment of depression and anxiety-like behaviors. One of the ways that astroglia modulate neuroplasticity is through the formation and maintenance of perineuronal nets (PNNs). Perineuronal nets are important extracellular matrix components that respond to stress and are implicated in anxiety-like behaviors. Normally, astroglial cells continuously turnover PNNs by degrading and donating PNN proteins; however, chronic stress slows PNN protein degradation and increases cortical PNN expression overall. In this report, we used weighted gene co-expression network analysis and eigengene analysis to further delineate the pathways and key regulators involved in the astroglial-PNN relationship following chronic stress. Our analyses indicate that chronic variable stress induces the expression of PNNs through inhibition of trophic pathways and key transcription factors in astroglial cells. These data further support the integral role of astroglial cells in the neuroplasticity hypothesis of depression through their modulation of anxiety-like behaviors and PNNs.

Astroglial cells are emerging as key players in the development and homeostatic maintenance of neurons and neuronal networks. Astroglial cell functions are critical to neuronal migration and maturation, myelination, and synapse dynamics, however little is known about astroglial phenotypic changes over development. Furthermore, astroglial cells express steroid hormone receptors and show rapid responses to hormonal manipulations, however, despite important sex differences in telencephalic regions such as the cortex and hippocampus few studies have examined sex differences in astroglial cells in development and outside of the hypothalamus and amygdala. To phenotype cortical astroglial cells across postnatal development while considering potential sex differences, we used translating ribosome affinity purification together with RNA sequencing (TRAPseq) and immunohistochemistry to phenotype the entire astroglial translatome in males and females at key developmental time points: P1, P4, P7, P14, P35 and in adulthood. Overall, we found two distinct astroglial phenotypes between early (P1-P7) and late development (P14-Adult). We also noted that although astroglia show few basal sex differences in adulthood, they show significant sex differences in developmental gene expression patterns, with peak sex differences observed at P7. At least part of the sex differences observed at P7 appear to be due to males reaching a more mature astroglial phenotype earlier than females. Together, these data clearly delineate and phenotype astroglia across development and identify sex differences in astroglial developmental programs. Importantly, these developmental sex differences could have an impact on the construction and maintenance of neuronal networks and potential developmental windows of vulnerability to neurologic and psychiatric disease.

Previous research has shown that fibroblast growth factor 2 protein (FGF2) can act as an anxiolytic and anti-depressive agent in rodents. Levels of hippocampal FGF2 and FGF2 receptors are decreased in post-mortem brains of individuals with mood disorders. No changes in FGF2 were noted in the post-mortem brains of individuals with mood disorders that were successfully treated with anti-depressant medication prior to death. Mutations in the FGF2 gene in humans have been shown to predict non-responsiveness to the therapeutic effects of selective serotonin reuptake inhibitors (SSRIs). These findings suggest that FGF2 may potentially be a target of and/or required for the therapeutic effects of antidepressant medications. To test this, we employed a rodent model of depressive behaviour, chronic variable stress (CVS) in conjunction with antidepressant treatment (fluoxetine) in wild-type (WT) and FGF2 knockout mice (FGF2KO) and examined depressive and anxiety behaviors. Results showed that fluoxetine reversed the effects of CVS on depressive and anxiety behaviours in wild-type mice only, suggesting that the FGF2 gene is indeed necessary for the therapeutic effects of fluoxetine. Interestingly, CVS decreased hippocampal FGF2 levels and fluoxetine partially reversed this effect. Because FGF2 has been previously shown to modify HPA activity through hippocampal glucocorticoid receptors (GR), we examined levels of glucocorticoid receptors and found a decrease in GR in response to CVS, with a further decrease in FGF2KO. No effect of fluoxetine on GR was observed in either WT or FGF2KO mice. This suggests that further changes in glucocorticoid receptors are not necessary for the anti-depressant effects of fluoxetine in WT mice, although decreased glucocorticoid receptors in response to FGF2 deletion may preclude the therapeutic actions of fluoxetine in FGF2KO. Whether astroglia, astroglial functions, or HPA changes are the downstream target of FGF2-mediated changes induced by fluoxetine remains to be determined, however, the current study reaffirms the potential of FGF2 as a novel therapeutic target in the treatment of depression and anxiety disorders.

Recent studies have suggested that cortical astroglia play an important role in depressive-like behaviors. Potential astroglial contributions have been proposed based on their neuroplastic functions such as glutamate recycling and synaptic plasticity. However, the specific mechanisms by which astroglial cells contribute or protect against a depressive phenotype remain unknown.

Recent studies have suggested that cortical astroglia play an important role in depressive-like behaviors. Potential astroglial contributions have been proposed based on their known neuroplastic functions, such as glutamate recycling and synaptic plasticity. However, the specific mechanisms by which astroglial cells may contribute or protect against a depressive phenotype remain unknown. To delineate astroglial changes that accompany depressive-like behavior, we used astroglial-specific bacTRAP mice exposed to chronic variable stress (CVS) and profiled the astroglial translatome using translating ribosome affinity purification (TRAP) in conjunction with RNAseq. As expected, CVS significantly increased anxiety- and depressive-like behaviors and corticosterone levels and decreased GFAP expression in astroglia, although this did not reflect a change in the total number of astroglial cells. TRAPseq results showed that CVS decreased genes associated with astroglial plasticity: RhoGTPases, growth factor signaling, and transcription regulation, and increased genes associated with the formation of extracellular matrices such as perineuronal nets (PNNs). PNNs inhibit neuroplasticity and astroglia contribute to the formation, organization, and maintenance of PNNs. To validate our TRAPseq findings, we showed an increase in PNNs following CVS. Degradation of PNNs in the prefrontal cortex of mice exposed to CVS reversed the CVS-induced behavioral phenotype in the forced swim test. These data lend further support to the neuroplasticity hypothesis of depressive behaviors and, in particular, extend this hypothesis beyond neuronal plasticity to include an overall decrease in genes associated with cortical astroglial plasticity following CVS. Further studies will be needed to assess the antidepressant potential of directly targeting astroglial cell function in models of depression.

This study aims to understand how preservice programs prepare future teachers to use ICT to develop students’ information literacy skills. A survey was conducted from January 2014 through May 2014 with 413 future teachers in four French Canadian universities. In the spring of 2015, qualitative data were also collected from 48 students in their final year of an initial teacher training program. Our findings suggest that although future teachers receive formal ICT training as part of their program, information literacy is not formally addressed. Nevertheless, information literacy is perceived to be an important skill. In addition to a lack of formal training, future teachers perceive that barriers such as time constraints and lack of access to necessary technologies in the classroom will prevent them from helping students develop information literacy skills. Based on these results, we propose some practical implications and recommendations for preservice programs and education policy makers. Cette étude vise à mieux comprendre comment la formation initiale en enseignement prépare les futurs enseignants à utiliser les TIC pour développer les compétences informationnelles des élèves. Dans un premier temps, une enquête a été réalisée entre janvier et mai 2014 auprès de 413 futurs enseignants dans quatre universités québécoises. Dans un second temps, au printemps 2015, des données qualitatives ont été recueillies auprès de 48 futurs enseignants au cours du dernier trimestre de leur formation initiale. Nos analyses suggèrent que si les futurs enseignants reçoivent une formation à l’utilisation pédagogique des TIC, les compétences informationnelles ne sont pas explicitement abordées, et ce, bien qu’elles soient perçues comme essentielles. De plus, les contraintes de temps et l’accessibilité aux outils informatiques sont pressenties comme des défis importants. Sur la base des suggestions des participants, nous dégageons des retombées pratiques pour la formation initiale et pour les détenteurs d’enjeux en éducation.

L’objectif general de cette these etait d’explorer le developpement personnel de jeunes a risque de delinquance et de decrochage scolaire a travers leur participation a un programme d’intervention psychosociale nomme « Bien dans mes Baskets » (BdmB). Ce programme utilise le basketball parascolaire comme outil d’intervention et il a comme particularite qu’une bonne partie de ses entraineurs-intervenants detiennent une formation professionnelle en travail social ou domaines connexes. Cette these presente les resultats de trois etudes faisant partie d’un projet de recherche plus vaste portant sur l’evaluation du programme BdmB. Une premiere etude a explore le processus de transfert, a d’autres domaines d’activites, des habiletes de vie ciblees par le programme BdmB. Des entretiens semi-directifs ont ete realises aupres de 14 anciens participants et sept anciennes participantes du programme. Nos resultats suggerent que trois principaux facteurs semblent avoir joue un role dans le processus de transfert des habiletes de vie developpees au sein de BdmB, soit la presence de contextes favorisant l’apprentissage experientiel, la valeur relative accordee aux differents domaines d’activites et la trajectoire de vie. Il ressort egalement de nos donnees qu’au-dela du processus de transfert sur une base individuelle, il est possible qu’un transfert puisse s’operer dans la communaute. L’objectif de la deuxieme etude etait d’explorer comment et dans quelle mesure les experiences au sein de BdmB ont pu servir de levier au processus d’empowerment. Des entretiens semi-directifs ont ete realises aupres de sept anciennes participantes de BdmB. Nos resultats suggerent que la pratique sportive, combinee a une intervention psychosociale, peut contribuer au developpement d’un plus grand controle sur sa vie. Cette amelioration serait la resultante cumulative de divers apprentissages, dont le developpement et le transfert d’habiletes de vie et la capacite a resister aux influences externes negatives presentes dans leurs milieux de vie respectifs, ainsi que l’impact positif des experiences vecues au sein de BdmB sur la perseverance scolaire et les aspirations professionnelles. Une troisieme etude avait pour objectif d’evaluer l’impact du programme BdmB sur le sentiment d’appartenance a l’ecole et la perception de soutien social. Un devis quasi experimental a ete utilise pour evaluer l’impact du programme aupres des athletes-etudiants(es) actuels. Le groupe d’intervention etait compose des athletes-etudiants de BdmB et les groupes de comparaison etaient constitues des etudiants de la meme ecole ne participant pas au programme et pratiquant ou non un autre sport. Les individus ont ete sondes a deux reprises a l’aide d’un questionnaire auto administre sur une periode de deux annees scolaires. Les resultats de l’etude indiquent que le groupe BdmB a developpe un meilleur sentiment d’appartenance et a percu un meilleur soutien social par rapport aux groupes de comparaison.

Psychosocial interventions are an essential part of the treatment for people with severe mental illness such as schizophrenia. The criteria regarding what makes an intervention "evidence-based" along with a current list of evidence-based interventions are presented. Although many evidence-based interventions exist, implementation studies reveal that few, if any, are ever implemented in a given setting. Various theories and approaches have been developed to better understand and overcome implementation obstacles. Among these, merging two evidence-based interventions, or offering an evidence-based intervention within an evidence-based service, are increasingly being reported and studied in the literature. Five such merges are presented, along with their empirical support: cognitive behavior therapy (CBT) with skills training; CBT and family psychoeducation; supported employment (SE) and skills training; SE and cognitive remediation; and SE and CBT.