Implementing trauma-informed care in a special education setting: An initial exploration of a multi-tiered model.

Implementing trauma-informed care in a special education environment serving youth from historically marginalized communities with high levels of exposure to potentially traumatic events (PTEs) requires a systematic tiered approach consistent with public health guidelines. Little is known about the implementation of this framework in special education settings where youth have significant emotional and behavioral difficulties. To address this need, a consultant-community partnership was forged between a hospital providing mental health services and a therapeutic day school that serves a special education cooperative. The current case study explores the design and implementation of a three-tiered model of trauma-informed care in a special education setting. This study will address the specific practices implemented at each tier, discuss successes and challenges, and summarize future directions for research, practice, and policy.

Effects of nitrous oxide and ketamine on electrophysiological and molecular responses in the prefrontal cortex of mice: A comparative study.

Nitrous oxide (N2O; laughing gas) has recently reported to produce rapid antidepressant effects, but little is known about the underlying mechanisms. We performed transcriptomics, in situ hybridization, and electrophysiological studies to examine the potential shared signatures induced by 1 h inhalation of 50% N2O and a single subanesthetic dose of ketamine (10 mg/kg, i.p.) in the medial prefrontal cortex (mPFC) in adult mice. Both treatments similarly affected the transcription of several negative regulators of mitogen-activated protein kinases (MAPKs), namely, dual specificity phosphatases (DUSPs). The effects were primarily located in the pyramidal cells. Notably, the overall effects of N2O on mRNA expression were much more prominent and widespread compared to ketamine. Ketamine caused an elevation of the spiking frequency of putative pyramidal neurons and increased gamma activity (30-100 Hz) of cortical local field potentials. However, N2O produced no such effects. Spiking amplitudes and spike-to-local field potential phase locking of putative pyramidal neurons and interneurons in this brain area showed no uniform changes across treatments. Our findings suggest that N2O and subanesthetic-dose ketamine target MAPK pathway in the mPFC but produce varying acute electrophysiological responses.

Bumetanide induces post-traumatic microglia-interneuron contact to promote neurogenesis and recovery.

Although the Na-K-Cl cotransporter (NKCC1) inhibitor bumetanide has prominent positive effects on the pathophysiology of many neurological disorders, the mechanism of action is obscure. Attention paid to elucidating the role of Nkcc1 has mainly been focused on neurons, but recent single cell mRNA sequencing analysis has demonstrated that the major cellular populations expressing NKCC1 in the cortex are non-neuronal. We used a combination of conditional transgenic animals, in vivo electrophysiology, two-photon imaging, cognitive behavioural tests and flow cytometry to investigate the role of Nkcc1 inhibition by bumetanide in a mouse model of controlled cortical impact (CCI). Here, we found that bumetanide rescues parvalbumin-positive interneurons by increasing interneuron-microglia contacts shortly after injury. The longitudinal phenotypic changes in microglia were significantly modified by bumetanide, including an increase in the expression of microglial-derived BDNF. These effects were accompanied by the prevention of CCI-induced decrease in hippocampal neurogenesis. Treatment with bumetanide during the first week post-CCI resulted in significant recovery of working and episodic memory as well as changes in theta band oscillations 1 month later. These results disclose a novel mechanism for the neuroprotective action of bumetanide mediated by an acceleration of microglial activation dynamics that leads to an increase in parvalbumin interneuron survival following CCI, possibly resulting from increased microglial BDNF expression and contact with interneurons. Salvage of interneurons may normalize ambient GABA, resulting in the preservation of adult neurogenesis processes as well as contributing to bumetanide-mediated improvement of cognitive performance.

High-intensity training with short and long intervals regulate cortical neurotrophic factors, apoptosis markers and chloride homeostasis in rats with stroke.

BACKGROUND/PURPOSE: The optimal endurance exercise parameters remain to be defined to potentiate long-term functional recovery after stroke. We aim to assess the effects of individualized high-intensity interval training (HIIT) with either long or short intervals on neurotrophic factors and their receptors, apoptosis markers and the two-main cation-chloride cotransporters in the ipsi- and contralesional cerebral cortices in rats with cerebral ischemia. Endurance performance and sensorimotor functions were also assessed METHODS: Rats with a 2 h transient middle cerebral artery occlusion (tMCAO) performed work-matched HIIT4 (intervals: 4 min) or HIIT1 (intervals: 1 min) on treadmill for 2 weeks. Incremental exercises and sensorimotor tests were performed at day 1 (D1), D8, and D15 after tMCAO. Molecular analyses were achieved in both the paretic and non-paretic triceps brachii muscles and the ipsi- and contralesional cortices at D17 RESULTS: Gains in endurance performance are in a time-dependent manner from the first week of training. This enhancement is supported by the upregulation of metabolic markers in both triceps brachii muscles. Both regimens alter the expression of neurotrophic markers and chloride homeostasis in a specific manner in the ipsi- and contralesional cortices. HIIT acts on apoptosis markers by promoting anti-apoptotic proteins in the ipsilesional cortex CONCLUSION: HIIT regimens seem to be of clinical relevance in the critical period of stroke rehabilitation by strongly improving aerobic performance. Also, the observed cortical changes suggest an influence of HIIT on neuroplasticity in both ipsi- and contralesional hemispheres. Such neurotrophic markers might be considered as biomarkers of functional recovery in individuals with stroke.

Acceptability and initial promise of trainings for community stakeholders serving refugee and immigrant families.

Cumulative traumatic migration experiences are compounded by escalating chronic distress related to the current sociopolitical climate for refugee and immigrant children and families. The aim of this open trial was to conduct a preliminary evaluation of You're Not Alone, a rapidly mounted, strengths-based, community-focused capacity building training initiative for stakeholders interacting with refugee and immigrant children and families in the Chicago area. Trainings, based on Trauma-Informed Care (TIC) and psychological first aid frameworks, adapted education and universal health promotion strategies for population-specific chronic traumatic stress. Two groups of participants (N = 948), who attended either mandatory (n = 659 educators) or voluntary (n = 289 community stakeholders) trainings, completed surveys at pretraining, post-training, and 6-week follow-up. Outcome indices included participant satisfaction, acceptability of training model, and changes in knowledge, attitudes, and behaviors. Over 90% of participants reported satisfaction and acceptability of trainings. For educators, hierarchical linear modeling analyses demonstrated significant increases in trauma knowledge, refugee and immigrant-specific knowledge, positive attitudes toward TIC over time, and a decrease in negative attitudes toward immigrants. Over 95% of participants indicated that they learned and intended to use new strategies to help serve refugee and immigrant children and families. At follow-up, over 80% of those who completed the survey had utilized at least one strategy, and over 55% indicated that they were using resources that they learned about in the training. This study demonstrates that capacity-building trainings swiftly developed and disseminated to community stakeholders can produce positive change in knowledge, attitudes, and practices. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

[Maternal-fetal outcomes in women with gestational diabetes in an intensive control program]. / Desenlaces materno-fetales en mujeres con diabetes gestacional en un programa de control intensivo.

Background: Gestational diabetes mellitus (GDM) is first diagnosed during pregnancy and it is the most frequent maternal hyperglycemia. Objective: To know fetal and maternal outcomes in an intensive control program in pregnant women with and without DMG at the Instituto Mexicano del Seguro Social (Mexican Institute for Social Security) Regional General Hospital No. 6, in Ciudad Madero, Tamaulipas. Material and methods: A descriptive and retrospective study, which included 800 outcomes of pregnant women between January 2009 and June 2020. Anthropometric data and pregnancy outcomes were collected. The intensive control program consisted of face-to-face consultations of 1 to 4 weeks, granted according to the degree of metabolic control, with which it was given nutritional counseling, recommendations for physical activity, and in some cases pharmacological treatment. Results: The prevalence of GDM was 36.2%. There were no statistically significant differences between the two groups, except for respiratory distress syndrome, which was more common in GDM (9.4%, p = 0.06). Patients with GDM had a lower prevalence of macrosomy (6.1%) compared to the control group (6.6%). All women admitted to the program in the first trimester had fewer fetal and maternal complications. Conclusions: This study demonstrates the effectiveness and efficiency of implementing an intensive control program in women with GDM, by reducing and equalizing maternal and fetal outcomes compared to a group of women without the disease.

Introducción: la diabetes mellitus gestacional (DMG) se diagnóstica por primera vez en el embarazo y es la hiperglucemia materna más frecuente. Objetivo: conocer los desenlaces fetales y maternos en un programa de control intensivo en mujeres embarazadas con y sin DMG en el Hospital General Regional No. 6 del Instituto Mexicano del Seguro Social (IMSS) en Ciudad Madero, Tamaulipas. Material y métodos: estudio descriptivo y retrospectivo que incluyó 800 desenlaces de mujeres gestantes entre enero de 2009 y junio de 2020. Se recopilaron datos antropométricos y desenlaces del embarazo. El programa de control intensivo consistió en consultas presenciales de una a cuatro semanas, otorgadas según el grado de control metabólico, en las que se proporcionó consejería nutricional, recomendaciones de actividad física y en algunos casos tratamiento farmacológico. Resultados: la prevalencia de DMG fue de 36.2%. No hubo diferencias estadísticamente significativas en ambos grupos, a excepción del síndrome de distrés respiratorio, que fue más frecuente en DMG (9.4%, p = 0.06). Las pacientes con DMG tuvieron menor prevalencia de macrosomía (6.1%) a diferencia del grupo control (6.6%). Toda mujer ingresada al programa en el primer trimestre tuvo menores complicaciones fetales y maternas. Conclusiones: este estudio demuestra la eficacia y eficiencia de implementar un programa de control intensivo en mujeres con DMG, al reducir e igualar los desenlaces maternos y fetales en comparación con un grupo de mujeres sin la enfermedad.

Transcranial magnetic stimulation set-up for small animals.

Transcranial magnetic stimulation (TMS) is widely applied on humans for research and clinical purposes. TMS studies on small animals, e.g., rodents, can provide valuable knowledge of the underlying neurophysiological mechanisms. Administering TMS on small animals is, however, prone to technical difficulties, mainly due to their small head size. In this study, we aimed to develop an energy-efficient coil and a compatible experimental set-up for administering TMS on rodents. We applied a convex optimization process to develop a minimum-energy coil for TMS on rats. As the coil windings of the optimized coil extend to a wide region, we designed and manufactured a holder on which the rat lies upside down, with its head supported by the coil. We used the set-up to record TMS-electromyography, with electromyography recorded from limb muscles with intramuscular electrodes. The upside-down placement of the rat allowed the operator to easily navigate the TMS without the coil blocking their field of view. With this paradigm, we obtained consistent motor evoked potentials from all tested animals.

Everyday Acts of Resistance: Mexican, Undocumented Immigrant Children and Adolescents Navigating Oppression With Mentor Support.

Study aims were to examine oppression in education among Mexican immigrant youth with undocumented status and how mentors and other adults helped them resist oppression. Qualitative, narrative one-on-one interviews were conducted with 17 Mexican immigrant young adults with undocumented or DACA status in the U.S. Participants provided retrospective accounts from childhood through older adolescence. Analyses revealed critical junctures in which participants experienced oppression: (1) developmental milestones and school events, (2) college application process, (3) unforeseen life events, and (4) incidents of racial discrimination. Mentors and other adults helped participants to resist oppression through advocacy, social capital efforts, role modeling, and emotional, instrumental, and financial support. This study fills gaps in the literature on mentoring and immigrant youth who are undocumented.

The structural violence of DACA and youth resistance.

OBJECTIVES: This study examined how youth who have received Deferred Action for Childhood Arrivals (DACA) experience structural violence and their responses to that violence. METHOD: Participants included 20 Latinx individuals, between the ages of 16 and 29, who migrated to the U.S. before age 16. The majority held DACA status. In-depth qualitative, narrative interviews were conducted with each participant. RESULTS: Narratives revealed multiple ways that DACA youth experience structural violence, including (a) challenges with the application process, (b) the financial burden created by the lack of access to federal financial aid for higher education, and (c) fears surrounding DACA. Youth responded to structural violence via (a) paying it forward, (b) radical hope, (c) social support, and (d) undocumented pride. CONCLUSIONS: Narratives demonstrate the ways in which young people experience structural violence despite the benefits of DACA and how some resist this violence. Implications for a legislative pathway to citizenship are discussed. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Time-dependent cortical plasticity during moderate-intensity continuous training versus high-intensity interval training in rats.

The temporal pattern of cortical plasticity induced by high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) is required to clarify their relative benefits to prevent neurological disorders. The purpose of this study is to define the time-dependent effects of work-matched HIIT and MICT on cortical plasticity, endurance, and sensorimotor performances over an 8-week training period in healthy rats. Adult healthy rats performed incremental exercise tests and sensorimotor tests before and at 2, 4, and 8 weeks of training. In parallel, cortical markers related to neurotrophic, angiogenic, and metabolic activities were assessed. Results indicate that HIIT induced an early and superior endurance improvement compared to MICT. We found significant enhancement of speed associated with lactate threshold (SLT) and maximal speed (Smax) in HIIT animals. MICT promoted an early increase in brain-derived neurotrophic factor and angiogenic/metabolic markers but showed less influence at 8 weeks. HIIT upregulated the insulin-like growth factor-1 (IGF-1) as well as neurotrophic, metabolic/angiogenic markers at 2 and 8 weeks and downregulated the neuronal K-Cl cotransporter KCC2 that regulates GABAA-mediated transmission. HIIT and MICT are effective in a time-dependent manner suggesting a complementary effect that might be useful in physical exercise guidelines for maintaining brain health.

Contribution of astrocytes to familial risk and clinical manifestation of schizophrenia.

Previous studies have implicated several brain cell types in schizophrenia (SCZ), but the genetic impact of astrocytes is unknown. Considering their high complexity in humans, astrocytes are likely key determinants of neurodevelopmental diseases, such as SCZ. Human induced pluripotent stem cell (hiPSC)-derived astrocytes differentiated from five monozygotic twin pairs discordant for SCZ and five healthy subjects were studied for alterations related to high genetic risk and clinical manifestation of SCZ in astrocyte transcriptomics, neuron-astrocyte co-cultures, and in humanized mice. We found gene expression and signaling pathway alterations related to synaptic dysfunction, inflammation, and extracellular matrix components in SCZ astrocytes, and demyelination in SCZ astrocyte transplanted mice. While Ingenuity Pathway Analysis identified SCZ disease and synaptic transmission pathway changes in SCZ astrocytes, the most consistent findings were related to collagen and cell adhesion associated pathways. Neuronal responses to glutamate and GABA differed between astrocytes from control persons, affected twins, and their unaffected co-twins and were normalized by clozapine treatment. SCZ astrocyte cell transplantation to the mouse forebrain caused gene expression changes in synaptic dysfunction and inflammation pathways of mouse brain cells and resulted in behavioral changes in cognitive and olfactory functions. Differentially expressed transcriptomes and signaling pathways related to synaptic functions, inflammation, and especially collagen and glycoprotein 6 pathways indicate abnormal extracellular matrix composition in the brain as one of the key characteristics in the etiology of SCZ.

Pharmacological and optical activation of TrkB in Parvalbumin interneurons regulate intrinsic states to orchestrate cortical plasticity.

Elevated states of brain plasticity typical for critical periods of early postnatal life can be reinstated in the adult brain through interventions, such as antidepressant treatment and environmental enrichment, and induced plasticity may be critical for the antidepressant action. Parvalbumin-positive (PV) interneurons regulate the closure of developmental critical periods and can alternate between high and low plasticity states in response to experience in adulthood. We now show that PV plasticity states and cortical networks are regulated through the activation of TrkB neurotrophin receptors. Visual cortical plasticity induced by fluoxetine, a widely prescribed selective serotonin reuptake inhibitor (SSRI) antidepressant, was lost in mice with reduced expression of TrkB in PV interneurons. Conversely, optogenetic gain-of-function studies revealed that activation of an optically activatable TrkB (optoTrkB) specifically in PV interneurons switches adult cortical networks into a state of elevated plasticity within minutes by decreasing the intrinsic excitability of PV interneurons, recapitulating the effects of fluoxetine. TrkB activation shifted cortical networks towards a low PV configuration, promoting oscillatory synchrony, increased excitatory-inhibitory balance, and ocular dominance plasticity. OptoTrkB activation promotes the phosphorylation of Kv3.1 channels and reduces the expression of Kv3.2 mRNA providing a mechanism for the lower excitability. In addition, decreased expression and puncta of Synaptotagmin2 (Syt2), a presynaptic marker of PV interneurons involved in Ca2+-dependent neurotransmitter release, suggests lower inputs onto pyramidal neurons suppressing feed-forward inhibition. Together, the results provide mechanistic insights into how TrkB activation in PV interneurons orchestrates the activity of cortical networks and mediating antidepressant responses in the adult brain.

Is High-Intensity Interval Training Suitable to Promote Neuroplasticity and Cognitive Functions after Stroke?

Stroke-induced cognitive impairments affect the long-term quality of life. High-intensity interval training (HIIT) is now considered a promising strategy to enhance cognitive functions. This review is designed to examine the role of HIIT in promoting neuroplasticity processes and/or cognitive functions after stroke. The various methodological limitations related to the clinical relevance of studies on the exercise recommendations in individuals with stroke are first discussed. Then, the relevance of HIIT in improving neurotrophic factors expression, neurogenesis and synaptic plasticity is debated in both stroke and healthy individuals (humans and rodents). Moreover, HIIT may have a preventive role on stroke severity, as found in rodents. The potential role of HIIT in stroke rehabilitation is reinforced by findings showing its powerful neurogenic effect that might potentiate cognitive benefits induced by cognitive tasks. In addition, the clinical role of neuroplasticity observed in each hemisphere needs to be clarified by coupling more frequently to cellular/molecular measurements and behavioral testing.

Elevated expression of endogenous glial cell line-derived neurotrophic factor impairs spatial memory performance and raises inhibitory tone in the hippocampus.

Parvalbumin-positive interneurons (PV+) are a key component of inhibitory networks in the brain and are known to modulate memory and learning by shaping network activity. The mechanisms of PV+ neuron generation and maintenance are not fully understood, yet current evidence suggests that signalling via the glial cell line-derived neurotrophic factor (GDNF) receptor GFRα1 positively modulates the migration and differentiation of PV+ interneurons in the cortex. Whether GDNF also regulates PV+ cells in the hippocampus is currently unknown. In this study, we utilized a Gdnf "hypermorph" mouse model where GDNF is overexpressed from the native gene locus, providing greatly increased spatial and temporal specificity of protein expression over established models of ectopic expression. Gdnfwt/hyper mice demonstrated impairments in long-term memory performance in the Morris water maze test and an increase in inhibitory tone in the hippocampus measured electrophysiologically in acute brain slice preparations. Increased PV+ cell number was confirmed immunohistochemically in the hippocampus and in discrete cortical areas and an increase in epileptic seizure threshold was observed in vivo. The data consolidate prior evidence for the actions of GDNF as a regulator of PV+ cell development in the cortex and demonstrate functional effects upon network excitability via modulation of functional GABAergic signalling and under epileptic challenge.

Protective Role of Low Ethanol Administration Following Ischemic Stroke via Recovery of KCC2 and p75NTR Expression.

A striking result from epidemiological studies show a correlation between low alcohol intake and lower incidence for ischemic stroke and severity of derived brain injury. Although reduced apoptosis and inflammation has been suggested to be involved, little is known about the mechanism mediating this effect in vivo. Increase in intracellular chloride concentration and derived depolarizing GABAAR-mediated transmission are common consequences following various brain injuries and are caused by the abnormal expression levels of the chloride cotransporters NKCC1 and KCC2. Downstream pro-apoptotic signaling through p75NTR may link GABAA depolarization with post-injury neuronal apoptosis. Here, we show that changes in GABAergic signaling, Cl- homeostasis, and expression of chloride cotransporters in the post-traumatic mouse brain can be significantly reduced by administration of 3% ethanol to the drinking water. Ethanol-induced upregulation of KCC2 has a positive impact on neuronal survival, preserving a large part of the cortical peri-infarct zone, as well as preventing the massive post-ischemic upregulation of the pro-apoptotic protein p75NTR. Importantly, intracortical multisite in vivo recordings showed that ethanol treatment could significantly ameliorate stroke-induced reduction in cortical activity. This surprising finding discloses a pathway triggered by low concentration of ethanol as a novel therapeutically relevant target.

The Kainate Receptor Subunit GluK2 Interacts With KCC2 to Promote Maturation of Dendritic Spines.

Kainate receptors (KAR) play a crucial role in the plasticity and functional maturation of glutamatergic synapses. However, how they regulate structural plasticity of dendritic spines is not known. The GluK2 subunit was recently shown to coexist in a functional complex with the neuronal K-Cl cotransporter KCC2. Apart from having a crucial role in the maturation of GABAergic transmission, KCC2 has a morphogenic role in the maturation of dendritic spines. Here, we show that in vivo local inactivation of GluK2 expression in CA3 hippocampal neurons induces altered morphology of dendritic spines and reduction in mEPSC frequency. GluK2 deficiency also resulted in a strong change in the subcellular distribution of KCC2 as well as a smaller somatodendritic gradient in the reversal potential of GABAA. Strikingly, the aberrant morphology of dendritic spines in GluK2-deficient CA3 pyramidal neurons was restored by overexpression of KCC2. GluK2 silencing in hippocampal neurons significantly reduced the expression of 4.1N and functional form of the actin filament severing protein cofilin. Consistently, assessment of actin dynamics using fluorescence recovery after photobleaching (FRAP) of ß-actin showed a significant increase in the stability of F-actin filaments in dendritic spines. In conclusion, our results demonstrate that GluK2-KCC2 interaction plays an important role in the structural maturation of dendritic spines. This also provides novel insights into the connection between KAR dysfunction, structural plasticity, and developmental disorders.

Novel carbon film induces precocious calcium oscillation to promote neuronal cell maturation.

Different types of carbon materials are biocompatible with neural cells and can promote maturation. The mechanism of this effect is not clear. Here we have tested the capacity of a carbon material composed of amorphous sp3 carbon backbone, embedded with a percolating network of sp2 carbon domains to sustain neuronal cultures. We found that cortical neurons survive and develop faster on this novel carbon material. After 3 days in culture, there is a precocious increase in the frequency of neuronal activity and in the expression of maturation marker KCC2 on carbon films as compared to a commonly used glass surface. Accelerated development is accompanied by a dramatic increase in neuronal dendrite arborization. The mechanism for the precocious maturation involves the activation of intracellular calcium oscillations by the carbon material already after 1 day in culture. Carbon-induced oscillations are independent of network activity and reflect intrinsic spontaneous activation of developing neurons. Thus, these results reveal a novel mechanism for carbon material-induced neuronal survival and maturation.

Dominant mutations in ITPR3 cause Charcot-Marie-Tooth disease.

OBJECTIVE: ITPR3, encoding inositol 1,4,5-trisphosphate receptor type 3, was previously reported as a potential candidate disease gene for Charcot-Marie-Tooth neuropathy. Here, we present genetic and functional evidence that ITPR3 is a Charcot-Marie-Tooth disease gene. METHODS: Whole-exome sequencing of four affected individuals in an autosomal dominant family and one individual who was the only affected individual in his family was used to identify disease-causing variants. Skin fibroblasts from two individuals of the autosomal dominant family were analyzed functionally by western blotting, quantitative reverse transcription PCR, and Ca2+ imaging. RESULTS: Affected individuals in the autosomal dominant family had onset of symmetrical neuropathy with demyelinating and secondary axonal features at around age 30, showing signs of gradual progression with severe distal leg weakness and hand involvement in the proband at age 64. Exome sequencing identified a heterozygous ITPR3 p.Val615Met variant segregating with the disease. The individual who was the only affected in his family had disease onset at age 4 with demyelinating neuropathy. His condition was progressive, leading to severe muscle atrophy below knees and atrophy of proximal leg and hand muscles by age 16. Trio exome sequencing identified a de novo ITPR3 variant p.Arg2524Cys. Altered Ca2+ -transients in p.Val615Met patient fibroblasts suggested that the variant has a dominant-negative effect on inositol 1,4,5-trisphosphate receptor type 3 function. INTERPRETATION: Together with two previously identified variants, our report adds further evidence that ITPR3 is a disease-causing gene for CMT and indicates altered Ca2+ homeostasis in disease pathogenesis.

You're not alone: A public health response to immigrant/refugee distress in the current sociopolitical context.

Recent political events and policy changes in the United States have fueled antirefugee/immigrant rhetoric and an increase of xenophobic harassment and intimidation, which together present a significant threat to the physical and mental health of refugee/immigrant children and families. This article aims to provide an overview of how the current sociopolitical context threatens the public health of refugee and immigrant communities and to describe the role of psychologists in advocating for social justice and responding to this urgent public health need through interprofessional collaboration and translation of scientific knowledge into multilevel intervention development. The case study of the You're Not Alone (YNA) initiative describes swiftly mobilized advocacy efforts (e.g., press conference, webinars, resources development and dissemination) and participatory development and roll-out of community capacity-building trainings to address the needs of refugee/immigrant children and families. Trainings aimed to raise awareness of the refugee/immigrant experience and to equip refugee/immigrant community members and providers across a variety of public sectors to implement culturally responsive and trauma-informed strategies to promote resilience, respond to distress, and prevent mental health crises. Between March 2017 and June 2018, a total of 1,642 individuals attended 48 training events. The role of psychologists in future policy and advocacy efforts to promote mental health among refugee/immigrant families is discussed as well as implications for how other marginalized communities affected by the current sociopolitical climate might benefit from broadening the scope of this public health response. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

Bumetanide Prevents Brain Trauma-Induced Depressive-Like Behavior.

Brain trauma triggers a cascade of deleterious events leading to enhanced incidence of drug resistant epilepsies, depression, and cognitive dysfunctions. The underlying mechanisms leading to these alterations are poorly understood and treatment that attenuates those sequels are not available. Using controlled-cortical impact as an experimental model of brain trauma in adult mice, we found a strong suppressive effect of the sodium-potassium-chloride importer (NKCC1) specific antagonist bumetanide on the appearance of depressive-like behavior. We demonstrate that this alteration in behavior is associated with an impairment of post-traumatic secondary neurogenesis within the dentate gyrus of the hippocampus. The mechanism mediating the effect of bumetanide involves early transient changes in the expression of chloride regulatory proteins and qualitative changes in GABA(A) mediated transmission from hyperpolarizing to depolarizing after brain trauma. This work opens new perspectives in the early treatment of human post-traumatic induced depression. Our results strongly suggest that bumetanide might constitute an efficient prophylactic treatment to reduce neurological and psychiatric consequences of brain trauma.