Visual EMDR stimulation mitigates acute varied stress effects on morphology of hippocampal neurons in male Wistar rats.

Introduction: Stress is a pervasive health concern known to induce physiological changes, particularly impacting the vulnerable hippocampus and the morphological integrity of its main residing cells, the hippocampal neurons. Eye Movement Desensitization and Reprocessing (EMDR), initially developed to alleviate emotional distress, has emerged as a potential therapeutic/preventive intervention for other stress-related disorders. This study aimed to investigate the impact of Acute Variable Stress (AVS) on hippocampal neurons and the potential protective effects of EMDR. Methods: Rats were exposed to diverse stressors for 7 days, followed by dendritic morphology assessment of hippocampal neurons using Golgi-Cox staining. Results: AVS resulted in significant dendritic atrophy, evidenced by reduced dendritic branches and length. In contrast, rats receiving EMDR treatment alongside stress exposure exhibited preserved dendritic morphology comparable to controls, suggesting EMDR's protective role against stressinduced dendritic remodeling. Conclusions: These findings highlight the potential of EMDR as a neuroprotective intervention in mitigating stress-related hippocampal alterations.

Portal Vein Doppler tracks volume status in patients with severe tricuspid regurgitation: A Proof-of-Concept Study.

BACKGROUND: Renal and liver congestion are associated with adverse outcomes in patients with tricuspid regurgitation (TR). Currently, there are no valid sonographic indicators of fluid status in this population. Intra-renal venous Doppler (IRVD) is a novel method for quantifying renal congestion but its interpretation can be challenging in severe TR due to altered hemodynamics. This study explores the potential of portal vein Doppler (PVD) as an alternative marker for decongestion during volume removal in patients with severe TR. METHODS: 42 patients with severe TR undergoing decongestive therapy were prospectively enrolled. Inferior vena cava diameter (IVCd), PVD and IRVD were sequentially assessed during volume removal. Improvement criteria were Portal Vein Pulsatility Fraction (PVPF) < 70% and Renal Venous Stasis Index (RVSI) < 0.5 for partial improvement, and PVPF <30% and RVSI <0.2 for complete improvement. RESULTS: After volume removal, PVPF significantly improved from 130 ± 39% to 47 ± 44% (p < 0.001), while IRVD improved from 0.72 ± 0.08 to 0.54 ± 0.22 (p < 0.001). A higher proportion of patients displayed improvement in PVD compared to IRVD (partial: 38% vs. 29%, complete: 41% vs. 7%) (p < 0.001). IRVD only improved in patients with concomitant improvement in severe TR. PVD was the only predictor of achieving ≥5 litres of negative fluid balance (AUC 0.83 p = 0.001). CONCLUSIONS: This proof-of-concept study suggests that PVD is the only sonographic marker that can track volume removal in severe TR, offering a potential indicator for decongestion in this population. Further intervention trials are warranted to determine if PVD-guided decongestion improves patient outcomes in severe TR.

K252a Prevents Microglial Activation Induced by Anoxic Stimulation of Carotid Bodies in Rats.

Inducing carotid body anoxia through the administration of cyanide can result in oxygen deprivation. The lack of oxygen activates cellular responses in specific regions of the central nervous system, including the Nucleus Tractus Solitarius, hypothalamus, hippocampus, and amygdala, which are regulated by afferent pathways from chemosensitive receptors. These receptors are modulated by the brain-derived neurotrophic factor receptor TrkB. Oxygen deprivation can cause neuroinflammation in the brain regions that are activated by the afferent pathways from the chemosensitive carotid body. To investigate how microglia, a type of immune cell in the brain, respond to an anoxic environment resulting from the administration of NaCN, we studied the effects of blocking the TrkB receptor on this cell-type response. Male Wistar rats were anesthetized, and a dose of NaCN was injected into their carotid sinus to induce anoxia. Prior to the anoxic stimulus, the rats were given an intracerebroventricular (icv) infusion of either K252a, a TrkB receptor inhibitor, BDNF, or an artificial cerebrospinal fluid (aCSF). After the anoxic stimulus, the rats were perfused with paraformaldehyde, and their brains were processed for microglia immunohistochemistry. The results indicated that the anoxic stimulation caused an increase in the number of reactive microglial cells in the hypothalamic arcuate, basolateral amygdala, and dentate gyrus of the hippocampus. However, the infusion of the K252a TrkB receptor inhibitor prevented microglial activation in these regions.

Risk Factors Associated with the Development of Hospital-Acquired Infections in Hospitalized Patients with Severe COVID-19.

Recognition of risk factors for hospital-acquired infections (HAI) in patients with COVID-19 is warranted. We aimed to describe factors associated with the development of HAI in patients with severe COVID-19. We conducted a retrospective cohort study including all adult patients admitted with severe COVID-19 between March 2020 and November 2020. The primary outcome was HAI development. Bivariate and multiple logistic regression models were constructed. Among 1540 patients, HAI occurred in 221 (14%). A total of 299 episodes of HAI were registered. The most common HAI were hospital-acquired/ventilation-associated pneumonia (173 episodes) and primary bloodstream infection (66 episodes). Death occurred in 387 (35%) patients and was more frequent in patients with HAI (38% vs. 23%, p < 0.01). Early mechanical ventilation (aOR 18.78, 95% CI 12.56-28.07), chronic kidney disease (aOR 3.41, 95% CI 1.4-8.27), use of corticosteroids (aOR 2.95, 95% CI 1.92-4.53) and tocilizumab (aOR 2.68, 95% CI 1.38-5.22), age ≥ 60 years (aOR 1.91, 95% CI 1.27-2.88), male sex (aOR 1.52, 95% CI 1.03-2.24), and obesity (aOR 1.49, 95% CI 1.03-2.15) were associated with HAI. In patients with severe COVID-19, mechanical ventilation within the first 24 h upon admission, chronic kidney disease, use of corticosteroids, use of tocilizumab, age ≥ 60 years, male sex, and obesity were associated with a higher risk of HAI.

Acoustic Stress Induces Opposite Proliferative/Transformative Effects in Hippocampal Glia.

The hippocampus is a brain region crucially involved in regulating stress responses and highly sensitive to environmental changes, with elevated proliferative and adaptive activity of neurons and glial cells. Despite the prevalence of environmental noise as a stressor, its effects on hippocampal cytoarchitecture remain largely unknown. In this study, we aimed to investigate the impact of acoustic stress on hippocampal proliferation and glial cytoarchitecture in adult male rats, using environmental noise as a stress model. After 21 days of noise exposure, our results showed abnormal cellular proliferation in the hippocampus, with an inverse effect on the proliferation ratios of astrocytes and microglia. Both cell lineages also displayed atrophic morphologies with fewer processes and lower densities in the noise-stressed animals. Our findings suggest that, stress not only affects neurogenesis and neuronal death in the hippocampus, but also the proliferation ratio, cell density, and morphology of glial cells, potentially triggering an inflammatory-like response that compromises their homeostatic and repair functions.

Immediate Early Gene c-fos in the Brain: Focus on Glial Cells.

The c-fos gene was first described as a proto-oncogene responsible for the induction of bone tumors. A few decades ago, activation of the protein product c-fos was reported in the brain after seizures and other noxious stimuli. Since then, multiple studies have used c-fos as a brain activity marker. Although it has been attributed to neurons, growing evidence demonstrates that c-fos expression in the brain may also include glial cells. In this review, we collect data showing that glial cells also express this proto-oncogene. We present evidence demonstrating that at least astrocytes, oligodendrocytes, and microglia express this immediate early gene (IEG). Unlike neurons, whose expression changes used to be associated with depolarization, glial cells seem to express the c-fos proto-oncogene under the influence of proliferation, differentiation, growth, inflammation, repair, damage, plasticity, and other conditions. The collected evidence provides a complementary view of c-fos as an activity marker and urges the introduction of the glial cell perspective into brain activity studies. This glial cell view may provide additional information related to the brain microenvironment that is difficult to obtain from the isolated neuron paradigm. Thus, it is highly recommended that detection techniques are improved in order to better differentiate the phenotypes expressing c-fos in the brain and to elucidate the specific roles of c-fos expression in glial cells.

Orthopaedic Trauma Research Priorities in Latin America: Developing Consensus Through a Modified Delphi Approach.

BACKGROUND: Despite a substantial burden of musculoskeletal injury, orthopaedic trauma studies in Latin America are lacking. The purpose of the present study was to identify research priorities among orthopaedic trauma surgeons in Latin America. METHODS: Research questions were solicited from members of the Asociación de Cirujanos Traumatólogos de las Américas. Participants rated questions by importance from 1 to 9. All questions were redistributed with an aggregate rating, and participants rerated questions with knowledge of group responses. RESULTS: Seventy-eight participants completed the first survey and were included in subsequent surveys. The mean age was 51.8 years, and most participants were male (92%), had completed an orthopaedic trauma fellowship (60.3%), and participated in research (80.8%). Seventeen countries were represented; 5 respondents were from a high-income country, 67 were from an upper middle-income country, and 6 were from a lower middle-income country. Sixty-five questions were identified. Six questions were rated from 1 to 3 ("more important") by >70% of participants: (1) What is the optimal treatment protocol for elderly patients with hip fracture? (2) What is the most effective initial and definitive management of musculoskeletal injury, including timing and surgical strategy, for the polytraumatized patient? (3) What is the ideal state of open fracture treatment, including timeliness and method of antibiotics, debridement, surgical fixation, and closure or coverage, at each hospital level in the health-care system? (4) What patient and fracture characteristics predict infection after musculoskeletal injury? (5) What is the current state of treatment for fracture-related infection, including timeliness and method of antibiotics and surgical intervention, at each hospital level in the health-care system? (6) What is the optimal protocol for temporary management for the hemodynamically unstable patient with a pelvic or acetabular fracture? CONCLUSIONS: This modified Delphi study of orthopaedic trauma surgeons in Latin America identified geriatric hip fractures, polytrauma, open fractures, musculoskeletal infection, and pelvic and acetabular fractures as top research priorities. This information is important for resource allocation and goal setting for orthopaedic trauma in the region.

Biopsychological correlates of repetitive and restricted behaviors in autism spectrum disorders.

BACKGROUND: Autism Spectrum Disorder (ASD) is considered a neurodevelopmental condition that is characterized by alterations in social interaction and communication, as well as patterns of restrictive and repetitive behaviors (RRBs). RRBs are defined as broad behaviors that comprise stereotypies, insistence on sameness, and attachment to objects or routines. RRBs can be divided into lower-level behaviors (motor, sensory, and object-manipulation behaviors) and higher-level behaviors (restrictive interests, insistence on sameness, and repetitive language). According to the DSM-5, the grade of severity in ASD partially depends on the frequency of RRBs and their consequences for disrupting the life of patients, affecting their adaptive skills, and increasing the need for parental support. METHODS: We conducted a systematic review to examine the biopsychological correlates of the symptomatic domains of RRBs according to the type of RRBs (lower- or higher-level). We searched for articles from the National Library of Medicine (PubMed) using the terms: autism spectrum disorders, ASD, and autism-related to executive functions, inhibitory control, inflexibility, cognitive flexibility, hyper or hypo connectivity, and behavioral approaches. For describing the pathophysiological mechanism of ASD, we also included animal models and followed PRISMA guidelines. RESULTS: One hundred and thirty-one articles were analyzed to explain the etiology, continuance, and clinical evolution of these behaviors observed in ASD patients throughout life. CONCLUSIONS: Biopsychological correlates involved in the origin of RRBs include alterations in a) neurotransmission system, b) brain volume, c) inadequate levels of growth factors, d) hypo- or hyper-neural connectivity, e) impairments in behavioral inhibition, cognitive flexibility, and monitoring and f) non-stimulating environments. Understanding these lower- and higher-level of RRBs can help professionals to improve or design novel therapeutic strategies.

General anesthesia in infants: neurobiological and neuropsychological concerns.

General anesthetics are crucial drugs for surgical interventions, which are indicated to induce analgesia, diminish pain, and reduce anxiety in order to facilitate invasive procedures. In pediatric patients, benefits of general anesthetics also include abolishment of motility. Besides their probed benefits on surgery, the recent warning of the Food and Drug Administration (FDA) on the use of general anesthetics in children yielded a controversy on their potential neurotoxic effects. In this review, the main facts of the cerebral development are studied, and the available evidence concerning the use of general anesthesia on the neuropsychological development of children is analyzed. Most of the studies found were uncontrolled retrospective cohorts for which conclusions are difficult to obtain. However, a few group of controlled studies, including the Mayo Anesthesia Safety in Kids study (MASK), have partially supported the FDA warning. Cumulated evidence appears to support the safety use of general anesthetics, but no conclusive data supporting that it may induce massive effects on the cognitive development of exposed children has been reported. Important evidence suggests that specific cognitive functions may result altered under long-term expositions. Such data must be considered for those involved in anesthetic procedures.

La anestesia general es una herramienta imprescindible para el proceso quirúrgico, ya que disminuye el dolor, reduce la ansiedad y genera inconsciencia. Sin ella, las cirugías serían dolorosas, riesgosas y emocionalmente traumáticas. La reciente emisión de una alerta sobre el uso de fármacos anestésicos en niños menores de 3 años por parte de la Food and Drug Administration (FDA) de los Estados Unidos generó controversia en torno a sus posibles efectos negativos. En este artículo se abordan los principales hitos del desarrollo neurobiológico del niño y se revisan las posibles consecuencias neuropsicológicas del uso de anestesia general en esta población. La mayoría de los reportes que abordan este tema son de tipo retrospectivo y arrojan resultados controversiales por sus inherentes dificultades metodológicas. Sin embargo, el estudio prospectivo sobre seguridad del uso de anestesia general en niños de la Clínica Mayo (MASK, Mayo Anesthesia Safety in Kids), junto con otros estudios a gran escala, han confirmado algunos datos obtenidos en los estudios experimentales que dieron sustento a la alerta emitida por la FDA. Así, las evidencias hasta ahora publicadas sugieren que el uso de anestesia general es seguro para el desarrollo cognitivo general del niño, aunque evidencian también alteraciones focalizadas en procesos cognitivos específicos que deben ser consideradas por el médico y la familia ante un procedimiento quirúrgico-anestésico.

Anestesia general en infantes: consideraciones neurobiológicas y neuropsicológicas / General anesthesia in infants: neurobiological and neuropsychological concerns

Resumen La anestesia general es una herramienta imprescindible para el proceso quirúrgico, ya que disminuye el dolor, reduce la ansiedad y genera inconsciencia. Sin ella, las cirugías serían dolorosas, riesgosas y emocionalmente traumáticas. La reciente emisión de una alerta sobre el uso de fármacos anestésicos en niños menores de 3 años por parte de la Food and Drug Administration (FDA) de los Estados Unidos generó controversia en torno a sus posibles efectos negativos. En este artículo se abordan los principales hitos del desarrollo neurobiológico del niño y se revisan las posibles consecuencias neuropsicológicas del uso de anestesia general en esta población. La mayoría de los reportes que abordan este tema son de tipo retrospectivo y arrojan resultados controversiales por sus inherentes dificultades metodológicas. Sin embargo, el estudio prospectivo sobre seguridad del uso de anestesia general en niños de la Clínica Mayo (MASK, Mayo Anesthesia Safety in Kids), junto con otros estudios a gran escala, han confirmado algunos datos obtenidos en los estudios experimentales que dieron sustento a la alerta emitida por la FDA. Así, las evidencias hasta ahora publicadas sugieren que el uso de anestesia general es seguro para el desarrollo cognitivo general del niño, aunque evidencian también alteraciones focalizadas en procesos cognitivos específicos que deben ser consideradas por el médico y la familia ante un procedimiento quirúrgico-anestésico.

Abstract General anesthetics are crucial drugs for surgical interventions, which are indicated to induce analgesia, diminish pain, and reduce anxiety in order to facilitate invasive procedures. In pediatric patients, benefits of general anesthetics also include abolishment of motility. Besides their probed benefits on surgery, the recent warning of the Food and Drug Administration (FDA) on the use of general anesthetics in children yielded a controversy on their potential neurotoxic effects. In this review, the main facts of the cerebral development are studied, and the available evidence concerning the use of general anesthesia on the neuropsychological development of children is analyzed. Most of the studies found were uncontrolled retrospective cohorts for which conclusions are difficult to obtain. However, a few group of controlled studies, including the Mayo Anesthesia Safety in Kids study (MASK), have partially supported the FDA warning. Cumulated evidence appears to support the safety use of general anesthetics, but no conclusive data supporting that it may induce massive effects on the cognitive development of exposed children has been reported. Important evidence suggests that specific cognitive functions may result altered under long-term expositions. Such data must be considered for those involved in anesthetic procedures.

Inhibitory control failures and blunted cortisol response to psychosocial stress in amphetamine consumers after 6 months of abstinence.

BACKGROUND: Amphetamine abuse has been conceived as an addictive illness where stress regulation and inhibitory control may be crucial factors determining chronicity and relapse. Since amphetamine consumption may disrupt the cerebral systems regulating inhibition and stress behaviors, deregulation on these systems may be expected even after long-term abstinence periods. The present study aimed to evaluate the ability of abstinent amphetamine consumers to regulate stress parameters and to inhibit cognitive patterns under the acute trier social stress test (TSST) paradigm. MATERIALS AND METHODS: A cohort study was conducted in a sample of 44 young individuals (average age: 24.6 years). The sample included 22 amphetamine consumers recruited from an addiction treatment center and 22 healthy nonconsumers belonging to the same sociodemographic conditions. Both groups were exposed to the TSST once the consumers completed 6 months in abstinence. To evaluate stress reactivity, we collected five saliva samples distributed before, during, and after stress exposure. Inhibitory capacity was also assessed before and after stress using the Stroop and d2 cancellation tests. RESULTS: Under stress conditions, cortisol measures were significantly lower in amphetamine consumers (1105.34 ± 756.958) than in healthy nonconsumers (1771.86 ± 1174.248) P = 0.022. Without stress, amphetamine consumers also showed lower cortisol values (1027.61 ± 709.8) than nonconsumers (1844.21 ± 1099.15) P = 0.016. Regarding inhibitory capacity, stress also was associated to consumer's lower scores on the Stroop (5.17 ± 8.34 vs. 10.58 ± 7.83) P = 0.032 and d2 tests (190.27 ± 29.47 vs. 218.00 ± 38.08) P = 0.010. CONCLUSION: We concluded that both the stress regulatory system and executive function system (attentional/inhibitory control) represent key vulnerability conditions to the long-term effect of compulsive amphetamine consumption.

Male rats exhibit higher pro-BDNF, c-Fos and dendritic tree changes after chronic acoustic stress.

Prolonged or intense exposure to environmental noise (EN) has been associated with a number of changes in auditory organs as well as other brain structures. Notably, males and females have shown different susceptibilities to acoustic damage as well as different responses to environmental stressors. Rodent models have evidence of sex-specific changes in brain structures involved in noise and sound processing. As a common effect, experimental models have demonstrated that dendrite arborizations reconfigure in response to aversive conditions in several brain regions. Here, we examined the effect of chronic noise on dendritic reorganization and c-Fos expression patterns of both sexes. During 21 days male and female rats were exposed to a rats' audiogram-fitted adaptation of a noisy environment. Golgi-Cox and c-Fos staining were performed at auditory cortices (AC) and hippocampal regions. Sholl analysis and c-Fos counts were conducted for evidence of intersex differences. In addition, pro-BDNF serum levels were also measured. We found different patterns of c-Fos expression in hippocampus and AC. While in AC expression levels showed rapid and intense increases starting at 2 h, hippocampal areas showed slower rises that reached the highest levels at 21 days. Sholl analysis also evidenced regional differences in response to noise. Dendritic trees were reduced after 21 days in hippocampus but not in AC. Meanwhile, pro-BDNF levels augmented after EN exposure. In all analyzed variables, exposed males were the most affected. These findings suggest that noise may exert differential effects on male and female brains and that males could be more vulnerable to the chronic effects of noise.

Male/female Differences in Radial Arm Water Maze Execution After Chronic Exposure to Noise.

INTRODUCTION: Noise is one of the main sources of discomfort in modern societies. It affects physiology, behavior, and cognition of exposed subjects. Although the effects of noise on cognition are well known, gender role in noise-cognition relationship remains controversial. AIM: We analyzed the effects of noise on the ability of male and female rats to execute the Radial Arm Water Maze (RAWM) paradigm. MATERIALS AND METHODS: Male and female Wistar rats were exposed to noise for 3 weeks, and the cognitive effects were assessed at the end of the exposure. RAWM execution included a three-day training phase and a reversal-learning phase conducted on the fourth day. Escape latency, reference memory errors, and working memory errors were quantified and compared between exposed and non-exposed subjects. RESULTS: We found that male rats were in general more affected by noise. Execution during the three-day learning phase evidenced that male exposed rats employed significantly more time to acquire the task than the non-exposed. On the other hand, the exposed females solved the paradigm in latencies similar to control rats. Both, males and females diminished their capacity to execute on the fourth day when re-learning abilities were tested. CONCLUSION: We conclude that male rats might be less tolerable to noise compared to female ones and that spatial learning may be a cognitive function comparably more vulnerable to noise.

Environmental noise exposure modifies astrocyte morphology in hippocampus of young male rats.

BACKGROUND: Chronic exposure to noise induces changes on the central nervous system of exposed animals. Those changes affect not only the auditory system but also other structures indirectly related to audition. The hippocampus of young animals represents a potential target for these effects because of its essential role in individuals' adaptation to environmental challenges. OBJECTIVE: The aim of the present study was to evaluate hippocampus vulnerability, assessing astrocytic morphology in an experimental model of environmental noise (EN) applied to rats in pre-pubescent stage. MATERIALS AND METHODS: Weaned Wistar male rats were subjected to EN adapted to the rats' audiogram for 15 days, 24 h daily. Once completed, plasmatic corticosterone (CORT) concentration was quantified, and immunohistochemistry for glial fibrillary acidic protein was taken in hippocampal DG, CA3, and CA1 subareas. Immunopositive cells and astrocyte arborizations were counted and compared between groups. RESULTS: The rats subjected to noise exhibited enlarged length of astrocytes arborizations in all hippocampal subareas. Those changes were accompanied by a marked rise in serum CORT levels. CONCLUSIONS: These findings confirm hippocampal vulnerability to EN and suggest that glial cells may play an important role in the adaptation of developing the participants to noise exposure.

Rapid Eye Movement Sleep Deprivation Produces Long-Term Detrimental Effects in Spatial Memory and Modifies the Cellular Composition of the Subgranular Zone.

Sleep deprivation (SD) affects spatial memory and proliferation in the dentate gyrus. It is unknown whether these deleterious effects persist in the long run. The aim of this study was to evaluate the proliferation, differentiation and maturation of neural progenitors as well as spatial memory 21 days after suffering SD. Sixty-day old male Balb/C mice were exposed to 72-h REM-SD. Spatial memory, cell fate, apoptosis and expression levels of insulin-like growth factor 1 receptor (IGF-1R) were evaluated in the hippocampus at 0, 14, and 21 days after SD or control conditions. After 21-days recovery period, memory performance was assessed with the Barnes maze, we found a significant memory impairment in SD mice vs. control (94.0 ± 10.2 s vs. 25.2 ± 4.5 s; p < 0.001). The number of BrdU+ cells was significantly decreased in the SD groups at day 14 (controls = 1.6 ± 0.1 vs. SD mice = 1.2 ± 0.1 cells/field; p = 0.001) and at day 21 (controls = 0.2 ± 0.03 vs. SD mice = 0.1 ± 0.02 cells/field; p < 0.001). A statistically significant decrease was observed in neuronal differentiation (1.4 ± 0.1 cells/field vs. 0.9 ± 0.1 cells/field, p = 0.003). Apoptosis was significantly increased at day 14 after SD (0.53 ± 0.06 TUNEL+ cells/field) compared to controls (0.19 ± 0.03 TUNEL+ cells/field p < 0.001) and at 21-days after SD (SD mice 0.53 ± 0.15 TUNEL+ cells/field; p = 0.035). At day 0, IGF-1R expression showed a statistically significant reduction in SD animals (64.6 ± 12.2 units) when compared to the control group (102.0 ± 9.8 units; p = 0.043). However, no statistically significant differences were found at days 14 and 21 after SD. In conclusion, a single exposition to SD for 72-h can induce deleterious effects that persist for at least 3 weeks. These changes are characterized by spatial memory impairment, reduction in the number of hippocampal BrdU+ cells and persistent apoptosis rate. In contrast, changes IGF-1R expression appears to be a transient event. Highlight Sleep deprivation affects spatial memory and proliferation in the dentate gyrus. To date it is unknown whether these deleterious effects are persistent over a long period of time. We analyzed the effects of sleep deprivation in the hippocampus after 21 days of recovery sleep. Our findings indicate that after sleep recovery, the detrimental effects of SD can be observed for at least 2 weeks, as shown by a reduction in memory performance, changes in the hippocampal cellular composition and higher apoptotic rate over a long period of time.

Sex-related effects of sleep deprivation on depressive- and anxiety-like behaviors in mice.

Anxiety and depressive symptoms are generated after paradoxical sleep deprivation (PSD). However, it is not clear whether PSD produces differential effects between females and males. The aim of this study was to assess the effect of PSD on anxiety- and depressive-like behaviors between sexes. Male and female BALB/c mice were divided in three groups: the control group, the 48-h PSD group and the 96-h PSD group. Immediately after PSD protocols, the forced swimming and open field test were applied. Sucrose consumption test was used to evaluate the middle-term effect of PSD. We found that corticosterone serum levels showed significant differences in the 96-h PSD females as compared to 96-h PSD males. In the open-field test, the 48-h and 96-h PSD females spent more time at the periphery of the field, and showed high locomotion as compared to males. In the elevated plus maze, the 48-h PSD females spent more time in closed arms than males, which is compatible with anxiety-like behavior. The forced swim test indicated that the 96-h PSD males spent more time swimming as compared to the 96-h PSD females. Remarkably, the 96-h PSD males had lower sucrose intake than the 96-h PSD females, which suggest that male mice have proclivity to develop a persistent depressive-like behavior late after PSD. In conclusion, male mice showed a significant trend to depressive-like behaviors late after sleep deprivation. Conversely, female have a strong tendency to display anxiety- and depressive-like behaviors immediately after sleep deprivation.

Extra-neurohypophyseal axonal projections from individual vasopressin-containing magnocellular neurons in rat hypothalamus.

Conventional neuroanatomical, immunohistochemical techniques, and electrophysiological recording, as well as in vitro labeling methods may fail to detect long range extra-neurohypophyseal-projecting axons from vasopressin (AVP)-containing magnocellular neurons (magnocells) in the hypothalamic paraventricular nucleus (PVN). Here, we used in vivo extracellular recording, juxtacellular labeling, post-hoc anatomo-immunohistochemical analysis and camera lucida reconstruction to address this question. We demonstrate that all well-labeled AVP immunopositive neurons inside the PVN possess main axons joining the tract of Greving and multi-axon-like processes, as well as axonal collaterals branching very near to the somata, which project to extra-neurohypophyseal regions. The detected regions in this study include the medial and lateral preoptical area, suprachiasmatic nucleus (SCN), lateral habenula (LHb), medial and central amygdala and the conducting systems, such as stria medullaris, the fornix and the internal capsule. Expression of vesicular glutamate transporter 2 was observed in axon-collaterals. These results, in congruency with several previous reports in the literature, provided unequivocal evidence that AVP magnocells have an uncommon feature of possessing multiple axon-like processes emanating from somata or proximal dendrites. Furthermore, the long-range non-neurohypophyseal projections are more common than an "occasional" phenomenon as previously thought.