ABSTRACT

SUMMARY: Systemic inflammatory response syndrome (SIRS) is a potentially fatal reaction to various forms of tissue damage and infections that cause damage to various organs. Furthermore, the brain is damaged earlier than other organs, resulting in diffuse brain dysfunction. The central clinical symptom of SIRS is delirium and emotional changes are involved in disease development. Although the amygdala is known to play a major role, the mechanisms underlying emotional changes in the early stages of SIRS have not been elucidated. Therefore, changes to dopamine levels in the amygdala were observed using an in vivo model of lipopolysaccharide (LPS)- induced SIRS to clarify the biochemical mechanisms activated in the early stages of SIRS. Extracellular dopamine was collected from the amygdala of free moving rats via microdialysis and then analyzed by high-performance liquid chromatography. In addition, emotional changes were assessed with the open field and sucrose preference tests. In the LPS group, dopamine release in the amygdala increased remarkably immediately after LPS administration, peaking at 120 min. Thereafter, dopamine release temporarily decreased, but then significantly increased again after 180 min. The present results suggest that diffuse brain dysfunction in the early stages of SIRS may involve altered dopamine levels in the amygdala.

El síndrome de respuesta inflamatoria sistémica (SRIS) es una reacción potencialmente fatal a diversas formas de daño tisular e infecciones que causan injuria a varios órganos. Además, el cerebro se daña antes que otros órganos, lo que provoca una disfunción cerebral difusa. El síntoma clínico central del SIRS es el delirio y los cambios emocionales están involucrados en el desarrollo de la enfermedad. Aunque se sabe que la amígdala desempeña un papel importante, no se han dilucidado los mecanismos que subyacen a los cambios emocionales en las primeras etapas del SRIS. Por lo tanto, en el estudio se provocaron cambios en los niveles de dopamina en la amígdala utilizando un modelo in vivo de SRIS inducido por lipopolisacáridos (LPS) para dilucidar los mecanismos bioquímicos activados en las primeras etapas del SRIS. La dopamina extracelular se recogió de la amígdala de ratas en movimiento libre mediante microdiálisis y luego se analizó mediante cromatografía líquida de alta resolución. Además, se evaluaron los cambios emocionales con las pruebas de campo abierto y de preferencia de sacarosa. En el grupo de LPS, la liberación de dopamina en la amígdala aumentó de manera notable inmediatamente después de la administración de LPS, alcanzando un máximo a los 120 minutos. A partir de entonces, la liberación de dopamina disminuyó temporalmente, pero luego volvió a aumentar significativamente después de 180 min. Los resultadosactuales sugieren que la disfunción cerebral difusa en las primeras etapas del SIRS puede implicar niveles alterados de dopamina en la amígdala.

ABSTRACT

Addictive behaviors related to Internet are becoming more common and this tool has been essential once it enables home office, entertainment, homeschooling, and easy access to information. Despite the easiness brought by technology, the exaggerated use has affected users in different ways, including in the development of psychiatric disorders. This study aimed to assess internet addiction, depression, anxiety, attention-deficit/hyperactivity disorder (ADHD), attention, impulsivity, and stress in 48 adolescents (26 young women and 22 young men), aged from 15 to 18 years, with a mean age of 16.74 (0.61), mostly students of public schools, during COVID-19, to investigate correlations between these variables according to sex and sociodemographic aspects. To assess the factors, the Internet Addiction Test (IAT); the Swanson, Nolan, and Pelham Rating Scale (SNAP-IV) Questionnaire ; the Depression, Anxiety, and Stress scale for brazilian adolescents (EDAE-A); the Barratt Impulsiveness Scale (BIS-11); and a sociodemographic questionnaire were applied. The data collection was performed in schools located in southern Brazil. The results indicated that 12 out of 48 adolescents were considered addicted to the Internet. Moreover, Internet addiction was a predictor of depression in regression analysis (p<0.001). In addition, participants classified as more addicted to the Internet scored lower averages in general attention (p<0.035) and higher averages in behavioral symptoms of inattention and ADHD (p<0.050), stress (p<0.003), anxiety (p<0.016), and depression (p<0.015), with effect sizes ranging from moderate to high. Therefore, the intense internet use by adolescents might cause psychological consequences such as depression in adolescents. Family support and professional intervention might help in the reduction of symptoms and consequences of internet addiction as well as in its prevention.(AU)

A dependência de internet é cada vez mais comum, pois essa ferramenta tem se tornado imprescindível, uma vez que possibilita home office, entretenimento, educação domiciliar e fácil acesso às informações. No entanto, o uso exagerado da tecnologia afeta os usuários de diversas formas, inclusive no desenvolvimento de transtornos psiquiátricos. Este estudo visou avaliar a dependência de internet, depressão, ansiedade, hiperatividade, atenção, impulsividade e estresse em 48 adolescentes (26 meninas e 22 meninos) de 15 a 18 anos, com idade média de 16,74 (0,61), estudantes de escolas públicas do Sul do Brasil durante a covid-19, para investigar correlações entre as variáveis anteriores de acordo com gênero e aspectos sociodemográficos. Para avaliar, aplicou-se o Internet Addiction Test (IAT), um teste de atenção, escala SNAP IV, escala de depressão, ansiedade e estresse para adolescentes (EDAE-A), escala de impulsividade de Barratt e um questionário sociodemográfico. Os resultados indicaram que 12 adolescentes foram considerados viciados em internet, e que a dependência desta foi preditora da depressão na análise de regressão (p < 0,001). Ainda, os participantes classificados como adictos tiveram médias mais baixas em atenção geral (p < 0,035) e mais altas em sintomas comportamentais de desatenção e hiperatividade (p < 0,050), estresse (p < 0,003), ansiedade (p < 0,016) e depressão (p < 0,015), com efeitos que variaram de moderado a alto. Portanto, o uso intenso da internet por adolescentes pode ter consequências psicológicas, como a depressão. Bom apoio familiar e intervenção profissional podem ajudar na redução dos sintomas e consequências, bem como na prevenção da dependência.(AU)

La adicción a Internet es cada vez más habitual, puesto que esta herramienta es esencial para el trabajo remoto, el entretenimiento, la educación domiciliar y el fácil acceso a la información. Sin embargo, su uso exagerado afecta a la vida de las personas de diferentes maneras, incluso en el desarrollo de trastornos psiquiátricos. El objetivo de este estudio fue evaluar la adicción a Internet, depresión, ansiedad, hiperactividad, atención, impulsividad y estrés en 48 adolescentes (26 muchachas y 22 muchachos), de entre 15 y 18 años, con una edad promedio de 16,74 (0,61), en su mayoría estudiantes de escuelas públicas del Sur de Brasil, durante la pandemia de la COVID-19, para investigar las correlaciones entre las variables mencionadas según género y aspectos sociodemográficos. Para evaluar los factores, se aplicaron el Test de Adicción a Internet (TAI), un test de atención, la escala SNAP IV, la Escala de Depresión, Ansiedad y Estrés para adolescentes (EDAE-A), la escala de impulsividad de Barratt y un cuestionario sociodemográfico. Los resultados indicaron que 12 adolescentes fueron considerados adictos a Internet, además, la adicción a Internet fue un predictor de la depresión en el análisis de regresión (p<0,001). Igualmente, los participantes clasificados como más adictos a Internet tuvieron promedios más bajos en atención general (p<0,035), y más altos en síntomas conductuales de falta de atención e hiperactividad (p<0,050), estrés (p<0,003), ansiedad (p<0,016) y depresión (p<0,015), con efectos que varían de moderado a alto. Por lo tanto, el uso intenso podría producir consecuencias psicológicas como la depresión en los adolescentes. Tener un buen apoyo familiar e intervención profesional puede ayudar a reducir los síntomas y las consecuencias de la adicción a Internet, así como prevenirla.(AU)

ABSTRACT

BACKGROUND@#Amygdala plays an important role in the neurobiological basis of panic disorder (PD), and the amygdala contains different subregions, which may play different roles in PD. The aim of the present study was to examine whether there are common or distinct patterns of functional connectivity of the amygdala subregions in PD using resting-state functional magnetic resonance imaging and to explore the relationship between the abnormal spontaneous functional connectivity patterns of the regions of interest (ROIs) and the clinical symptoms of PD patients.@*METHODS@#Fifty-three drug-naïve, non-comorbid PD patients and 70 healthy controls (HCs) were recruited. Seed-based resting-state functional connectivity (rsFC) analyses were conducted using the bilateral amygdalae and its subregions as the ROI seed. Two samples t test was performed for the seed-based Fisher's z -transformed correlation maps. The relationship between the abnormal spontaneous functional connectivity patterns of the ROIs and the clinical symptoms of PD patients was investigated by Pearson correlation analysis.@*RESULTS@#PD patients showed increased rsFC of the bilateral amygdalae and almost all the amygdala subregions with the precuneus/posterior cingulate gyrus compared with the HC group (left amygdala [lAMY]: t  = 4.84, P  <0.001; right amygdala [rAMY]: t  = 4.55, P  <0.001; left centromedial amygdala [lCMA]: t  = 3.87, P  <0.001; right centromedial amygdala [rCMA]: t  = 3.82, P  = 0.002; left laterobasal amygdala [lBLA]: t  = 4.33, P  <0.001; right laterobasal amygdala [rBLA]: t  = 4.97, P  <0.001; left superficial amygdala [lSFA]: t  = 3.26, P  = 0.006). The rsFC of the lBLA with the left angular gyrus/inferior parietal lobule remarkably increased in the PD group ( t  = 3.70, P  = 0.003). And most of the altered rsFCs were located in the default mode network (DMN). A significant positive correlation was observed between the severity of anxiety and the rsFC between the lSFA and the left precuneus in PD patients ( r  = 0.285, P  = 0.039).@*CONCLUSIONS@#Our research suggested that the increased rsFC of amygdala subregions with DMN plays an important role in the pathogenesis of PD. Future studies may further explore whether the rsFC of amygdala subregions, especially with the regions in DMN, can be used as a biological marker of PD.

ABSTRACT

Post-traumatic stress disorder (PTSD) has been reported to be associated with a higher risk of cardiovascular disease. The amygdala may have an important role in regulating cardiovascular function. This study aims to explore the effect of amygdala glutamate receptors (GluRs) on cardiovascular activity in a rat model of PTSD. A compound stress method combining electrical stimulation and single prolonged stress was used to prepare the PTSD model, and the difference of weight gain before and after modeling and the elevated plus maze were used to assess the PTSD model. In addition, the distribution of retrogradely labeled neurons was observed using the FluoroGold (FG) retrograde tracking technique. Western blot was used to analyze the changes of amygdala GluRs content. To further investigate the effects, artificial cerebrospinal fluid (ACSF), non-selective GluR blocker kynurenic acid (KYN) and AMPA receptor blocker CNQX were microinjected into the central nucleus of the amygdala (CeA) in the PTSD rats, respectively. The changes in various indices following the injection were observed using in vivo multi-channel synchronous recording technology. The results indicated that, compared with the control group, the PTSD group exhibited significantly lower weight gain (P < 0.01) and significantly decreased ratio of open arm time (OT%) (P < 0.05). Retrograde labeling of neurons was observed in the CeA after microinjection of 0.5 µL FG in the rostral ventrolateral medulla (RVLM). The content of AMPA receptor in the PTSD group was lower than that in the control group (P < 0.05), while there was no significant differences in RVLM neuron firing frequency and heart rate (P > 0.05) following ACSF injection. However, increases in RVLM neuron firing frequency and heart rate were observed after the injection of KYN or CNQX into the CeA (P < 0.05) in the PTSD group. These findings suggest that AMPA receptors in the amygdala are engaged in the regulation of cardiovascular activity in PTSD rats, possibly by acting on inhibitory pathways.

ABSTRACT

Integrating multisensory inputs to generate accurate perception and guide behavior is among the most critical functions of the brain. Subcortical regions such as the amygdala are involved in sensory processing including vision and audition, yet their roles in multisensory integration remain unclear. In this study, we systematically investigated the function of neurons in the amygdala and adjacent regions in integrating audiovisual sensory inputs using a semi-chronic multi-electrode array and multiple combinations of audiovisual stimuli. From a sample of 332 neurons, we showed the diverse response patterns to audiovisual stimuli and the neural characteristics of bimodal over unimodal modulation, which could be classified into four types with differentiated regional origins. Using the hierarchical clustering method, neurons were further clustered into five groups and associated with different integrating functions and sub-regions. Finally, regions distinguishing congruent and incongruent bimodal sensory inputs were identified. Overall, visual processing dominates audiovisual integration in the amygdala and adjacent regions. Our findings shed new light on the neural mechanisms of multisensory integration in the primate brain.

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The amygdala is an important hub for regulating emotions and is involved in the pathophysiology of many mental diseases, such as depression and anxiety. Meanwhile, the endocannabinoid system plays a crucial role in regulating emotions and mainly functions through the cannabinoid type-1 receptor (CB1R), which is strongly expressed in the amygdala of non-human primates (NHPs). However, it remains largely unknown how the CB1Rs in the amygdala of NHPs regulate mental diseases. Here, we investigated the role of CB1R by knocking down the cannabinoid receptor 1 (CNR1) gene encoding CB1R in the amygdala of adult marmosets through regional delivery of AAV-SaCas9-gRNA. We found that CB1R knockdown in the amygdala induced anxiety-like behaviors, including disrupted night sleep, agitated psychomotor activity in new environments, and reduced social desire. Moreover, marmosets with CB1R-knockdown had up-regulated plasma cortisol levels. These results indicate that the knockdown of CB1Rs in the amygdala induces anxiety-like behaviors in marmosets, and this may be the mechanism underlying the regulation of anxiety by CB1Rs in the amygdala of NHPs.

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O conceito de psicopatia é habitualmente associado a uma psicopatologia caracterizada pela falta de empatia, manipulação, agressividade, impulsividade, egocentrismo, crueldade e criminalidade. Já amplamente aceito pela comunidade científica, o conceito costuma ser utilizado em contextos jurídico-penais na validação de seu funcionamento punitivo. Dentre as concepções que alicerçaram o surgimento histórico desse conceito, destaca-se o papel do criminoso nato de Lombroso. Nesse sentido, este estudo buscou evidenciar como o conceito contemporâneo de psicopatia se firma enquanto modernização das concepções lombrosianas acerca do criminoso nato. Para isso, nos apoiamos na psicopatolologia para realizar um estudo comparativo entre as produções de Lombroso e as pesquisas contemporâneas acerca da psicopatia. Dentre as principais similaridades, destacamos a ênfase atribuída à suposta natureza criminal, etiologicamente decorrente de sua configuração orgânica. No mais, tais concepções também se assemelham no destaque de um déficit afetivo e moral, assim como na descrição da tendência a ser canhoto, egoísta, mentiroso, resistente à dor, narcisista, impulsivo, promíscuo, cruel, maléfico e inapto ao trabalho. Assim como fez Lombroso, as pesquisas acerca da psicopatia costumam ser realizadas com sujeitos já previamente criminalizados; condicionando uma seletividade étnico-racial e de classe. Descritos como sujeitos perigosos, incuráveis e intratáveis, ambas as concepções promovem a defesa do acirramento da punição jurídico-penal. Concluímos que a criminalidade nata de Lombroso continua a ser expressa no conceito de psicopatia, visto que as funções jurídico-penais e socioeconômicas de sua definição exercem o mesmo papel na legitimação científica da violência de Estado, encarceramento em massa e racismo estrutural.(AU)

Psychopathy is usually associated with a psychopathology characterized by a lack of empathy, manipulation, aggressiveness, impulsivity, egocentrism, cruelty, and criminality. Widely accepted by the scientific community, this concept is often used in legal and criminal contexts to validate its punitive functioning. Among the conceptions that underpinned the historical emergence of psychopathy, Lombroso's born criminal stands out. Hence, this study analyzes how the contemporary concept of psychopathy updates Lombrosian conceptions about the born criminal. To do so, we rely on psychopathology to conduct a comparative study between Lombroso's work and contemporary research on psychopathy. Among the main similarities, we highlight the emphasis given to the supposed criminal nature, etiologically arising from its organic configuration. Moreover, such conceptions emphasize an affective and moral deficit, and describe a tendency toward left-handedness, selfishness, lying, pain-resistance, narcissism, impulsivity, promiscuousness, cruelty, maliciousness and unfitness for work. As did Lombroso, research on psychopathy is usually conducted with individuals who have already been criminalized, conditioning an ethnic-racial and class selectivity. By describing these subjects as dangerous, incurable and intractable, both conceptions advocate for increased legal and penal punishment. In conclusion, Lombroso's natural criminality continues to underpin the concept of psychopathy, since its legal-criminal and socioeconomic functions play the same role in scientifically legitimizing state violence, mass incarceration, and structural racism.(AU)

La psicopatía es un concepto generalmente asociado a una psicopatología que se caracteriza por la falta de empatía, la manipulación, agresividad, impulsividad, egocentrismo, crueldad y criminalidad. Ya ampliamente aceptado por la comunidad científica, este concepto se utiliza a menudo en contextos legales para validar su funcionamiento punitivo. Entre los conceptos que fundamentaron el surgimiento histórico de este concepto, destaca el papel del criminal nato de Lombroso. En este contexto, este estudio buscó mostrar cómo el concepto contemporáneo de psicopatía se establece como la modernización de las concepciones lombrosianas sobre el criminal nato. Para eso, se utiliza la psicopatología para realizar un estudio comparativo entre las producciones de Lombroso y la investigación contemporánea sobre psicopatía. Entre las principales similitudes, destaca el énfasis atribuido a su supuesta naturaleza criminal, resultado etiológico de su configuración orgánica. Además, estas concepciones también son similares al resaltar un déficit afectivo y moral, así como al describir la tendencia a ser zurdo, egoísta, mentiroso, resistente al dolor, narcisista, impulsivo, promiscuo, cruel, malévolo e inadecuado para el trabajo. Como hizo Lombroso, los estudios sobre psicopatía se suelen realizar con sujetos que ya han sido criminalizados; condicionando una selectividad étnica, racial y de clase. Calificados como sujetos peligrosos, incurables e intratables, ambas concepciones promueven la defensa del aumento de la pena legal. Se concluye que la criminalidad nata de Lombroso continúa expresándose en el concepto de psicopatía, ya que las funciones penales y socioeconómicas de su definición juegan el mismo papel en la legitimación científica de la violencia estatal, encarcelamiento masivo y racismo estructural.(AU)

ABSTRACT

OBJECTIVES@#To explore the damage effects of chronic restraint stress (CRS) on amygdala cells through the rat CRS model.@*METHODS@#The rat CRS model was established, and the changes in body weight and adrenal mass in control group and CRS group were monitored at 1 d, 7 d, 14 d and 21 d. The behavior changes were evaluated by the percentage of retention time of open arms and open arm entries using the elevated plus maze (EPM). ELISA was used to detect the concentrations of rat's corticotropin releasing hormone (CRH), adrenocorticotropic hormone (ACTH) and cortisol. The changes of expression of glucocorticoid receptor (GR) and glial fibrillary acidic protein (GFAP) in amygdala were determined by immunohistochemistry and Western blotting. Ultrastructure changes of glial cell were observed by transmission electron microscopy. The apoptosis rate of amygdala was measured by flow cytometry.@*RESULTS@#Compared with the control group at the same time points, body weight of CRS 1 d, 7 d, 14 d and 21 d groups increased slowly, but adrenal mass increased significantly; the serum level of CRH, cortisol and ACTH increased significantly at 7 d, 14 d and 21 d respectively; the expression of GR in amygdala was increased while that of GFAP was decreased; EPM test suggested that the percentage of retention time of open arms and open arm entries decreased significantly after 14 d. The CRS group showed different degrees of glial cell damage in amygdala, and the apoptosis rate of glial cell was significantly increased in 21 d group.@*CONCLUSIONS@#This study successfully established a CRS model in rats, and anxiety-like behavioral changes in model rats may be caused by apoptosis of amygdala astrocytes.

ABSTRACT

Chronic stress leads to many psychiatric disorders, including social and anxiety disorders that are associated with over-activation of neurons in the basolateral amygdala (BLA). However, not all individuals develop psychiatric diseases, many showing considerable resilience against stress exposure. Whether BLA neuronal activity is involved in regulating an individual's vulnerability to stress remains elusive. In this study, using a mouse model of chronic social defeat stress (CSDS), we divided the mice into susceptible and resilient subgroups based on their social interaction behavior. Using in vivo fiber photometry and in vitro patch-clamp recording, we showed that CSDS persistently (after 20 days of recovery from stress) increased BLA neuronal activity in all the mice regardless of their susceptible or resilient nature, although impaired social interaction behavior was only observed in susceptible mice. Increased anxiety-like behavior, on the other hand, was evident in both groups. Notably, the CSDS-induced increase of BLA neuronal activity correlated well with the heightened anxiety-like but not the social avoidance behavior in mice. These findings provide new insight to our understanding of the role of neuronal activity in the amygdala in mediating stress-related psychiatric disorders.

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Epilepsy is a common neurological disorder characterized by hyperexcitability in the brain. Its pathogenesis is classically associated with an imbalance of excitatory and inhibitory neurons. Calretinin (CR) is one of the three major types of calcium-binding proteins present in inhibitory GABAergic neurons. The functions of CR and its role in neural excitability are still unknown. Recent data suggest that CR neurons have diverse neurotransmitters, morphologies, distributions, and functions in different brain regions across various species. Notably, CR neurons in the hippocampus, amygdala, neocortex, and thalamus are extremely susceptible to excitotoxicity in the epileptic brain, but the causal relationship is unknown. In this review, we focus on the heterogeneous functions of CR neurons in different brain regions and their relationship with neural excitability and epilepsy. Importantly, we provide perspectives on future investigations of the role of CR neurons in epilepsy.

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OBJECTIVE@#To investigate the underlying molecular mechanisms by which silence information regulator (SIRT) 2 and glutaminase (GLS) in the amygdala regulate social behaviors in autistic rats.@*METHODS@#Rat models of autism were established by maternal sodium valproic acid (VPA) exposure in wild-type rats and SIRT2-knockout ( SIRT2 -/-) rats. Glutamate (Glu) content, brain weight, and expression levels of SIRT2, GLS proteins and apoptosis-associated proteins in rat amygdala at different developmental stages were examined, and the social behaviors of VPA rats were assessed by a three-chamber test. Then, lentiviral overexpression or interference vectors of GLS were injected into the amygdala of VPA rats. Brain weight, Glu content and expression level of GLS protein were measured, and the social behaviors assessed.@*RESULTS@#Brain weight, amygdala Glu content and the levels of SIRT2, GLS protein and pro-apoptotic protein caspase-3 in the amygdala were increased in VPA rats, while the level of anti-apoptotic protein Bcl-2 was decreased (all P<0.01). Compared with the wild-type rats, SIRT2 -/- rats displayed decreased expression of SIRT2 and GLS proteins in the amygdala, reduced Glu content, and improved social dysfunction (all P<0.01). Overexpression of GLS increased brain weight and Glu content, and aggravated social dysfunction in VPA rats (all P<0.01). Knockdown of GLS decreased brain weight and Glu content, and improved social dysfunction in VPA rats (all P<0.01).@*CONCLUSIONS@#The glutamate circulatory system in the amygdala of VPA induced autistic rats is abnormal. This is associated with the upregulation of SIRT2 expression and its induced increase of GLS production; knocking out SIRT2 gene or inhibiting the expression of GLS is helpful in maintaining the balanced glutamate cycle and in improving the social behavior disorder of rats.

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Abstract Recent studies suggested that safranal exerts anticonvulsant properties. The present study aimed to investigate the effect of safranal on epileptic activities in the amygdala electrical kindling model in male rats. Animals were implanted with a recording electrode on the skull and a tripolar in the amygdala. After 10 days of recovery, the afterdischarge (AD) threshold of each animal was determined and stimulated once daily the AD threshold for full kindling development. Then, parameters including afterdischarge duration (ADD), stage 4 latency (S4L), stage 5 duration (S5D), and stimulation threshold were determined before and after injection of safranal (0.05, 0.1, 0.2 ml/ kg; i.p). While the dose of 0.05 ml/kg had no significant effect, the dose of 0.1 ml/kg increased the AD threshold as well as S4L and decreased the S5D (P<0.05). Injection of 0.2 ml/kg of the safranal significantly decreased the ADD and S5D (P<0.05) and 83.3% of animals had no stage 4 and stage 5 of kindling (P<0.001). Based on the obtained data safranal has anticonvulsant effects dosedependently. It seems that a dose of 0.2 ml/kg is the minimum effective dose. Further investigation is warranted to conduct the clinical implications for the treatment of epileptic disorders

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RESUMEN: En terminología médica el término amígdala cerebral es utilizado para denominar a la estructura que según la Terminologia Neuroanatomica y Terminologia Anatomica se conoce como cuerpo amigadaloide, la cual está constituida por diversos núcleos y es responsable de las emociones, el comportamiento, regulación de la ansiedad, la agresión, el miedo, la memoria emocional, la cognición social y las respuestas al estrés. Siendo la amígdala cerebral una estructura tan importante el objetivo de este estudio fue: analizar el significado del término amígdala cerebral en la Terminologia Neuronatomica y en la Terminologia Anatomica y contrastar si el origen de sus raíces greco latinas concuerdan con la función de esta estructura acorde con los requerimientos de la FIPAT. Para ello se consultó los diccionarios de la Lengua Española, Diccionario DGE Griego Español, Diccionario VOX Griego Español, Diccionario Médico, Biológico, Histológico y Etimológico de la Universidad de Salamanca y Diccionario de Términos Médicos de la Real Academia Nacional de Medicina, así como algunos artículos y libros clásicos de anatomía. Los resultados indicaron que el término amígdala tiene el mismo significado en griego como en latín, en donde ἀμυγδαλέα, ἀμυγδαλέας (pr. amygdaléa, amygdaléas) es el árbol del almedro y ἀμυγδάλη, ἀμυγδάλης (pr. amygdále, amygdáles) significa almendra. Conociendo tanto la anatomía como la fisiología de esta estructura su forma no se asemeja a la de una almendra y su denominación actual no está acorde con los requerimientos de la FIPAT por lo cual consideramos que esta debe ser revisada.

SUMMARY: In medical terminology the term brain amygdala is used to refer to the structure that according to the Terminologia Neuroanatomica and Terminologia Anatomica is known as the amydaloid body, which is made up of various nuclei and is responsible for emotions, behavior, regulation of the anxiety, aggression, fear, emotional memory, social cognition, and responses to stress. Being the cerebral amygdala such an important structure, the objective of this study was: to analyze the meaning of the term cerebral amygdala in Terminologia Neuroanatomica and in Terminologia Anatomica and to contrast if the origin of its Greek Latin roots agrees with the function of this structure according to the requirements of the FIPAT. For this, the dictionaries of the Royal Spanish Academy, the DGE Greek Spanish Dictionary, the VOX Greek Spanish Dictionary, the Medical, Biological, Histological and Etymological Dictionary of the University of Salamanca, the Dictionary of the Royal National Academy of Medicine, as well as some articles and classic books of anatomy. The results indicated that the term amygdala has the same meaning in Greek as in Latin, where? ἀμυγδαλέα, ἀμυγδαλέας (pr. Amygdaléa, amygdaléas) is the almond tree andἀμυγδάλη, ἀμυγδάλης (pr. amygdále, amygdáles) means almond. Knowing both the anatomy and the physiology of this structure, its shape does not resemble that of an almond and its current name is not in accordance with the requirements of the FIPAT, for which we consider that it should be revised.

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Objective: To investigate whether poor antidepressant tolerability is associated with functional brain changes in children and adolescents of parents with bipolar I disorder (at-risk youth). Methods: Seventy-three at-risk youth (ages 9-20 years old) who participated in a prospective study and had an available baseline functional magnetic resonance imaging (fMRI) scan were included. Research records were reviewed for the incidence of adverse reactions related to antidepressant exposure during follow-up. The sample was divided among at-risk youth without antidepressant exposure (n=21), at-risk youth with antidepressant exposure and no adverse reaction (n=12), at-risk youth with antidepressant-related adverse reaction (n=21), and healthy controls (n=20). The fMRI task was a continuous performance test with emotional distracters. Region-of-interest mean activation in brain areas of the fronto-limbic emotional circuit was compared among groups. Results: Right amygdala activation in response to emotional distracters significantly differed among groups (F3,66 = 3.1, p = 0.03). At-risk youth with an antidepressant-related adverse reaction had the lowest amygdala activation, while at-risk youth without antidepressant exposure had the highest activation (p = 0.004). Conclusions: Decreased right amygdala activation in response to emotional distracters is associated with experiencing an antidepressant-related adverse reaction in at-risk youth. Further studies to determine whether amygdala activation is a useful biomarker for antidepressant-related adverse events are needed.

ABSTRACT

The periaqueductal gray (PAG) is a complex mesencephalic structure involved in the integration and execution of active and passive self-protective behaviors against imminent threats, such as immobility or flight from a predator. PAG activity is also associated with the integration of responses against physical discomfort (e.g., anxiety, fear, pain, and disgust) which occurs prior an imminent attack, but also during withdrawal from drugs such as morphine and cocaine. The PAG sends and receives projections to and from other well-documented nuclei linked to the phenomenon of drug addiction including: (i) the ventral tegmental area; (ii) extended amygdala; (iii) medial prefrontal cortex; (iv) pontine nucleus; (v) bed nucleus of the stria terminalis; and (vi) hypothalamus. Preclinical models have suggested that the PAG contributes to the modulation of anxiety, fear, and nociception (all of which may produce physical discomfort) linked with chronic exposure to drugs of abuse. Withdrawal produced by the major pharmacological classes of drugs of abuse is mediated through actions that include participation of the PAG. In support of this, there is evidence of functional, pharmacological, molecular. And/or genetic alterations in the PAG during the impulsive/compulsive intake or withdrawal from a drug. Due to its small size, it is difficult to assess the anatomical participation of the PAG when using classical neuroimaging techniques, so its physiopathology in drug addiction has been underestimated and poorly documented. In this theoretical review, we discuss the involvement of the PAG in drug addiction mainly via its role as an integrator of responses to the physical discomfort associated with drug withdrawal.

ABSTRACT

Pathophysiological mechanisms involved in orofacial pain and their relationship with emotional disorders have emerged as an important research area for multidisciplinary studies. In particular, temporomandibular disorders (TMD) have been evaluated clinically from both physiological and psychological perspectives. We hypothesized that an altered neuronal activity occurs in the amygdala and the dorsal raphe nucleus (DR), encephalic regions involved in the modulation of painful and emotional information. Adult male Wistar rats were used in an experimental complete Freund's adjuvant (CFA)-induced temporomandibular joint (TMJ) inflammation model. CFA was applied for 1 or 10 days, and the animals were euthanized for brain samples dissection for FosB/ΔFosB and parvalbumin (PV) immunostaining. Our results were consistent in showing that the amygdala and DR were activated in the persistent inflammatory phase (10 days) and that the expression of PV+ interneurons in the amygdala was decreased. In contrast, in the DR, the expression of PV+ interneurons was increased in persistent states of CFA-induced TMJ inflammation. Moreover, at 10 days of inflammation, there was an increased co-localization of PV+ and FosB/ΔFosB+ neurons in the basolateral and central nucleus of the amygdala. Different nuclei of the amygdala, as well as portions of the DR, were activated in the persistent phase (10 days) of TMJ inflammation. In conclusion, altered activity of the amygdala and DR was detected during persistent inflammatory nociception in the temporomandibular joint. These regions may be essential for both sensory and affective dimensions of orofacial pain.

ABSTRACT

La isquemia cerebral es el tipo de accidente cerebrovascular más común, generando altas tasas de mortalidad y morbilidad a nivel mundial. El entendimiento de la fisiopatología de la lesión cerebral ha requerido de la implementación de modelos experimentales que permitan evaluar los fenómenos celulares, sobre todo aquellos a largo plazo. Por tal razón, el objetivo del presente trabajo fue evaluar las áreas exofocales a un mes y cuatro meses post-isquemia cerebral en un modelo experimental. Ratas Wistar fueron sometidas a una isquemia focal transitoria (t-MCAo) y un grupo fueron sacrificados al mes y otro grupo a los cuatro meses post-isquemia para su posterior análisis histológico. Los cortes fueron teñidos con Nissl y se realizó inmunohistoquímica de la proteína Tau. Nuestros resultados muestran tres áreas de lesión exofocal tanto al mes como a los cuatro meses post-isquemia: el giro dentado, la amígdala y el tálamo. Estas regiones se han asociado al control emocional, lo cual sugiere que a largo término post-isquemia se tengan en cuenta hallazgos clínicos que evalúen cambios emocionales en los pacientes que han sufrido un evento isquémico cerebral.

Cerebral ischemia is the most common type of stroke, which generates high mortality and morbidity rates worldwide. The understanding of the pathophysiology of brain injury has required the implementation of experimental models that allow the evaluation of cellular phenomena, especially those in the long-term. For this reason, the objective of the present work was to evaluate the exofocal areas at one month and four months after cerebral ischemia. Wistar rats were subjected to transient focal ischemia (t-MCAo) and one group was sacrificed one month and another group at four months' post-ischemia for subsequent histological analysis. The cuts were stained with Nissl and immunohistochemistry of the Tau protein was performed. Our results show three areas of exofocal lesion both one month and four months' post-ischemia: the thalamus, the dentate gyrus, and the amygdala. These regions have been associated with emotional control, which suggests that in the long-term post-ischemia clinical findings that evaluate emotional changes in patients who have suffered a cerebral ischemic event should be considered.

ABSTRACT

OBJECTIVE@#To investigate the effects of central nucleus of amygdala (CeA) lesion on the initiation and expression of sodium appetite in sodium-deficient rats.@*METHODS@#Three groups of SD rats (n=6 in each group) were treated with bilateral CeA lesion, sham lesion or no lesion. After the recovery, the rats were fed with low-sodium diets for 14 days to establish a sodium-deficient rat model. The double-bottle selection in single cage test was used to observe the intake of 0.3 mol/L NaCl and DW in 5 timepoint with 24 hours in sodium-deficient rats. Immunofluorescence staining of aldosterone-sensitive neurons in the nucleus tractus solitarii (NTS)was used to investigate the effect of CeA lesion or not on the activity of aldosterone-sensitive neurons in rats with or without sodium deficiency.@*RESULTS@#After fed with low-sodium diet for14 days, the volume and preference rate of 0.3 mol/L NaCl intake of the rats within 24 h were significantly increased compared with those before low-sodium diet (P＜0.01). The intake volume and the preference rate of 0.3 mol/L NaCl in CeA lesion rats were significantly decreased than those in CeA sham lesion rats and normal rats in the sodium-deficient condition (P＜0.01). The CeA lesion had no effects on the activity of aldosterone-sensitive neurons in NTS in rats with low-sodium diet.@*CONCLUSION@#Low-sodium diet induces an increase in the expression of sodium appetite in rats. CeA lesions inhibit the behavioral expression of sodium appetite in sodium-deficient rats but have no effects on the initiation of sodium appetite in rats with sodium-deficient rats.

ABSTRACT

Mindfulness is a process in which all thoughts, feelings, sensations, and all phenomena that happen to me are uncritically recognized as they are, so that they are eventually accepted and released without identifying or automatically responding to them. The clinical effects of mindfulness-based therapy have already been demonstrated in several studies. However, consistent results have not been reported for the mechanism of mindfulness-based treatment. Thus, this review aimed to describe a systematic review of the literature and research on the mechanisms of mindfulness-based interventions. Experienced meditators showed a physiological change in a ‘wakeful hypometabolic state’ during mindfulness meditation. In mindfulness meditation, it is known that certain areas other than brain activation during relaxation are additionally activated, particularly activation of fronto-limbic and fronto-parietal neural networks. The psychological mechanisms include meta-cognitive awareness, emotion regulation, reduction of automatic and self-referential thinking, concentration control, self-compassion, improvement of value clarification and self-regulation, exposure, extinction, and reconsolidation. Of the brain regions with changes in activity associated with mindfulness meditation, prefrontal cortex, the default mode network including cortical midline structures were associated with emotion regulation, concentration control, and reduction of automatic and self-referential thinking. In addition, brain regions associated with mindfulness meditation have been reported in the hippocampus, amygdala, and medical frontal cortices associated with memory reconsolidation and fear extinction. Thus, mindfulness-based interventions have a psychological and neurobiological effect with a special mechanism different from other psychological interventions, so that mindfulness based intervention can be an effective therapeutic intervention with a different mechanism from other psychological techniques.

ABSTRACT

Nociceptin/orphanin FQ (N/OFQ) and its receptor, nociceptin opioid peptide (NOP) receptor, are localized in brain areas implicated in depression including the amygdala, bed nucleus of the stria terminalis, habenula, and monoaminergic nuclei in the brain stem. N/OFQ inhibits neuronal excitability of monoaminergic neurons and monoamine release from their terminals by activation of G protein-coupled inwardly rectifying K⁺ channels and inhibition of voltage sensitive calcium channels, respectively. Therefore, NOP receptor antagonists have been proposed as a potential antidepressant. Indeed, mounting evidence shows that NOP receptor antagonists have antidepressant-like effects in various preclinical animal models of depression, and recent clinical studies again confirmed the idea that blockade of NOP receptor signaling could provide a novel strategy for the treatment of depression. In this review, we describe the pharmacological effects of N/OFQ in relation to depression and explore the possible mechanism of NOP receptor antagonists as potential antidepressants.