The Interplay between Neurotransmitters and Calcium Dynamics in Retinal Synapses during Development, Health, and Disease.

The intricate functionality of the vertebrate retina relies on the interplay between neurotransmitter activity and calcium (Ca2+) dynamics, offering important insights into developmental processes, physiological functioning, and disease progression. Neurotransmitters orchestrate cellular processes to shape the behavior of the retina under diverse circumstances. Despite research to elucidate the roles of individual neurotransmitters in the visual system, there remains a gap in our understanding of the holistic integration of their interplay with Ca2+ dynamics in the broader context of neuronal development, health, and disease. To address this gap, the present review explores the mechanisms used by the neurotransmitters glutamate, gamma-aminobutyric acid (GABA), glycine, dopamine, and acetylcholine (ACh) and their interplay with Ca2+ dynamics. This conceptual outline is intended to inform and guide future research, underpinning novel therapeutic avenues for retinal-associated disorders.

[Research progress on the neural mechanism of the regulation of social isolation on innate behaviors].

Innate behavior is mainly controlled by genetics, but is also regulated by social experiences such as social isolation. Studies in animal models such as Drosophila and mice have found that social isolation can regulate innate behaviors through the changes at the molecular level, such as hormone, neurotransmitter, neuropeptide level, and at the level of neural circuits. In this review, we summarized the research progress on the regulation of social isolation on various animal innate behaviors, such as sleep, reproduction and aggression by altering the expression of conserved neuropeptides and neurotransmitters, hoping to deepen the understanding of the key and conserved signal pathways that regulate innate behavior by social isolation.

Functions and mechanisms of adenosine and its receptors in sleep regulation.

Sleep is a natural and recurring state of life. Long-term insomnia can lead to physical and mental fatigue, inattention, memory loss, anxiety, depression and other symptoms, imposing immense public health and economic burden worldwide. The sleep and awakening regulation system is composed of many nerve nuclei and neurotransmitters in the brain, and it forms a neural network that interacts and restricts each other to regulate the occurrence and maintenance of sleep-wake. Adenosine (AD) is a neurotransmitter in the central nervous system and a driver of sleep. Meanwhile, the functions and mechanisms underlying sleep-promoting effects of adenosine and its receptors are still not entirely clear. However, in recent years, the increasing evidence indicated that adenosine can promote sleep through inhibiting arousal system and activating sleep-promoting system. At the same time, astrocyte-derived adenosine in modulating sleep homeostasis and sleep loss-induced related cognitive and memory deficits plays an important role. This review, therefore, summarizes the current research on the functions and possible mechanisms of adenosine and its receptors in the regulation of sleep and homeostatic control of sleep. Understanding these aspects will provide us better ideas on clinical problems such as insomnia, hypersomnia and other sleep disorders.

Viés da Escalada, Daemons de Otimização, e a Influência da Narrativa Social Aceleracionista / Hill-Climbing Bias, Optimization Daemons, and the Influence of Accelerated Social Narratives

O fenômeno de aceleração social, intimamente ligado a nossa modernização tecnológica e os sistemas políticos e sociais que adotamos, vem sendo alvo de questionamentos por parte da teoria crítica por diversos filósofos e sociólogos, principalmente em relação a se tal "aceleração" seja algo que, possa ser justificável pelo bem comum da sociedade. De fato, as rápidas mudanças que ocorreram no último século causaram uma tremenda mudança em nossos estilos-de-vida, e na maneira como experienciamos o mundo. Que a nossa sociedade mudou e continua a mudar é um fato evidente quando olhamos criticamente para o passado e presente, e comparamos diferentes épocas da história humana. Neste ensaio tentaremos explorar algumas possíveis hipóteses que fundamentem o comportamento aceleracionista em certos fatores e mecanismo biológicos que caracterizam os sistemas de motivação e saciação humanos. Também tentaremos mostrar como certos fenômenos sociais podem auxiliar em fortalecer este tipo de comportamento, e suas possíveis origens evolutivas. Este estudo tem como objetivo principal fundamentar a Tese Aceleracionista em evidências neurofisiológicas, cognitivo-comportamentais, evolutivas e sociais.

The phenomenon of social acceleration is closely linked to our technological modernization and the political and social systems we have adopted, and it has been questioned by several philosophers and sociologists, especially in relation to whether such acceleration is something that can be justified for the common good of society. In fact, the rapid changes that have occurred in the last century have caused a tremendous change in our lifestyles, and in the way we experience the world. That society have changed and continues to change is an evident fact when we look critically to the past and our present and compare different times in human history. In this essay we will try to explore some possible hypotheses that underpin accelerated behavior, in certain biological factors and mechanisms that characterize human motivation and satiation systems. We will also try to show how certain social phenomena can help to strengthen this type of behavior, and its possible evolutionary origins. The main objective of this study is to base the Accelerationist Thesis on neurophysiological, cognitive-behavioral, evolutionary and also social evidence.

Bases de la estimulación cerebral profunda / Bases of deep brain stimulation

INTRODUCCIÓN: La estimulación cerebral profunda es una terapia eficaz que está siendo utilizada en un número creciente de indicaciones. Los mecanismos mediante los cuales ejerce efecto terapéutico aún se desconocen en su mayor parte, si bien cada vez se dispone de más datos sobre su influencia en diversos niveles. OBJETIVO: Revisar la bibliografía existente sobre el mecanismo de acción de la estimulación cerebral profunda. Desarrollo. La estimulación cerebral profunda actúa sobre el tejido cerebral estimulado en varios niveles, molecular, celular y de redes neuronales. En su efectividad intervienen factores espaciales, temporales y eléctricos, pero fundamentalmente parece ejercer su función mediante la sustitución de patrones de disparo anómalos, presentes en ciertas enfermedades neurológicas y psiquiátricas. Otros mecanismos, como la neuroprotección o la neurogénesis, permanecen en estudio. CONCLUSIONES: Aunque aún se desconocen muchos efectos por los cuales la estimulación cerebral profunda actúa en el cerebro, parece un tratamiento complejo, con efectos a gran escala, en los que parece primar la corrección de circuitopatías como mecanismo principal

INTRODUCTION: Deep brain stimulation is an effective therapy that is being used in an increasing number of indications. The mechanisms by which it exerts its therapeutic effect are still largely unknown, although there is increasing evidence of its influence at various levels. AIM: To review the existing literature on the mechanism of action of deep brain stimulation. DEVELOPMENT. Deep brain stimulation acts on brain tissue that is stimulated at various levels: molecular, cellular and neural networks. Spatial, temporal and electrical factors are involved in its effectiveness, but it mainly seems to perform its function by replacing anomalous firing patterns, which are present in certain neurological and psychiatric diseases. Other mechanisms, such as neuroprotection or neurogenesis, remain under study. CONCLUSIONS: Although many of the effects by which deep brain stimulation acts on the brain are still unknown, it seems to be a complex treatment, with large-scale effects, in which the correction of circuitopathies seems to prevail as the main mechanism

De la compuerta a la neuromatriz y neuromodulación / From gate and neuromodulation to neuromatrix

The following article presents a review of the evolution of the gate and neuromatrix theories as well as their contribution in the development of neuromodulation to the present day. Nowadays the mechanism of action of neuromodulation is better to understand by dividing it according to the level where it acts (local, central or peripheral). Patient selection is crucial to optimize the effectiveness of the device; although the indications for pain that support current guidelines are failed back syndrome, complex regional pain syndrome and lower limb ischemic pain and refractory angina; neuromodulation is already being extended to multiple fields of action that affect the future, such as the improvement of human capacities.

El siguiente artículo consiste en una revisión no sistemática de la evolución de la teoría de la compuerta y la neuromatriz, así como su aporte en el desarrollo de los dispositivos de neuromodulación. Para entender mejor el mecanismo de acción de la neuromodulación se divide según el nivel en que actúe sea local, central o periférico. La selección de pacientes es crucial para optimizar la eficacia del dispositivo; aunque las indicaciones para manejo del dolor que soportan las guías actuales son síndrome de espalda fallida, síndrome doloroso regional complejo y dolor tipo isquémico en miembros inferiores y dolor por angina refractaria; actualmente la neuromodulación se está extendiendo a múltiples campos de acción entre los cuales se encuentra el mejoramiento de las capacidades humanas.

La geometría funcional como fundamento de la estructura y la función del aparato psíquico / Functional geometry as the basis of the psychic apparatus 'structure and function / La geometria funcional com a fonament de l'estructura i la funció de l’aparell psíquic

El proceso evolutivo del sistema nervioso central (SNC) no solo afectó a los genes, al desarrollo, la anatomía o la cognición, sino y fundamentalmente, la organización neural. Desde un enfoque puramente teórico analizaremos lo que a nuestro juicio define la estructura y el posterior funcionamiento del aparato psíquico, la geometría funcional. Esbozaremos un modelo posible que explica, a través de los principios metodológicos aportados por la lógica transcursiva, los aspectos funcionales del SNC que le dan sustento a la psiquis

The evolutionary process of the central nervous system (CNS) not only affected genes, development, anatomy or cognition but fundamentally, the neural organization. From a purely theoretical approach, we will analyze what, in our opinion, defines the structure and the subsequent functioning of the psychic apparatus, the functional geometry. We will outline a possible model that explains, through the methodological principles provided by the transcursive logic, the functional aspects of the CNS that give support to the psyche

El procés evolutiu del sistema nerviós central (SNC) no només va afectar els gens, el desenvolupament, l'anatomia o la cognició, sinó, i fonamentalment, l'organització neural. Des d'un enfocament purament teóric, analitzarem el que al nostre ju­dici defineix l'estructura i el posterior funcionament de l'aparell psíquic, la geometria funcional. Esbossarem un model possible que explica, a través dels principis metodológics aportats per la lógica transcursiva, els aspectes funcionals del SNC que sustenten la psique

Vigencia del efecto placebo: su biología desde la genética a la conducta / Biological and genetic mechanisms underlying the placebo effect

The placebo effect has been seldom studied in the history of medicine. However, during the last decades, the great impact of this phenomenon in clinical practice, ranging from surgical to psychiatric field, has been revealed. Research elucidated both the psychological mechanisms and genetic polymorphisms that affect the susceptibility of individuals to express this phenomenon. We herein review the psychological mechanisms, brain structures (anterior cingulate cortex, nucleus accumbens, dorsolateral prefrontal cortex, insular cortex, thalamus) and neurotransmission systems involved (opioid, dopaminergic, cannabinoid, serotoninergic, cholecystokinin). These are the clue to recognize the polymorphisms that have been identified so far. The biological basis of both the placebo effect and its alter ego, the nocebo effect, are well recognized, and related to corresponding psychological processes. Finally, the implications of the findings in clinical practice and medical training are discussed.

La depresión: un predictor de demencia / Depression: a predictor of dementia

Algunos estudios sugieren que hasta un tercio de los casos de Alzheimer, la demencia más común en nuestra sociedad, puede ser prevenido con la eliminación de algunos factores de riesgo. Barnes y Yaffe encontraron que un 10% de casos de Alzheimer eran atribuibles a la depresión, pero en la literatura científica no queda claro su papel etiológico en el desarrollo de demencia. El objetivo de la revisión es analizar la evidencia científica sobre la hipótesis de que la depresión aumenta el riesgo de desarrollar demencia. Se realizó una revisión sistemática y metaanálisis con literatura científica publicada hasta la fecha, con una cobertura temporal entre 1990 y 2014. Diez de los artículos encontrados cumplían con los criterios de selección -similitud en a) tamaño y características de la muestra (procedencia, edad…), b) procedimiento de recogida de datos, c) método de estudio de la relación (comparación inter- como intragrupal), d) método estadístico de análisis de los resultados- y calidad previamente establecidos. Los valores de odds ratio de los estudios analizados oscilan entre 1,72 y 3,59, y los de hazard ratio de entre 1,72 a 5,44, lo que indica que los sujetos con historia de depresión tienen mayor riesgo de desarrollar demencia que aquellos que no la han tenido (AU)

Many studies suggest that in 10-25% of cases of Alzheimer's, the most common dementia in our society, can be prevented with the elimination of some risk factors. Barnes and Yaffe found that one-third of Alzheimer's cases are attributable to depression, but in the scientific literature it is not clear if it has a real causal effect on the development of dementia. The purpose of this study is to analyse the scientific evidence on the hypothesis that depression increases the risk of developing dementia. A systematic review and a meta-analysis were performed on the scientific literature published up until the present day, searching articles that were published between 1990 and 2014. Ten of the studies found met the selection criteria -similar to a) size and characteristics of the sample (origin, age…), b) process of gathering data c) method of studying the relationship (within and/or between group comparison), and d) statistical analysis of the results- and the previously established quality. The value of odds ratio varied from 1.72 to 3.59, and the hazard ratio from 1,72 to 5.44. This indicates that the subjects with a history of depression have a higher risk of developing dementia than others who did not suffer depression (AU)

Sistemas de neurotransmisión, alteraciones neuroanatómicas y muerte celular en la esquizofrenia: actualización y perspectivas / Neurotransmitter systems, neuroanatomical pathology and cell death in schizophrenia: update and perspectives

La esquizofrenia incluye una alteración del juicio de realidad que se caracteriza por la presentación de ideas delirantes que pueden ir acompañadas de alucinaciones de alguna modalidad sensorial. Estos síntomas se presentan en la esquizofrenia, pero también pueden resultar de una amplia variedad de trastornos neurológicos y psiquiátricos. Asimismo, puede ser inducida químicamente. A pesar de que la presentación de psicosis es clínicamente similar, se desconoce si involucra mecanismos neurobiológicos distintos para cada situación. Los pacientes que sufren esquizofrenia no sólo exhiben diversas alteraciones neuroanatómicas sino, además, alteraciones en la neurotransmisión de diferentes sistemas. Actualmente, las teorías más aceptadas proponen una sobreactivación del sistema dopaminérgico y una hipofunción del sistema glutamatérgico. Adicionalmente, otros sistemas involucrados en la fisiopatología de la esquizofrenia son la vía del óxido nítrico, así como los sistemas GABAérgico, glicinérgico y serotonérgico. Más aún, dichos sistemas interactúan entre sí modulando el desarrollo del sistema nervioso y la supervivencia de las células. Las alteraciones descritas en este artículo podrían formar una misma secuencia de eventos. La investigación en este campo habrá de enfocarse en dilucidar esa cadena para acercarse aún más a sus extremos inicial, que le da origen, y final, que tiene implicaciones terapéuticas.

Schizophrenia is a thought disorder characterized by delusional thinking which may be accompanied by hallucinations involving any sensory modality. Schizophrenia may be associated with several neurologic and psychiatric disorders. Also, it may be induced by drugs. In spite of the similarity in psychoses symptomatology, it is unknown if it involves the same underlying neurobiologic mechanisms in those cases. Schizophrenic patients exhibit not only neuroanatomical alterations, but also, distortion of several neurotransmitter systems. Nowadays, the main theories in this regard involve dopaminergic hyperfunction and glutamatergic hypofunction. Additionally, other systems involved in the schizophrenia pathophysiology are the nitric oxide pathway as well as GABAergic, glycinergic and serotonergic systems. Furthermore, those systems interact with each other to modulate nervous system development and cell survival. The alterations described in this paper may be part of a single cascade of events. Research in this field should focus on the elucidation of this chain to find its limits, the initial stage that originates it, and the final stage that has therapeutic implications.

Consecuencias de la enfermedad de Parkinson en la calidad de vida / Consequences of Parkinson’s disease on quality of life

La enfermedad de Parkinson (EP), se identifica como una enfermedad neurodegenerativa, que tiende a atacar al Sistema Nervioso Central, dañando severamente regiones neuronales de la sustancia negra. A nivel mundial la EP ocupa la segunda posición como la enfermedad de degeneración neuronal con mayor prevalencia. Los orígenes de la EP resultan multifactoriales, pues al presente se desconoce una única causa biológica o genética que explique su etiología de forma plena y satisfactoria. Se reconocen en la actualidad una variedad de siete tipos de Parkinsonismo, que producen afectaciones en sus distintas etapas, tanto a nivel de los sistemas de serotonina, noradrenalina como acetilcolina. Los drásticos efectos que provoca la EP sobre la Calidad de Vida (CV) de los pacientes, puede ser evaluada científica y cuantitativamente, desde las múltiples pruebas y evaluaciones que han surgido dentro del campo de las ciencias de la salud. Los cuatro síntomas más comunes para el reconocimiento del Parkinsonismo, son la inestabilidad postural, la rigidez corporal, la bradicinesia y los temblores. La EP continúa siendo poco intervenida en sus etapas tempranas de aparición, especialmente en naciones en vías de desarrollo, por lo que se requiere mayor unidad entre disciplinas científicas y sistemas públicos de salud, para mejorar la CV de estas poblaciones...

Parkinson's disease (PD), is identified as a neurodegenerative disease, tending to attack the Central Nervous System, severely damaging neural regions of substantia nigra. Globally PD ranks second as the most prevalent neuronal degeneration disease. The origins of PD are multifactorial, because nowadays a unique biological or genetic cause to explain the etiology of full and satisfactory way is unknown. They now recognize a variety of seven types of Parkinsonism, producing affectations in its various stages, both at the serotonin, norepinephrine and acetylcholine systems. The drastic effects caused by PD on Quality of Life (QoL) of patients, can be evaluated quantitatively and scientifically and from the multiple tests and evaluations that have emerged within the field of health sciences. The four most common symptoms of Parkinsonism recognition are postural instability, body rigidity, bradykinesia and tremors. PD is still little intervened in the early stages of emergence, especially in developing nations, so that greater unity between scientific disciplines and public health systems are required to improve the QoL’s populations...

Mapping and signaling of neural pathways involved in the regulation of hydromineral homeostasis

Several forebrain and brainstem neurochemical circuitries interact with peripheral neural and humoral signals to collaboratively maintain both the volume and osmolality of extracellular fluids. Although much progress has been made over the past decades in the understanding of complex mechanisms underlying neuroendocrine control of hydromineral homeostasis, several issues still remain to be clarified. The use of techniques such as molecular biology, neuronal tracing, electrophysiology, immunohistochemistry, and microinfusions has significantly improved our ability to identify neuronal phenotypes and their signals, including those related to neuron-glia interactions. Accordingly, neurons have been shown to produce and release a large number of chemical mediators (neurotransmitters, neurohormones and neuromodulators) into the interstitial space, which include not only classic neurotransmitters, such as acetylcholine, amines (noradrenaline, serotonin) and amino acids (glutamate, GABA), but also gaseous (nitric oxide, carbon monoxide and hydrogen sulfide) and lipid-derived (endocannabinoids) mediators. This efferent response, initiated within the neuronal environment, recruits several peripheral effectors, such as hormones (glucocorticoids, angiotensin II, estrogen), which in turn modulate central nervous system responsiveness to systemic challenges. Therefore, in this review, we shall evaluate in an integrated manner the physiological control of body fluid homeostasis from the molecular aspects to the systemic and integrated responses.

Desde la corteza auditiva a la cóclea: progresos en el sistema eferente auditivo / From auditory cortex to cochlea: progress in the auditory efferent system

El sistema eferente auditivo está constituido por el sistema olivococlear y por vías descendentes que provienen de la corteza auditiva y se dirigen a la cóclea. El sistema olivococlear se divide en una porción medial y una lateral, con neuronas que inervan a las células ciliadas externas y a fibras del nervio auditivo respectivamente. El principal neurotransmisor de las sinapsis olivococleares es acetilcolina, y tanto las células ciliadas externas como las fibras del nervio auditivo poseen receptores para esta molécula. El sistema eferente córtico-coclear se origina en la capa V y VI de la corteza auditiva y proyecta a los colículos inferiores y complejo olivar superior, donde a través del sistema olivococlear se conecta con el órgano receptor auditivo. En este artículo se revisan importantes hallazgos obtenidos en los últimos años que involucran (i) nuevos neurotransmisores y receptores del sistema eferente auditivo; (ii) vías descendentes de la corteza auditiva y su rol fisiológico sobre las respuestas cocleares y (iii) rol del sistema eferente auditivo en patologías audiológicas y neuropsiquiátricas.

The auditory efferent system is composed by the olivocochlear fibers and descending projections that originate in the auditory cortex and end in the cochlea. The olivocochlear system is divided into a medial and lateral division, with fibers directed to the outer hair cells and to the auditory nerve fibers respectively. It is known that acetylcholine is the main neurotransmitter of the olivocochlear synapses and that outer hair cells and auditory nerve fibers have receptors to this molecule. The cortico-cochlear efferent system originates in layers V and VI of the auditory cortex. These descending projections are directed to the inferior colliculus and superior olivary complex, a site in which the olivocochlear fibers emerge and connect the brain with the cochlear receptor. In this article recent discoveries obtained in the last years are reviewed: (i) new neurotransmitters and receptors of the olivocochlear system; (ii) anatomy and physiology of descending pathways from the auditory cortex to the cochlea and, (iii) clinical role of auditory efferents in audiological and neuropsychiatric pathologies.

Suplementos nutricionales en trastornos de la conducta alimentaria / Nutritional supplements in eating disorders

Se consideran Trastornos de la Conducta Alimentaria (TCA) a una serie de entidades nosológicas diferenciadas que tienen como nexo común una alteración continuada en la ingesta o bien en la conducta relacionada con la ingesta. Dentro de dicha clasificación destacan los siguientes trastornos: Anorexia Nerviosa (AN) y Bulimia Nerviosa (BN). La AN es un trastorno de curso crónico caracterizado principalmente por una negativa o disminución de la ingesta acompañado de una distorsión de la imagen corporal con el consecuente miedo intenso a la ganancia de peso. Se estima una prevalencia vital en la adolescencia de dicho trastorno de aproximadamente el 0,5-1%1. En la BN la presencia de atracones de comida y la posterior conducta compensatoria (en forma de ejercicio intenso, uso de laxantes, diuréticos...) es lo que prima en el paciente. La prevalencia se estima entre un 2 y un 4% en mujeres jóvenes, iniciándose generalmente en etapas algo posteriores que la AN. Se cree que en su patogenia influyen factores biológicos, psicológicos y ambientales así como una cierta vulnerabilidad genética. Existen distintos tratamientos con eficacia avalada por parte de literatura científica, tanto terapias biológicas como psicológicas, a pesar de ello, nos encontramos con una efectividad parcial de dichas terapias siendo necesaria la búsqueda de nuevas dianas así como de nuevos tratamiento. Aunque la etiopatogenia de los TCA no esté clara, algunas de las disfunciones neurobiológicas encontradas permitirían considerar que la dieta y la administración de nutrientes podría ser relevante en el tratamiento de estos trastornos. Proponemos en este artículo una revisión de nuevos tratamientos enfocados al déficit nutricional (AU)

Eating disorders (EDs) are a series of differentiated nosological entities sharing the common link of a continuous alteration in food intake or in food intake-related behavior. Within this classification, the following disorders are noteworthy: anorexia nerviosa (AN) and bulimia nerviosa (BN). Anorexia nervosa is a chronic disorder characterized mainly by negative or decreased food intake accompanied by a distortion of body image and intense accompanying fear of weight gain. The estimated vital prevalence of this disorder in adolescence is approximately 0.5%-1%.1 The primary feature of BN is the presence of binge eating accompanied by compensatory behavior (in the form of intense exercise and the use of laxatives and diuretics, etc.). The prevalence of BN is estimated to be between 2% and 4% in young women, and it generally starts at somewhat later stages than AN. It is believed that biological, psychological, and environmental factors, as well as genetic vulnerability, influence the pathogenesis of EDs. A variety of therapies exist, both biological and psychological, whose effectiveness is supported by the scientific literature. Nonetheless, we find these therapies only partially effective and new targets as well as new treatments should be sought. Although the etiopathogenesis of EDs is unclear, some of the neurobiological dysfunction found suggests that diet and nutrient supplementation could be relevant in their treatment. We review in this article new treatments focusing on nutritional déficits (AU)

Fine-tuning of defensive behaviors in the dorsal periaqueductal gray by atypical neurotransmitters

This paper presents an up-to-date review of the evidence indicating that atypical neurotransmitters such as nitric oxide (NO) and endocannabinoids (eCBs) play an important role in the regulation of aversive responses in the periaqueductal gray (PAG). Among the results supporting this role, several studies have shown that inhibitors of neuronal NO synthase or cannabinoid receptor type 1 (CB1) receptor agonists cause clear anxiolytic responses when injected into this region. The nitrergic and eCB systems can regulate the activity of classical neurotransmitters such as glutamate and γ-aminobutyric acid (GABA) that control PAG activity. We propose that they exert a ‘fine-tuning’ regulatory control of defensive responses in this area. This control, however, is probably complex, which may explain the usually bell-shaped dose-response curves observed with drugs that act on NO- or CB1-mediated neurotransmission. Even if the mechanisms responsible for this complex interaction are still poorly understood, they are beginning to be recognized. For example, activation of transient receptor potential vanilloid type-1 channel (TRPV1) receptors by anandamide seems to counteract the anxiolytic effects induced by CB1 receptor activation caused by this compound. Further studies, however, are needed to identify other mechanisms responsible for this fine-tuning effect.

Pathophysiology of mood disorders in temporal lobe epilepsy / Fisiopatologia dos transtornos de humor na epilepsia do lobo temporal

OBJECTIVE: There is accumulating evidence that the limbic system is pathologically involved in cases of psychiatric comorbidities in temporal lobe epilepsy (TLE) patients. Our objective was to develop a conceptual framework describing how neuropathological, neurochemical and electrophysiological aspects might contribute to the development of psychiatric symptoms in TLE and the putative neurobiological mechanisms that cause mood disorders in this patient subgroup. METHODS: In this review, clinical, experimental and neuropathological findings, as well as neurochemical features of the limbic system were examined together to enhance our understanding of the association between TLE and psychiatric comorbidities. Finally, the value of animal models in epilepsy and mood disorders was discussed. CONCLUSIONS:TLE and psychiatric symptoms coexist more frequently than chance would predict. Alterations and neurotransmission disturbance among critical anatomical networks, and impaired or aberrant plastic changes might predispose patients with TLE to mood disorders. Clinical and experimental studies of the effects of seizures on behavior and electrophysiological patterns may offer a model of how limbic seizures increase the vulnerability of TLE patients to precipitants of psychiatric symptoms.

OBJETIVO: Há evidências crescentes do envolvimento do sistema límbico nas comorbidades psiquiátricas associadas à epilepsia do lobo temporal (ELT). Nosso objetivo foi descrever o panorama atual das alterações neuropatológicas, neuroquímicas e eletrofisiológicas que podem contribuir para o desenvolvimento de sintomas psiquiátricos na ELT e explorar possíveis mecanismos neurobiológicos que podem levar ao aparecimento das desordens de humor nesse subgrupo de pacientes. MÉTODOS: Achados clínicos, de modelos experimentais e neuropatológicos foram revistos, assim como características neuroquímicas do sistema límbico foram examinadas em conjunto para auxiliar nossa compreensão sobre a associação entre ELT e transtornos de humor. CONCLUSÕES: A ELT e os sintomas psiquiátricos coexistem numa frequência muito maior do que o acaso poderia sugerir. Alterações e desregulação de redes anatômicas essenciais, além de mudanças plásticas aberrantes ou deficientes, podem predispor o cérebro de pacientes com ELT a transtornos de humor. Estudos experimentais e clínicos sobre o efeito das crises no comportamento e nos padrões eletrofisiológicos podem oferecer um modelo de como as crises límbicas aumentam a vulnerabilidade a sintomas psiquiátricos em pacientes com ELT.

Serotonina e controle hipotalâmico da fome: uma revisão / Serotonin and hypothalamic control of hunger: a review

Este trabalho revisa a participação do sistema serotonérgico no controle da ingestão de alimentos e saciedade. É de grande interesse compreender a relevância desse sistema para o controle fisiológico do balanço energético e da obesidade. Mais de 35 anos de pesquisas sugerem que a serotonina (5-HT) desempenha um importante papel na saciedade. Assim, o sistema serotonérgico tem sido um alvo viável para o controle de peso. A 5-HT apresenta controle sobre a fome e a saciedade através de diversos receptores, com diferentes funções. O receptor 5-HT2C parece ser o mais importante na relação entre ingestão alimentar e balanço energético. Nesta revisão serão discutidos os mecanismos do sistema serotonérgico envolvidos no controle da ingestão de alimentos e saciedade.

This paper reviews involvement of the serotonergic system in the control of food intake and satiety. It is of great interest to understand the relevance of this system for physiological control of energy balance and obesity. Over 35 years of research suggest that serotonin (5-HT) plays an important role in satiety. Thus, the serotonergic system has been a viable target for weight control. The 5-HT has control over hunger and satiety through different receptors with distinct functions. The 5-HT2C receptor may be more important in the relationship between food intake and energy balance. This review will discuss the mechanisms of the serotonergic system involved in the control of food intake and satiety.

Comunicación neuronal y metabolismo sináptico en epilepsia infantil / Neuronal communication and synaptic metabolism in childhood epilepsy

Introducción. Los conocimientos que la neurociencia básica y el neurometabolismo están aportando en epilepsia pediátrica, y en concreto en mecanismos de comunicación sináptica, crecen rápidamente. Existe, no obstante, una desconexión entre estos avances y una visión que los integre de manera global y en la práctica clínica y terapéutica. Objetivos. Ofrecer una visión integradora de los diferentes mecanismos moleculares y metabólicos que se conocen y postulan en epilepsia pediátrica, y sugerir conceptos como el de ‘metabolismo sináptico’ y ‘fenotipos sinápticos’ como herramientas útiles para desarrollar este enfoque. Desarrollo. Se revisan los estudios más destacados que intentan explicar las características esenciales de la comunicación sináptica en el cerebro en desarrollo, a través de diferentes moléculas, básicamente proteínas sinápticas, canales iónicos (cotransportadores de cloro, sodio y potasio), la compartimentalización pre y postsináptica, y los principales actores metabólicos (neurotransmisores, metabolismo energético, factores de crecimiento y lípidos). A partir de esta combinación de mecanismos biológicos se sugieren ejemplos de ‘fenotipos sinápticos’ en dos casos concretos de epilepsia genética (SCN1A) y metabólica (epilepsia con respuesta a la piridoxina). Conclusiones. Una perspectiva holística, entendiendo la diversidad de elementos relacionados y que suceden en determinados momentos del neurodesarrollo, puede ayudar a delinear fenotipos, vías de metabolismo sináptico y conectividad cerebral, que faciliten no sólo la comprensión de la fisiopatología, sino nuevas aproximaciones terapéuticas en epilepsia pediátrica (AU)

Introduction. Basic neuroscience and neurometabolism are providing a rapidly increasing amount of knowledge on paediatric epilepsy and, more specifically, on the mechanisms involved in synaptic communication. There is, however, a mismatch between these advances and a vision that integrates them in a global way, in clinical and therapeutic practice. Aims. To offer an integrative view of the different molecular and metabolic mechanisms that are known and postulated in paediatric epilepsy, and to suggest concepts such as ‘synaptic metabolism’ and ‘synaptic phenotypes’ as useful tools for developing this approach. Development. We also review the most notable studies that attempt to explain the essential characteristics of synaptic communication in the developing brain by means of different molecules, essentially synaptic proteins, ion channels (chlorine, sodium and potassium co-transporters), and pre- and post-synaptic compartmentalisation, as well as the main players in metabolism (neurotransmitters, energy metabolism, growth factors and lipids). This combination of biological mechanisms has led to examples of ‘synaptic phenotypes’ being suggested in two specific cases of genetic (SCN1A) and metabolic epilepsy (epilepsy with response to pyridoxine). Conclusions. A holistic perspective, which takes into account the diversity of elements that are related and which take place at certain times in neurodevelopment, can help to define phenotypes, channels for synaptic metabolism and brain connectivity, which facilitate not only the understanding of the pathophysiology, but also new therapeutic approaches in paediatric epilepsy (AU)

Sobre la vigilia y el sueño / Upon waking and sleeping

Las últimas décadas han sido muy fructíferas en la tarea de descifrar los circuitos, los neurotransmisoresy las sustancias moduladoras implicadas en la regulación del ciclo sueño-vigilia, y se ha descubierto el papel de nuevas ustancias neuromoduladoras como la orexina o hipocretina. Llama la atención el hecho de que no se mencionan otras de estas sustancias muy estudiadas recientemente como son el óxido nítrico y la melatonina. El óxido nítrico es una sustancia gaseosa liberada por varios grupos neuronales esenciales en el control del estado encefálico global, en sumayoría involucrados en la excitación neuronal durante las transiciones entre sueño y vigilia yentre sueño no REM y REM.....

Unconventional neurotransmitters, neurodegeneration and neuroprotection

Neurotransmitters are also involved in functions other than conventional signal transfer between nerve cells, such as development, plasticity, neurodegeneration, and neuroprotection. For example, there is a considerable amount of data indicating developmental roles for the glutamatergic, cholinergic, dopaminergic, GABA-ergic, and ATP/adenosine systems. In this review, we discuss the existing literature on these "new" functions of neurotransmitters in relation to some unconventional neurotransmitters, such as the endocannabinoids and nitric oxide. Data indicating both transcriptional and post-transcriptional modulation of endocannabinoid and nitrinergic systems after neural lesions are discussed in relation to the non-conventional roles of these neurotransmitters. Knowledge of the roles of neurotransmitters in brain functions other than information transfer is critical for a more complete understanding of the functional organization of the brain and to provide more opportunities for the development of therapeutical tools aimed at minimizing neuronal death.