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.

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.

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.

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...

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.

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.

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.

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.

Involvement of nitric oxide in learning & memory processes.

Nitric oxide (NO), synthesized from the amino acid, L-arginine by nitric oxide synthase (NOS) has received attention as a neurotransmitter in the brain. NO has been found to induce cognitive behaviour in experimental animals. In order to show evidence for the involvement of NO in learning and memory processes, the reports indicating the effects of its precursor, donors, and inhibitors of its synthesis in mammals, birds, fishes and invertebrates have been reviewed. Further, learning and memory impairment occurring in man and animals due to defective NO activity in the brain due to pathological conditions such as epilepsy, stress, diabetes and side effects of therapeutic agents and reversal of this condition by L-arginine and NO donors have been included. In addition, the reports that indicate ageing-induced impairment of cognition that is known to occur in Alzheimer's disease due to deposition of the toxic protein, beta amyloid and the effect of L-arginine and NO donors in preventing dementia in these patients have been reviewed.

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.

Purinergic signalling: past, present and future

The discovery of non-adrenergic, non-cholinergic neurotransmission in the gut and bladder in the early 1960's is described as well as the identification of adenosine 5'-triphosphate (ATP) as a transmitter in these nerves in the early 1970's. The concept of purinergic cotransmission was formulated in 1976 and it is now recognized that ATP is a cotransmitter in all nerves in the peripheral and central nervous systems. Two families of receptors to purines were recognized in 1978, P1 (adenosine) receptors and P2 receptors sensitive to ATP and adenosine diphosphate (ADP). Cloning of these receptors in the early 1990's was a turning point in the acceptance of the purinergic signalling hypothesis and there are currently 4 subtypes of P1 receptors, 7 subtypes of P2X ion channel receptors and 8 subtypes of G protein-coupled receptors. Both short-term purinergic signalling in neurotransmission, neuromodulation and neurosecretion and long-term (trophic) purinergic signalling of cell proliferation, differentiation, motility, death in development and regeneration are recognized. There is now much known about the mechanisms underlying ATP release and extracellular breakdown by ecto-nucleotidases. The recent emphasis on purinergic neuropathology is discussed, including changes in purinergic cotransmission in development and ageing and in bladder diseases and hypertension. The involvement of neuron-glial cell interactions in various diseases of the central nervous system, including neuropathic pain, trauma and ischemia, neurodegenerative diseases, neuropsychiatric disorders and epilepsy are also considered.

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.

Dor neuropática: aspectos neuroquímicos: [revisão] / Dolor neuropático: aspectos neuroquímicos: [revisión] / Neuropathic pain: neurochemical aspects: [review]

JUSTIFICATIVA E OBJETIVOS: A dor neuropática é causada por lesão ou inflamação do sistema nervoso. É síndrome complexa, com mecanismos biológicos pouco esclarecidos, envolvendo teorias inflamatórias e imunes. O objetivo desta revisão foi descrever os principais fatores biológicos relacionados com a dor neuropática, associando de forma lógica as hipóteses sugeridas pela literatura. CONTEÚDO: Foram descritos os principais neuromediadores, canais iônicos e células, incluindo as do sistema imune envolvidos na excitabilidade neuronal, assim como enfatizada possível seqüência de ativação ou interação desses agentes na alteração neuroplástica decorrente da agressão ao nervo. CONCLUSÕES: Do estudo, foi possível concluir que os avanços no conhecimento da fisiopatologia da dor neuropática podem determinar novos alvos para abordagem farmacológica dessa síndrome.

BACKGROUND AND OBJECTIVES: Neuropathic pain is caused by damage or inflammation of the nervous system. It is a complex syndrome and its biological mechanisms, involving inflammatory and immunologic theories, are not clear. The objective of this review was to describe the main biologic factors associated with neuropathic pain, making a logical association between hypotheses suggested in the literature. CONTENTS: The main neuromediators, ion channels, and cells, including cells in the nervous system involved in neuronal excitation are described, and the possible activation sequence or interaction among those agents in the neoplastic change secondary to nerve damage are emphasized. CONCLUSIONS: It was possible to conclude that the advances on the knowledge of the pathophysiology of neuropathic pain can determine new pharmacologic approaches for this syndrome.

JUSTIFICATIVA Y OBJETIVOS: El dolor Neuropático lo causa la lesión o inflamación del sistema nervioso. Es un síndrome complejo, con mecanismos biológicos poco aclarados, que envuelve teorías inflamatorias e inmunes. El objetivo de esta revisión fue describir los principales factores biológicos relacionados con el dolor Neuropático, asociando de forma lógica a las hipótesis sugeridas por la literatura. CONTENIDO: Fueron descritos los principales neuromediadores, canales iónicos y células, incluyendo las del sistema inmune involucrados en la excitabilidad neuronal, como también la posible secuencia de activación o interacción de esos agentes en la alteración neuroplástica proveniente e la agresión al nervio. CONCLUSIONES: De ese estudio, se pudo concluir que los avances en el conocimiento de la fisiopatología del dolor Neuropático, pueden determinar nuevos objetivos para el abordaje farmacológico de ese síndrome.

Neurobiologia dos transtornos do controle dos impulsos / The neurobiology of impulse control disorders

OBJETIVO: Revisar os artigos sobre substratos neurobiológicos dos transtornos do controle dos impulsos. O jogo patológico é o foco central desta revisão na medida em que a maioria dos estudos biológicos dos formalmente classificados como transtornos do controle dos impulsos examinou este transtorno. MÉTODO: Foi feita uma busca no banco de dados Medline de artigos publicados de 1966 até o presente para identificar aqueles relevantes para serem revisados neste artigo. DESFECHOS: Estudos pré-clínicos sugerem que a neuromodulação das monoaminas cerebrais está associada à tomada de decisões impulsivas e aos comportamentos de risco. Os estudos clínicos implicam diversos sistemas de neurotransmissores (serotoninérgico, dopaminérgico, adrenérgico e opióide) na fisiopatologia do jogo patológico e de outros transtornos do controle dos impulsos. Estudos de neuroimagem preliminares têm indicado o córtex pré-frontal ventromedial e o estriato ventral como atuantes na fisiopatologia do jogo patológico e de outros transtornos do controle dos impulsos. As contribuições genéticas para o jogo patológico parecem substanciais e os estudos iniciais têm relacionado esse transtorno a polimorfismos alélicos específicos, ainda que os achados de varredura genômica ainda tenham que ser publicados. CONCLUSÃO: Mesmo que tenham sido logrados avanços significativos em nossa compreensão sobre os transtornos do controle dos impulsos, mais pesquisas são necessárias para ampliar o conhecimento existente e traduzir esses achados em avanços clínicos.

OBJECTIVE: To review the neurobiological substrates of impulse control disorders. Pathological gambling is a main focus of the review in that most biological studies of the formal impulse control disorders have examined this disorder. METHOD: The medical database Medline from 1966 to present was searched to identify relevant articles that were subsequently reviewed to generate this manuscript. RESULTS: Preclinical studies suggest that differential brain monoamine neuromodulation is associated with impulsive decision-making and risk-taking behaviors. Clinical studies implicate multiple neurotransmitter systems (serotonergic, dopaminergic, adrenergic, and opioidergic) in the pathophysiology of pathological gambling and other impulse control disorders. Initial neuroimaging studies have implicated the ventromedial prefrontal cortex and ventral striatum in the pathophysiology of pathological gambling and other impulse control disorders. Genetic contributions to pathological gambling seem substantial and initial studies have implicated specific allelic polymorphisms, although genome-wide analyses have yet to be published. CONCLUSION: Although significant advances have been made in our understanding of the neurobiology of impulse control disorders, more research is needed to extend existing knowledge and translate these findings into clinical advances.

Mecanismos neuroendócrinos envolvidos na puberdade de novilhas / Neuroendocrine mechanisms in puberty heifers / Mecanismos neuroendocrinos involucrados en la pubertad de novillas

Sob o ponto de vista fisiológico, a puberdade em novilhas Bos taurus e Bos indicus caracteriza-se por um aumento na concentração e freqüência pulsátil de LH e um decréscimo na sensibilidade do hipotálamo aos esteróides gonadais, com participação ou não de neurotransmissores com capacidade de estimular ou inibir a secreção de LH, o que resultará na primeira ovulação. Os eventos fisiológicos relacionados à primeira ovulação são similares, tanto nas novilhas Bos taurus, quanto nas novilhas Bos indicus, ocorrendo mais tardiamente nesta última. O sistema extensivo de criação do Zebu, adotado na maioria dos países sul-americanos, contribui para que a puberdade aconteça mais tardiamente, refletindo na idade ao primeiro parto. A idade à primeira ovulação é uma característica de alta herdabilidade, sendo a seleção genética, através da precocidade sexual, uma ferramenta para reduzir a idade ao primeiro parto e melhorar a eficiência reprodutiva do sistema de produção. Aliado à seleção genética, o uso de técnicas de manejo melhorando a qualidade nutricional e a oferta de alimentos, o cruzamento entre raças, a exposição das novilhas a touros e o uso de biotecnologias que permitam manipular a primeira ovulação, podem contribuir para o aumento da produtividade. Esta revisão tem como objetivo abordar aspectos fisiológicos relacionados à puberdade de novilhas Bos taurus e Bos indicus.

Under a physiological perspective, puberty in both Bos taurus and Bos indicus heifers is characterized by an increase in the LH concentration, frequency pulses, and decreasing of the hypothalamic-pituitary axis sensibility to gonadal steroid, with, or without, the participation of the neurotransmitters capable of either stimulating or to inhibiting the LH secretion, which will result in the first ovulation. The physiological events related to the first ovulation are similar for both Bos taurus and Bos indicus, occurring later for Bos indicus. The extensive Zebu management carried out in the majority of the South American countries contributes for puberty to occur later influencing the age of the first calving. Regarding the first ovulation, age is a characteristic of high heritability, as the genetic selection, through sexual precocity, is a tool for first¬calving age reduction; and the improvement of the nutritional quality and feeding supply, crossbreeding, heifer exposition to bulls and the use o biotechnologies which ensure the manipulation of the first ovulation might contribute for the productivity increasing. This review aims at approaching physiological aspects related to the puberty of both Bos taurus and Bos indicus heifers.

Mecanismos do ciclo sono-vigília / Sleep-wake cycle mechanisms

Três sub-divisões hipotalâmicas são importantes no ciclo sono-vigília: o hipotálamo anterior (núcleos gabaérgicos e núcleos supraquiasmáticos), o hipotálamo posterior (núcleo túbero-mamilar histaminérgico) e o hipotálamo lateral (sistema hipocretinas). O sistema gabaérgico inibitório do núcleo pré-óptico ventro-lateral (VLPO) do hipotálamo anterior é responsável pelo início e manutenção do sono NREM. Os neurônios supraquiasmáticos (NSQs) do hipotálamo anterior são responsáveis pelo ritmo circadiano do ciclo sono-vigília. Os núcleos aminérgicos, histaminérgicos, as hipocretinas e núcleos colinérgicos do prosencéfalo basal apresentam-se ativos durante a vigília, inibindo o núcleo pré-óptico ventro-lateral, promovendo a vigília. O processo de inibição-estimulação é a base do modelo da interação recíproca entre os grupos de células wake-off-sleep-on e células wake-off-sleep-on reguladores do ciclo sono-vigília. O modelo da interação recíproca também se aplica aos núcleos colinérgicos (células REM-on) e aminérgicos (células REM-off) do tronco cerebral no controle temporal do sono REM-NREM.

Fisiopatologia do transtorno afetivo bipolar: o que mudou nos últimos 10 anos? / Physiopathology of bipolar disorders: what have changed in the last 10 years?

Apesar dos crescentes esforços para o entendimento da neurobiologia do transtorno afetivo bipolar (TAB), sua exata fisiopatologia permanece indeterminada. Inicialmente, a pesquisa estava voltada para o estudo das aminas biogênicas, devido aos efeitos dos diversos agentes psicofarmacológicos. Mais recentemente, evidências apontam que disfunções nos sistemas de sinalização intracelular e de expressão gênica podem estar associadas ao TAB. Estas alterações podem estar associadas a interrupções nos circuitos reguladores do humor, como sistema límbico, estriado e córtex pré-frontal, sendo que os efeitos neuroprotetores do uso crônico dos estabilizadores de humor podem reverter este processo patológico. Este artigo tem como objetivo trazer uma atualização dos achados recentes sobre a neuroquímica do TAB.

Anormalidades neuropatológicas e neuroquímicas no transtorno afetivo bipolar / Neuropatological and neurochemical abnormalities in bipolar disorder

OBJETIVOS: Estudos pós-mortem, farmacológicos, de neuroimagem e em modelos animais têm demonstrado uma possível associação de mecanismos de sinalização intracelular na fisiopatologia do transtorno afetivo bipolar (TAB). Esse trabalho tem como objetivo revisar os achados em neuropatologia e bioquímica celular. MÉTODOS: Foi realizada uma pesquisa ao MEDLINE, entre 1980 e 2003, tendo sido utilizados os unitermos: bipolar disorder, signaling, second messengers e postmortem, além de referências cruzadas dos artigos selecionados. RESULTADOS: uropatológicos demonstraram uma diminuição do número de células neuronais e gliais, principalmente no córtex pré-frontal de pacientes bipolares. Estudos neuroquímicos demonstraram alterações nas vias do AMPc, fosfatidilinositol, Wnt/GSK-3beta e Ca++ intracelular nesses pacientes. CONCLUSÃO: Os achados de alterações neuropatológicas e neuroquímicas no TAB podem estar relacionados com a fisiopatologia deste transtorno e com os efeitos dos estabilizadores de humor. No entanto, mais estudos são necessários para esclarecer o papel das cascatas de sinalização intracelular na patogênese deste transtorno.