Cerebral localization of higher functions: anatomic structures before the identification of their memory function / Localização cerebral de funções superiores: estruturas anatômicas antes da identificação de suas funções de memória

The nature of memory and the search for its localization have been a subject of interest since Antiquity. After millennia of hypothetical concepts the core memory-related structures finally began to be identified through modern scientifically-based methods at the diencephalic, hippocampal, and neocortical levels. However, there was a clear temporal delay between the finding of these anatomic structures ignoring their function, and their identification related to memory function. Thus, the core structures begun to be identified with a pure anatomical view in the late Middle Ages on, while the memory function related to them was discovered much later, in the late Modern Period.

A natureza da memória e a busca de sua localização tem sido objeto de interesse desde a Antiguidade. Após milênios de conceitos hipotéticos as estruturas centrais relacionadas com a memória finalmente começaram a ser identificadas através de métodos modernos com base científica, nos níveis diencefálico, hipocampal e neocortical. Entretanto, houve um claro retardo temporal entre o achado dessas estruturas anatômicas ignorando sua função e sua identificação relacionada à função da memória. Assim, as estruturas centrais começaram a ser identificadas com uma visão puramente anatômica da Idade Média tardia em diante, enquanto a função da memória relacionada com as mesmas foi descoberta muito mais tarde, no Período Moderno tardio.

Cerebral localization of higher functions: Memory-related anatomic structures / Localização cerebral de funções superiores: estruturas anatômicas relacionadas com a memória. achados iniciais

ABSTRACT The nature of memory and the search for its localization have been a subject of interest since Antiquity. After millennia of theoretical concepts, shifting from the heart to the brain, then from the ventricles to solid parts, the core memory-related structures finally began to be identified through modern scientifically-based methods at the diencephalic and cortical (hippocampal and neocortical) levels, mostly in the late Modern period, culminating in the current state of knowledge on the subject.

RESUMO A natureza da memória e a busca de sua localização tem sido objeto de interesse desde a Antiguidade. Após milênios de conceitos teóricos, mudando do coração para o cérebro e daí dos ventrículos para as partes sólidas, as estruturas centrais relacionadas com a memória finalmente começaram a ser identificadas através de métodos modernos com base científica, nos níveis diencefálico e cortical (hipocampal e neocortical), principalmente no período Moderno tardio, aproximando-se do estado atual do conhecimento sobre o tema.

Apuntes sobre la evolución histórica de la obra de Pedro Ortiz Cabanillas y su teoría sociobiológica informacional / Notes on the historical evolution of the work of Pedro Ortiz Cabanillas and his sociobiological informational theory

RESUMEN La Teoría Sociobiológica Informacional propone una definición radicalmente distinta de los sistemas vivos, y con lo mismo es la única teoría neurológica existente que evade el problema mente-cerebro y que explica la naturaleza de la conciencia humana. Fue desarrollada por Pedro Ortiz Cabanillas entre 1984 y 2011. En este documento vamos a realizar un recuento de todas sus obras más importantes. Incluimos, adicionalmente, material inédito de los años 1998, 1999, 2006, y 2009.

ABSTRACT The Informational Sociobiological Theory proposes a radically-different definition of living systems and, therefore, is the only existing neurological theory that evades the mind-brain problem and explains the nature of human consciousness. It was developed by Pedro Ortiz Cabanillas between 1984 and 2011. In this document we are presenting a listing of his main works. We include, additionally, unpublished material of the years 1998, 1999, 2006, and 2009.

Regiones del encéfalo vinculadas a la interpretación del dolor / Regions of the brain involved with the interpretation of the pain

Introducción: Entre el lugar del daño tisular y la percepción del dolor, ocurre una serie de eventos electroquímicos que se conocen como nocicepción y comprenden cuatro procesos neurofisiológicos conocidos como: transducción, transmisión, modulación y percepción. Objetivo: Aportar información actualizada sobre las regiones del encéfalo vinculadas a la interpretación del dolor. Material y Método: Se realizó una revisión bibliográfica, con vistas a esclarecer la interpretación de la señal nociceptiva. Se consultaron treinta y cinco artículos científicos, se determinó escoger un total de veintinueve por su relación directa con el propósito de la búsqueda, veintitrés de los cuales corresponden a los últimos 5 años publicados en revistas internacionales y nacionales. Desarrollo: Los axones nociceptivos se clasifican como A δ; y C, participan en la conducción de los potenciales de acción de la periferia al sistema nervioso central. La transmisión de la señal en forma de potenciales de acción se descodifica en áreas relacionadas con aspectos cognoscitivos, afectivo, emocional y conductual del dolor. Este disímil conjunto de estructuras se reconoce en la actualidad como matriz encefálica del dolor. Conclusiones: La matriz del dolor, corresponde a áreas encefálicas como las cortezas somestésicas SI y SII, implicadas en el aspecto discriminativo del dolor. La corteza cingulada anterior y la corteza insular están asociadas al componente afectivo emocional del dolor(AU)

Introduction: A series of electrochemical events called nociception occur between the tissue damage and the perception of pain. They include four neurophysiological processes known as: transduction, transmission, perception, and modulation. Objective: To provide up-to-date information about the regions of the brain involved with the interpretation of pain. Material and Method: A bibliographic review was carried out with the aim of clarifying the interpretation of the nociceptive signal. Thirty-five scientific articles were consulted, and a total of twenty-nine were chosen due to their direct relationship with the aim of the search, twenty-three of which correspond to the last five years of publication in national and international journals. Development: Nociceptive axons are classified as Aδ; and C, and participate in the conduction of action potential of the peripheral nervous system (PNS). The transmission of the signal in the form of action potential is decoded in areas related to cognoscitive, affective, and emotional aspects, and the behavioral area of pain. This dissimilar group of structures is recognized at present as the brain matrix of pain. Conclusions: The pain matrix corresponds to brain areas such as SI and SII somatosensory cortices, implied in the discriminative aspect of pain. Both the anterior cingulate cortex (ACC) and the anterior insular cortex (AIC) are associated with the emotional and affective component of pain(AU)

Comparative proteomics of rat brain in the BCNU-induced model of cortical dysplasia / 中华急诊医学杂志

Objective To screen the differential proteins in the brain (neocortex and hippocampus) between the rats with cortical dysplasia (CD) and control ones,and investigate the role of their alteration in the development of epilepsy in CD.Methods Cortical dysplasia was induced in rat pups via in utero delivery of BCNU.A two-dimensional electrophoresis (2-DE)-based approach was used to construct the expression profiles of proteins in both the neocortex and hippocampus at different age groups (postnatal day 7 and 60) and to detect proteome changes between CD rats and control ones.Following gel image analysis,protein spots that differed in abundance between CD and control rats were identified by using Matrx-assisted laser desorption/ionization (MALDI) mass spectrometry (MS) and MS/MS.Results A total of 57 kinds of protein were screened out (P ＜ 0.05),in which 35 were found up-regulated and 22 were down-regulated compared with the control,35 from neonatal stage (postnatal day 7) and others from adult stage.Finally,12 among them were identified,including tubulin,alpha-lB,Beta-actin,tubulin beta-2A,GAP-43,UbCKmit,GAPDH and TMBr-3,etc.Conclusions Changed expression of specific proteins which were found in our study are involved in construction of brain 's cytoskeleton,synaptic function,mitochondrial function and so forth.Thus,they may be related to the pathogenic mechanisms of epileptogenicity of CD.

Modelo computacional preliminar de la formación de la superficie cerebral / Preliminary computation form of the cerebral surface development

La corteza cerebral es una lámina gris, formada por cuerpos de neuronas, que cubre los hemisferios cerebrales y cuyo grosor varía de 1,25 mm en el lóbulo occipital a 4 mm en el lóbulo anterior. Debido a los numerosos pliegues que presenta, la superficie cerebral es unas 30 veces mayor que la superficie del cráneo. Estos pliegues forman las circunvoluciones cerebrales, surcos y fisuras y delimitan áreas con funciones determinadas, divididas en cinco lóbulos. La formación de las circunvoluciones puede variar entre individuos y constituyen una característica importante de la formación del cerebro. Estos patrones se pueden representar, de forma matemática, como patrones de Turing. En este artículo se desarrolla un modelo fenomenológico que describe la formación de los patrones de las circunvoluciones que ocurren en la corteza cerebral mediante ecuaciones de reacción difusión con parámetros en el espacio de Turing. Para estudiar la formación de patrones se resuelven varios ejemplos numéricos sobre geometrías simplificadas de un cerebro. Para la solución numérica se utilizó el método de los elementos finitos en conjunto con el método de Newton-Raphson. Los ejemplos numéricos muestran que el modelo puede representar la formación de los pliegues de la corteza cerebral y reproducir patologías de la formación de las circunvoluciones, tales como polimicrogiria y lisencefalia.

Cerebral cortex is a gray layer including neuron bodies covering the cerebral hemispheres and whose thickness fluctuates from 1.25 mm in the occipital lobule to 4 mm in the anterior lobule. Due to the many folds present, la cerebral surface is a thirty times greater than the cranial surface. These folds create the cerebral convolutions, grooves and fissures defining areas with determined functions, divided into five lobules. La convolutions formation may to vary among subjects and are an important characteristic of brain formation. These patterns may be represented in a mathematical way like Turing patterns. The aim of present paper was to design a phenomenological model describing the formation of convolutions patterns occurring in the cerebral cortex by means of diffusion reaction equations with parameters in the Turing space. To study la formation of patterns it is necessary to solve some numerical examples on simplified geometries of a brain. For numerical solution authors used the finite elements method together with the Newton-Raphson method. The numerical examples demonstrate that this model may to represent the folds formation in the cerebral cortex and to reproduce pathologies of the convolutions formation, such as the polymicrogyria and lissencephalous.

Differential expression of Na+-K+-Cl- cotransporter 1 and K+-Cl- cotransporter 2 in the somata and dendrites of adult rat neocortical neurons[1] / 神经解剖学杂志

γ-aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the adult brain. However, electrophysiological findings indicate that GABA exerts excitation in dendrites of mature eorlieal neurons. Little is known about morphological basis of GABA-medi-ated excitation in dendrites of mature cortical neurons. The effect of activated GABAA receptors is mainly determined by intraceUular chloride ion, whose active influx is mainly mediated by Na+-K +-Cl- cotransporter isoform 1 (NKCC1) and exclusion is mainly executed by K+-Cl- cotransporter isoform 2 ( KCC2 ). In the present study, by using immunofluorescent double staining and fluorescent density analysis, the expression and distribution of NKCCI- and KCC2-immunoreactivities in the dendrite and soma of adult rat neocortical neurons were detected in vivo and in vitro. The present results showed that both cytoplasm and membrane of neuronal soma and dendrite expressed NKCC1, while KCC2 only expressed in membrane of soma and dendrite. The results also indicated that the dendrites rather than the somata of neurons expressed more NKCC1 in adult rat neocortex, while the level of KCC2 expression in the dendrite membrane was similar to that in the membrane of somata. The similar expression pattern of NKCC1 and KCC2 in the dendrites and the somata was also observed in neocortical neurons cultured for 20 days in vitro. The present results suggest that the more NKCC1 expreasion in dendrites may contribute to GABA-mediated excitation in neuronal dendrites of adult neocortex neurons.

Memory Consolidating During Sleep / 生物化学与生物物理进展

Sleep and memory are the basic function of the brain. A large number of studies from both humans and animals experiments have offered a substantive body of evidence supporting that sleep contributes crucially to memory consolidation. The processes of memory consolidation in hippocampus and cortex during sleep was reviewed and the primary cellular and molecular mechanism were briefly introduced.

The Effect of Resection Extent Upon Postoperative Outcome of Seizures and Memory in Anterior Temporal Lobectomy with Amygdalohippocampectomy / 대한간질학회지

PURPOSE: To investigate the relationship of the resection extent of hippocampus and temporal neocortex with the postsurgical outcome in patients with mesial temporal lobe epilepsy (TLE). METHODS: Sixty-eight patients with TLE underwent brain MRI pre- and post-operatively. They were divided into two groups by seizure outcomes:seizure free group (SF, N=54) and non-seizure free group (NSF, N=14). Patients were classified further according to the post-surgical memory changes:MD group (with postsurgical memory decline, N=15) and NMD group (without postsurgical memory decline, N=16). The hippocampal resection was estimated by subtracting the length of post-surgical hippocampus from the pre-surgical length. The resection of temporal neocortex was measured by comparing the resection lengths on superior, middle, inferior and basal temporal gyri shown on three dimensional brain MRI. RESULTS: The mean extent of hippocampal resection was significantly larger in SF than in NSF (33.2+/-7.5 mm vs. 24.8+/-7.4 mm p=0.001) while that between MD and NMD was not significantly different. The resection extent of temporal neocortex was not significantly different between SF and NSF as well as between MD and NMD, but the resection extent of basal temporal gyrus of left TLE was significantly larger in MD than in NMD. CONCLUSIONS: The hippocampal resection was significantly greater in SF. The overall resection extent of the temporal neocortex did not correlate to the surgical outcomes of seizures or memory although that of the basal temporal gyrus of the left TLE was larger in MD.

Effects of Experimental Ischemia on Expression of Protein Kinase C Isozyme in Rat Neocortex

Ischemia leads to a complex sequence of events culmination in the loss of functional integrity of the nervous system and, ultimately, in neuronal cell death. Intracellular accumulation of calcium ions following ischemia may alter protein kinase C(PKC) activity. But nature of change of the PKC activity depending on duration and degree of ischemia is not well understood. To understand the effect of the experimental focal ischemia on expression of PKC isozyme, we investigated the expression of PKC gamma, beta, alpha immunocytochemically and activities of cytochrome oxidase(CO) histochemically in focal ischemic brain of the rat. Two groups of focal ischemic infarction were produced in two groups of Sprague Dawley rats(200-300 gm) : Group I, Clip compression of left middle cerebral artery(MCA) for 10min and releases and sacrificed 48 hr later ; Group II, Electric coagulation of left MCA and killed 2-24 hr later. In the group I, CO activity and immunoreactivity(IR) for PKC gamma and beta were decreased generally in the left MCA territory, especially in layers II through IV of ischemic cortex. In the group II, decrease of CO activities and marked increase of three PKC isozyme IRs were noted in the layers I through IV. The isozymes displayed different localization in the control cortex, but the IRs of three isozymes markedly increased in the ischmic region, so that the difference among IR patterns disappeared. Although vacuolation and decrease of number of IR neuron were noted, there were remaining IR pyramidal neurons arounf vacuole in layers IV/V showing dense immuostaining in the cell body and apical dendrite. These results indicate that 10min acute ischemia inhibits activity of PKC gamma and beta and that prolonged ischemia longer than 2hr induces the expression of three PKC isozymes. Inhibition and possible induction of PKC are proposed to represent a critical step during ischemic neuronal injury.

Effects of Experimental Focal Ischemia of PV- and Calbindin-Immunoreactive Neuron of Rat Neocortex

To understand the changes in expression of calcium binding proteins(CaBP) during the experimental focal ischemia, expression of two kinds of CaBP, paralvumin(PV) and calbindin D-28K(Calbindin), immunocytochemically, and activities of cytochrome oxidase(CO) and acetylcholinesterase(AchE), histochemically, in focal ischemic brain of the rat were investigated. Two groups of focal ischemic infarction were produced in Sprague Dawley rats(200-350 mg):Group I, Clip compression of left middle cerebral artery(MCA) for 5-10 mins and release;Group II, Electric coagulation of left MCA for 2-24 hrs. In the group I, CO activity and PV- and Calbindin-immunoreactivity(IR) were decreased in the left MCA territory, and decreased in number of PV- and Calbindin-IR neurons and degree of IR, but AchE activity was nearly same as that of control cortex. In the group II, decrease of CO and AchE activities, and marked increase of PV- and Calbindin IRs were noted on neuropil in the layers I through VI of ischemic region. Characteristically pyramidal cells, which did not express the both CaBPs in the control cortex, of layer V of ischemic cortex showed PV- and Calbindin Irs in the cell body and apical dendrite. These findings suggest that 1) PV- and Calbindin-IR neurons, mainly non-pyramidal cells, are more vulnerable than pyramidal cell to ischemic injury, 2) CaBP may have some roles in hypoxic neuronal injury, and 3) PV and Calbindin-immunocytochemistry can be used as useful technique in evaluation of experimental ischemia.

Transplantation of fetal neocortex in rhesus monkey.

A feasibility study of neural transplantation in adult rhesus monkey was undertaken. Fresh and preserved neocortex containing multiplying and maturing neurons obtained from 55-70 gestation days were transplanted into the striatum, cerebellum and cerebral cortex of adult monkeys. Tissues were preserved for 4 days either at subzero temperature in the freezer compartment of the ordinary refrigerator in Ringer lactate or incubated in culture medium. While 2 monkeys out of 5 injected with preserved tissue had successful transplants after 4 months, all the 10 monkeys injected with fresh tissue had no transplants. The size of the two surviving transplants was small. The neurons in the transplants were mainly in clusters. Many of the cells were immature and some showed early degenerative changes. Neuronal processes were restricted to the transplants and thus showed lack of morphological integration with the host tissue. Further studies are in progress to define the nature of the embryonic tissue of primate which can grow and survive and also the role of neural grafts in functional recovery following experimental lesions of the brain regions.