Brain/MINDS: brain-mapping project in Japan

There is an emerging interest in brain-mapping projects in countries across the world, including the USA, Europe, Australia and China. In 2014, Japan started a brain-mapping project called Brain Mapping by Integrated Neurotechnologies for Disease Studies (Brain/MINDS). Brain/MINDS aims to map the structure and function of neuronal circuits to ultimately understand the vast complexity of the human brain, and takes advantage of a unique non-human primate animal model, the common marmoset (Callithrix jacchus). In Brain/MINDS, the RIKEN Brain Science Institute acts as a central institute. The objectives of Brain/MINDS can be categorized into the following three major subject areas: (i) structure and functional mapping of a non-human primate brain (the marmoset brain); (ii) development of innovative neurotechnologies for brain mapping; and (iii) human brain mapping; and clinical research. Brain/MINDS researchers are highly motivated to identify the neuronal circuits responsible for the phenotype of neurological and psychiatric disorders, and to understand the development of these devastating disorders through the integration of these three subject areas.     

脑电生物反馈训练对ADHD 儿童心理、行为的影响

目的：探讨脑电生物反馈治疗对ADHD儿童心理、行为的影响。方法：对45例ADHD儿童采用脑电生物反馈训练。20次为一个疗程。治疗前和治疗后20、40次分别用症状评定量表进行比较。结果：接受20次训练的ADHD儿童注意、情感、活动水平、异常行为、学业等方面的问题都有明显好转;接受40次训练的ADHD儿童注意、情感、活动水平、异常行为、学业等方面的问题改善十分明显。P值〈0.01差异显著。结论：脑电生物反馈训练能有效地改善儿童注意、情感、活动水平、异常行为、学业等方面的问题。     

Brain ankyrin. A membrane-associated protein with binding sites for spectrin, tubulin, and the cytoplasmic domain of the erythrocyte anion channel

Brain ankyrin was purified from pig brain membranes in milligram quantities by a procedure involving affinity chromatography on erythrocyte spectrinagarose. Brain ankyrin included two polypeptides of Mr = 210,000 and 220,000 that were nearly identical by peptide mapping and were monomers in solution. Brain ankyrin and erythrocyte ankyrin are closely related proteins with the following properties in common: 1) shared antigenic sites, 2) high-affinity binding to the spectrin beta subunit at the midregion of spectrin tetramers, 3) a binding site for the cytoplasmic domain of the erythrocyte anion channel, 4) a binding site for tubulin, 5) a similar domain structure with a protease-resistant domain of Mr = 72,000 that contains the spectrin-binding activity and domains of Mr = 95,000 (brain ankyrin) or 90,000 (erythrocyte ankyrin) that contain binding sites for both tubulin and the anion channel. Brain ankyrin is present at about 100 pmol/mg of membrane protein in demyelinated membranes based on radioimmunoassay with antibody raised against brain ankyrin and affinity purified on brain ankyrin-agarose. Brain spectrin tetramers are present at 30 pmol/mg of membrane protein. Brain ankyrin thus is present in sufficient amounts to attach spectrin to membranes. Brain ankyrin also may attach microtubules to membranes independently of spectrin and has the potential to interconnect microtubules and spectrin-associated actin filaments.     

Brain bank of the Brazilian aging brain study group—a milestone reached and more than 1,600 collected brains

INTRODUCTION: Brain banking remains a necessity for the study of aging brain processes and related neurodegenerative diseases. In the present paper, we report the methods applied at and the first results of the Brain Bank of the Brazilian Aging Brain Study Group (BBBABSG) which has two main aims: (1) To collect a large number of brains of elderly comprising non-demented subjects and a large spectrum of pathologies related to aging brain processes, (2) To provide quality material to a multidisciplinar research network unraveling multiple aspects of aging brain processes and related neurodegenerative diseases. METHODS: The subjects are selected from the Sao Paulo Autopsy Service. Brain parts are frozen and fixated. CSF, carotids, kidney, heart and blood are also collected and DNA is extracted. The neuropathological examinations are carried out based on accepted criteria, using immunohistochemistry. Functional status are assessed through a collateral source based on a clinical protocol. Protocols are approved by the local ethics committee and a written informed consent form is obtained. RESULTS: During the first 21 months, 1,602 samples were collected and were classified by Clinical Dementia Rating as CDR0: 65.7%; CDR0.5:12.6%, CDR1:8.2%, CDR2:5.4%, and CDR3:8.1%. On average, the cost for the processing each case stood at 400 US dollars. To date, 14 laboratories have been benefited by the BBBABSG. CONCLUSION: The high percentage of non- demented subjects and the ethnic diversity of this series may be significantly contributive toward aging brain processes and related neurodegenerative diseases understanding since BBBABSG outcomes may provide investigators the answers to some additional questions.     

Foxj1 在脑外伤后的表达变化

目的:探讨脑外伤后Foxj1在脑组织中的表达变化及其意义。方法:建立大鼠脑外伤模型,利用Western blot和免疫组织化学方法检测脑外伤后Foxj1在脑组织中表达的变化。结果:Western blot显示大鼠脑外伤后,Foxj1的表达逐步增高,伤后3 d升至最高点,之后逐渐降低;免疫组织化学的结果与Western blot一致。结论:脑外伤后Foxj1在脑组织中的表达增高,这种增高的表达参与了脑外伤后脑组织的病理生理和生化变化。     

Book Reviews

Books reviewed:
Bob Blank, Brain Policy: How the New Neuroscience will Change our Lives
Nora Machado, Using the Bodies of the Dead     

Picturing Personhood: Brain Scans and Biomedical Identity

Picturing Personhood: Brain Scans and Biomedical Identity . Joseph Dumit. Princeton: Princeton University Press, 2004. xii. 272 pp.     

Ishi's Brain: In Search of America's Last "Wild" Indian

Ishi's Brain: In Search of America's Last ”Wild„ Indian . Orin Starn. New York: W. W. Norton, 2005. 352 pp.     

Human Language and Our Reptilian Brain: The Subcortical Bases of Speech, Syntax, and Thought

Human Language and Our Reptilian Brain: The Subcortical Bases of Speech, Syntax, and Thought. Philip Lieberman. Cambridge, MA: Harvard University Press, 2000. 221 pp.     

Book Reviews

Book reviews in this article:
Pineal Research Reviews, Volume 4 edited by R. J. Reiter. Alan R. Liss.
Two Hemispheres—One Brain. Functions of the Corpus Callosum (Neurology and Neurobiology, Volume 17) edited by F. Lepore, M. Ptito, and H. H. Jasper. Alan R. Liss.
Molecular and Cellular Mechanisms of Anesthetics edited by S. H. Roth and K. W. Miller.
Memory, Imprinting and the Brain: An Inquiry into Mechanisms (Oxford Psychology Series, Volume 10) by G. Horn.     

Dendritic reorganization in pyramidal neurons in medial prefrontal cortex after chronic corticosterone administration.

Chronic stress produces deficits in cognition accompanied by alterations in neural chemistry and morphology. For example, both stress and chronic administration of corticosterone produce dendritic atrophy in hippocampal neurons (Woolley C, Gould E, McEwen BS. 1990. Exposure to excess glucocorticoids alters dendritic morphology of adult hippocampal pyramidal neurons. Brain Res 531:225-231; Watanabe Y, Gould E, McEwen BS, 1992b. Stress induces atrophy of apical dendrites of hippocampal CA3 pyramidal neurons. Brain Res 588:341-345). Prefrontal cortex is also a target for glucocorticoids involved in the stress response (Meaney MJ, Aitken DH. 1985. [(3)H]Dexamethasone binding in rat frontal cortex. Brain Res 328:176-180); it shows neurochemical changes in response to stress (e.g., Luine VN, Spencer RL, McEwen BS. 1993. Effect of chronic corticosterone ingestion on spatial memory performance and hippocampal serotonergic function. Brain Res 616:55-70; Crayton JW, Joshi I, Gulati A, Arora RC, Wolf WA. 1996. Effect of corticosterone on serotonin and catecholamine receptors and uptake sites in rat frontal cortex. Brain Res 728:260-262; Takao K, Nagatani T, Kitamura Y, Yamawaki S. 1997. Effects of corticosterone on 5-HT(1A) and 5-HT(2) receptor binding and on the receptor-mediated behavioral responses of rats. Eur J Pharmacol 333:123-128; Sandi C, Loscertales M. 1999. Opposite effects on NCAM expression in the rat frontal cortex induced by acute vs. chronic corticosterone treatments. Brain Res 828:127-134), and mediates many of the behaviors that are altered by chronic corticosterone administration (e.g., Lyons DM, Lopez JM, Yang C, Schatzberg AF. 2000. Stress-level cortisol treatment impairs inhibitory control of behavior in monkeys. J Neurosci 20:7816-7821). To determine if glucocorticoid-induced morphological changes also occur in medial prefrontal cortex, the effects of chronic corticosterone administration on dendritic morphology in this corticolimbic structure were assessed. Adult male rats received s.c. injections of either corticosterone (10 mg in 250 microL sesame oil; n = 8) or vehicle (250 microL; n = 8) daily for 3 weeks. A third group of rats served as intact controls (n = 4). Brains were stained using a Golgi-Cox procedure and pyramidal neurons in layer II-III of medial prefrontal cortex were drawn; dendritic morphology was quantified in three dimensions. Sholl analyses demonstrated a significant redistribution of apical dendrites in corticosterone-treated animals: the amount of dendritic material proximal to the soma was increased relative to intact rats, while distal dendritic material was decreased relative to intact animals. Thus, chronic glucocorticoid administration dramatically reorganized apical arbors in medial prefrontal cortex. This reorganization likely reflects functional changes and may contribute to stress-induced changes in cognition.     

Visualization of polyribosomes in the postsynaptic area of the squid giant synapse by electron spectroscopic imaging

Brain Cell Biology - Giant axons from squids (Loligo vulgaris andLoligo pealii) were studied by conventional electron microscopy and by electron spectroscopic imaging: electrons with a...     

Origins of the Human Brain

Origins of the Human Brain. J. P. Changeux and J. Chavaillon. eds. Oxford, England: Oxford University Press, 1995. 321 pp.     

Book Reviews

Book Reviewed in this article:
Molecular Biology of Brain and Endocrine Peptidergic Systems edited by Michel Chretien and Kenneth W. McKerns.
Neurotoxins in Neurochemistry edited by J. O. Dolly.     

Dendritic reorganization in pyramidal neurons in medial prefrontal cortex after chronic corticosterone administration

Chronic stress produces deficits in cognition accompanied by alterations in neural chemistry and morphology. For example, both stress and chronic administration of corticosterone produce dendritic atrophy in hippocampal neurons (Woolley C, Gould E, McEwen BS. 1990. Exposure to excess glucocorticoids alters dendritic morphology of adult hippocampal pyramidal neurons. Brain Res 531:225–231; Watanabe Y, Gould E, McEwen BS, 1992b. Stress induces atrophy of apical dendrites of hippocampal CA3 pyramidal neurons. Brain Res 588:341–345). Prefrontal cortex is also a target for glucocorticoids involved in the stress response (Meaney MJ, Aitken DH. 1985. [³H]Dexamethasone binding in rat frontal cortex. Brain Res 328:176–180); it shows neurochemical changes in response to stress (e.g., Luine VN, Spencer RL, McEwen BS. 1993. Effect of chronic corticosterone ingestion on spatial memory performance and hippocampal serotonergic function. Brain Res 616:55–70; Crayton JW, Joshi I, Gulati A, Arora RC, Wolf WA. 1996. Effect of corticosterone on serotonin and catecholamine receptors and uptake sites in rat frontal cortex. Brain Res 728:260–262; Takao K, Nagatani T, Kitamura Y, Yamawaki S. 1997. Effects of corticosterone on 5‐HT_1A and 5‐HT₂ receptor binding and on the receptor‐mediated behavioral responses of rats. Eur J Pharmacol 333:123–128; Sandi C, Loscertales M. 1999. Opposite effects on NCAM expression in the rat frontal cortex induced by acute vs. chronic corticosterone treatments. Brain Res 828:127–134), and mediates many of the behaviors that are altered by chronic corticosterone administration (e.g., Lyons DM, Lopez JM, Yang C, Schatzberg AF. 2000. Stress‐level cortisol treatment impairs inhibitory control of behavior in monkeys. J Neurosci 20:7816–7821). To determine if glucocorticoid‐induced morphological changes also occur in medial prefrontal cortex, the effects of chronic corticosterone administration on dendritic morphology in this corticolimbic structure were assessed. Adult male rats received s.c. injections of either corticosterone (10 mg in 250 μL sesame oil; n = 8) or vehicle (250 μL; n = 8) daily for 3 weeks. A third group of rats served as intact controls (n = 4). Brains were stained using a Golgi‐Cox procedure and pyramidal neurons in layer II‐III of medial prefrontal cortex were drawn; dendritic morphology was quantified in three dimensions. Sholl analyses demonstrated a significant redistribution of apical dendrites in corticosterone‐treated animals: the amount of dendritic material proximal to the soma was increased relative to intact rats, while distal dendritic material was decreased relative to intact animals. Thus, chronic glucocorticoid administration dramatically reorganized apical arbors in medial prefrontal cortex. This reorganization likely reflects functional changes and may contribute to stress‐induced changes in cognition. © 2001 John Wiley & Sons, Inc. J Neurobiol 49: 245–253, 2001     

Brain fatty acids in perinatal asphyxia

In hypoxic or ischemic states the release of fatty acids is proposed to have several harmful effects on brain structure and function. We therefore decided to study brain FFA in a simple, clinically related animal model resembling intrauterine perinatal asphyxia (PA). Cerebral blood flow (CBF), brain fatty acids (C14:0, C16:1, C16:0, C18:1, C1 8:0, sigma C), plasma glucose, lactate, beta-hydroxybutyrate (beta-OHB), non-esterified fatty acids (NEFA) and insulin were determined in PA and compared to the normoxic state. Brain C 14:0 FFA were not significantly different from normoxic rats. Brain FFA C 16:0 were comparable between groups but significantly decreased at 20 min of PA. C 18:0 FFA showed a trend to increase with the length of PA reaching significance at 10 min of asphyxia only and were declining at 20 min, however, not significantly. Brain C 16:1 and C 18:1 FFA concentrations were comparable between groups. The parameters cerebral blood flow, glucose and lactate showed a stepwise and significant increase with the length of PA, whereas beta-HOB, NEFA and insulin showed no changes. CBF, glucose and lactate showed a strong association whereas other parameters failed to correlate with each other. Only inconsistent trends of increased brain FFA were found and the association between brain glucose and brain FFA could be ruled out. Although CBF was manifold and significantly elevated in PA, brain FFA pattern suggests that the increase of CBF is obviously not mediated by brain FFA. We conclude that FFA may not be involved in the early phase-pathogenesis of PA.     

Book Reviews

Books review in this article:
Modulators, Mediators, and Specifiers in Brain Function. Interactions of Neuropeptides, Cyclic Nucleotides, and Phosphoproteins in Mechanisms Underlying Neuronal Activity, Behaviour, and Neuropsychiatric Disorders . Y. H. Ehrlich, J. Volavka, L. G. Davis, and E. G. Brunngraber (editors)
Advances in Neurology, Vol. 23: Huntington's Disease edited by T. N. Chase, N. S. Wexler, and A. Barbeau
Dopaminergic Ergot Derivatives and Motor Function edited by Kjell Fuxe and Donald B. Calne
Immunocytochemistry by Ludwig A. Sternberger
Molecular Neurobiology of the Mammalian Brain J. Eccles, P. L. McGeer and E. McGeer
Neurobiology of Chemical Transmission edited by Masanori Otsuka and Zach Hall     

Book Reviews

Books review in this article:
Ciba Foundation Symposium 91, Substance P in the Nervous System edited by R. Porter and M. O'Connor
Aging, Vol. 23: Aging Brain and Ergot Alkaloids edited by Alessandro Agnoli, Gaetano Crepaldi, Pier Franco Spano, and Marco Trabucchi
Neurophysiology: The Fundamentals by Robert A. Lavine     

Expression of Vascular Endothelial Growth Factor A and Its Type 1 Receptor in Supratentorial Neoplasm

Background:Vascular endothelial growth factor (VEGF) is one of the primary angiogenesis regulators in solid cancers. Brain solid tumors are life-threatening diseases in which angiogenesis is an important phase of tumor development and progression. In the present study, VEGF-A and VEGF receptor (VEGF-R1) gene expression was evaluated in CNS brain tumors.Methods:VEGF-A and VEGF-R1 expression was quantified using real-time PCR on fresh biopsies of 38 supratentorial brain tumors compared to 30 non-tumoral tissues. Then, the correlations were investigated with clinic-pathological and demographic factors of the patients.Results:PCR product sequencing confirmed the validity of qRT-PCR. Although VEGF-A and VEGF-R1 expression showed increasing trends with the progression of cell proliferation in different stages of astrocytoma, VEGF-R1 did not meet the 95% confidence interval in other brain tumors. An increasing trend in VEGF-A expression and a declining trend in VEGF-R1 expression from Stage I to II were observed in meningioma. VEGF-A and VEGF-R1 expression had no significant correlation with age and gender. Although peritumoral brain edema (PTBE) in astrocytoma was significantly associated with tumor stages, VEGF-A and VEGF-R1 were not correlated with PTBE in meningioma and metastasis.Conclusion:VEGF-A is a valuable factor for the prognosis of PTBE and malignancy in astrocytoma and is helpful in monitoring treatment approaches.Key Words: Angiogenesis, Brain edema, Brain neoplasm, Peritumoral brain, VEGF, VEGFR1     

Book Reviews

Book Review in this Article:
Arterial Behavior and Blood Circulation in the Brain by George Mchedlishvili.
Model Systems in Neurotoxicology. Alternative Approaches to Animal Testing edited by A. Shahar and A. M. Goldberg.