EL BLOG DEL AMEINNN
Y DE LAS NEUROCIENCIAS (MEXICO)
El blog tiene como finalidad facilitar la comunicación y compartir las cosas que nos son comunes a los egresados del Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, tambien tiene como
finalidad incluir los comentarios y contribuciones de la comunidad neurocientifica de Mexico
J. Pineal Res. 2011; 50:29–37
Gerardo Ramirez-Rodriguez, Leonardo Ortíz-López, Aline Domínguez-Alonso, Gloria A. Benítez-King and Gerd Kempermann
1Laboratory of Neurogenesis, Department of Neuropharmacology, National Institute of Psychiatry. Mexico D.F., Mexico; 2Department of Neuropharmacology, National Institute of Psychiatry, Mexico D.F., Mexico; 3CRTD –Center for Regenerative Therapies Dresden,
Dresden, Germany
Fig. 6. Schematic representation of melatonin effects altering dendrite complexity of new neurons. Chronic melatonin treatment (8 mg/kg) for 14 days increases dendrite complexity of new neurons identified by doublecortin staining (imagen de abajo) , while in mice treated with vehicle the number of immature neurons and neurons with more complex dendrites are lower than that in melatonin-treated mice (imagen de arriba). Draw box shows the events corresponding to the cell survival and dendrite maturation of the neurogenic process in which melatonin plays a role.
Abstract: In the course of adult hippocampal neurogenesis, the postmitotic maturation and survival phase is associated with dendrite maturation. Melatonin modulates the survival of new neurons with relative specificity. During this phase, the new neurons express microtubule-associated protein doublecortin (DCX). Here, we show that the entire population of cells expressing DCX is increased after 14 days of treatment with melatonin. As melatonin also affects microtubule polymerization which is important for neuritogenesis and dendritogenesis, we studied the consequences of chronic melatonin administration on dendrite maturation of DCX-positive cells. Treatment with melatonin increased the number of DCX-positive immature neurons with more complex dendrites. Sholl analysis revealed that melatonin treatment lead to greater complexity of the dendritic tree. In addition, melatonin increased the total volume of the granular cell layer. Besides its survival-promoting effect, melatonin thus also increases dendritic maturation in adult neurogenesis. This might open the opportunity of using melatonin as an adjuvant in attempts to extrinsically stimulate adult hippocampal neurogenesis in neuropsychiatric disease, dementia or cognitive ageing.
Eri Segi-Nishida, Jennifer L. Warner-Schmidt, and Ronald S. Duman*
Laboratory of Molecular Psychiatry, Department of Psychiatry and Pharmacology, Yale University School of Medicine, New Haven, CT 06508
Edited by Fred H. Gage, Salk Institute for Biological Studies, San Diego, CA, and approved May 7, 2008 (received for review November 15, 2007)
All classes of antidepressants increase hippocampal cell proliferation and neurogenesis, which contributes, in part, to the behavioral actions of these treatments. Among antidepressant treatments, electroconvulsive seizure (ECS) is the most robust stimulator of hippocampal cell proliferation and the most efficacious treatment for depression, but the cellular mechanisms underlying the actions of ECS are unknown. To address this question, we investigated the effect of ECS on proliferation of neural stem-like and/or progenitor cells in the subgranular zone of rat dentate gyrus. We define the neural differentiation cascade from stem-like cells to early neural progenitors (also referred to as quiescent and amplifying neural progenitors, respectively) by coexpression of selective cellular and mitotic activity markers. We find that at an early mitotic phase ECS increases the proliferation of quiescent progenitors and then at a later phase increases the proliferation of amplifying progenitors. We further demonstrate that vascular endothelial growth factor (VEGF) signaling is necessary for ECS induction of quiescent neural progenitor cell proliferation and is sufficient to produce this effect. These findings demonstrate that ECS and subsequent induction of VEGF stimulates the proliferation of neural stem-like cells and neural progenitor cells, thereby accounting for the superior neurogenic actions of ECS compared with chemical antidepressants.
Bearden CE, Thompson PM, Avedissian C, Klunder AD, Nicoletti M, Dierschke N, Brambilla P and Soares JC (2009) Altered
hippocampal morphology in unmedicated patients with major depressive illness. ASN NEURO 1(4):art:e00020.doi:10.1042/AN20090026
ABSTRACT
Despite converging evidence that major depressive illness is associated with both memory impairment and hippocampal pathology, findings vary widely across studies and it is not known whether these changes are regionally specific.
In the present study we acquired brain MRIs (magnetic resonance images) from 31 unmedicated patients with MDD (major depressive disorder; mean age 39.2 + -11.9 years; 77% female) and 31 demographically comparable controls. Three-dimensional parametric mesh models were created to examine localized alterations of hippocampal morphology. Although global volumes did not differ between groups, statistical mapping results revealed that in MDD patients, more severe depressive symptoms were associated with greater left hippocampal atrophy, particularly in CA1 (cornu ammonis 1) subfields and the subiculum. However, previous treatment with atypical antipsychotics was associated with a trend towards larger left hippocampal volume. Our findings suggest effects of illness severity on hippocampal size, as well as a possible effect of past history of atypical antipsychotic treatment, which may reflect prolonged neuroprotective effects. This possibility awaits confirmation in longitudinal studies.
Key words: antipsychotic, brain mapping, hippocampus,
mood disorder, neuroimaging, subiculum, unipolar depression.
Effect of plasma exchange in accelerating natalizumab clearance and restoring leukocyte function
B O. Khatri, S Man, G Giovannoni, A P. Koo, J-C Lee, B Tucky, F Lynn, S Jurgensen, J Woodworth, S Goelz, P W. Duda, M A. Panzara, R M. Ransohoff, and R J. Fox
Neurology. 2009 February 3; 72(5): 402–409. doi: 10.1212/01.wnl.0000341766.59028.9d.
Reactivation of Human Herpesvirus-6 in Natalizumab Treated Multiple Sclerosis Patients
Karen Yao, Susan Gagnon, Nahid Akhyani, Elizabeth Williams, Julie Fotheringham, Elliot Frohman, Olaf Stuve, Nancy Monson, Michael K. Racke, and Steven Jacobson
PLoS ONE. 2008; 3(4): e2028. Published online 2008 April 30. doi: 10.1371/journal.pone.0002028.
Immunologic, clinical, and radiologic status 14 months after cessation of natalizumab therapy
O Stüve, P D. Cravens, E M. Frohman, J T. Phillips, G M. Remington, G von Geldern, S Cepok, M P. Singh, J W. Cohen Tervaert, M De Baets, D MacManus, D H. Miller, E W. Radü, E M. Cameron, N L. Monson, S Zhang, R Kim, B Hemmer, and M K. Racke
Neurology. 2009 February 3; 72(5): 396–401. doi: 10.1212/01.wnl.0000327341.89587.76.
Increased numbers of circulating hematopoietic stem/progenitor cells are chronically maintained in patients treated with the CD49d blocking antibody natalizumab
Evaluation of Patients Treated with Natalizumab for Progressive Multifocal Leukoencephalopathy
Tarek A. Yousry, Eugene O. Major, Caroline Ryschkewitsch, Gary Fahle, Steven Fischer, Jean Hou, Blanche Curfman, Katherine Miszkiel, Nicole Mueller-Lenke, Esther Sanchez, Frederik Barkhof, Ernst-Wilhelm Radue, Hans R. Jäger, and David B. Clifford
N Engl J Med. Author manuscript; available in PMC 2007 July 30.
PMCID: PMC1934511
Published in final edited form as: N Engl J Med. 2006 March 2; 354(9): 924–933. doi: 10.1056/NEJMoa054693.
Remitting–relapsing multiple sclerosis patient refractory to conventional treatments and bone marrow transplantation who responded to natalizumab
Athanasia Mouzaki, Maria Koutsokera, Zoe Dervilli, Maria Rodi, Dimitra Kalavrizioti, Nikolaos Dimisianos, Ioannis Matsoukas, and Panagiotis Papathanasopoulos
Int J Gen Med. 2010; 3: 313–320. Published online 2010 October 5. doi: 10.2147/IJGM.S13648.
GLANCE: Results of a phase 2, randomized, double-blind, placebo-controlled study
A D. Goodman, H Rossman, A Bar-Or, A Miller, D H. Miller, K Schmierer, F Lublin, O Khan, N M. Bormann, M Yang, M A. Panzara, A W. Sandrock, and For the GLANCE Investigators
Neurology. 2009 March 3; 72(9): 806–812. doi: 10.1212/01.wnl.0000343880.13764.69.
