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Search Results: 1 - 10 of 655 matches for " Temugin Berta "
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Microglia and Spinal Cord Synaptic Plasticity in Persistent Pain
Sarah Taves,Temugin Berta,Gang Chen,Ru-Rong Ji
Neural Plasticity , 2013, DOI: 10.1155/2013/753656
Abstract: Microglia are regarded as macrophages in the central nervous system (CNS) and play an important role in neuroinflammation in the CNS. Microglial activation has been strongly implicated in neurodegeneration in the brain. Increasing evidence also suggests an important role of spinal cord microglia in the genesis of persistent pain, by releasing the proinflammatory cytokines tumor necrosis factor-alpha (TNFα), Interleukine-1beta (IL-1β), and brain derived neurotrophic factor (BDNF). In this review, we discuss the recent findings illustrating the importance of microglial mediators in regulating synaptic plasticity of the excitatory and inhibitory pain circuits in the spinal cord, leading to enhanced pain states. Insights into microglial-neuronal interactions in the spinal cord dorsal horn will not only further our understanding of neural plasticity but may also lead to novel therapeutics for chronic pain management. 1. Microglia-Synapse Interactions in Healthy CNS Microglia are derived from myeloid precursor cells in the periphery and penetrate the central nervous system (CNS) during embryogenesis [1]. They account for approximately 10–20% of all cells in the CNS, however their distribution varies from one region to another [2, 3]. Microglial density is particularly high in the hippocampus, basal ganglia, substantia nigra, and spinal cord [2, 4]. Microglia are regarded as the resident macrophages in the CNS and, similar to peripheral macrophages, they display different morphology depending upon their physiological states. In the resting physiological state, microglial cells are ramified with slender, radially projecting processes with similar thickness, length, and ramification, whereas in pathological states, microglia can be activated presenting an amoeboid morphology characterized by large soma, short/thick, and radially projecting processes with few ramifications [4–6]. Although most studies have focused on the role of activated microglia and synaptic transmission, both resting and activated microglia dynamically interact with synapses shaping their connectivity and function [7]. Microglial processes constantly and dynamically survey their environment and interact with nearby synapses [8, 9]. In mature CNS, it has been observed that microglial processes interact with axon terminals and dendritic spines in a transient manner, for an average of five minutes and at a rate of approximately one microglial contact per hour [10]. Notably, microglia processes are driven by neuronal activity and can simultaneously interact with both presynaptic and postsynaptic
Acute morphine activates satellite glial cells and up-regulates IL-1β in dorsal root ganglia in mice via matrix metalloprotease-9
Temugin Berta, Tong Liu, Yen-Chin Liu, Zhen-Zhong Xu, Ru-Rong Ji
Molecular Pain , 2012, DOI: 10.1186/1744-8069-8-18
Abstract: Subcutaneous morphine injection (10 mg/kg) induced robust peripheral glial responses, as evidenced by increased GFAP expression in DRGs but not in spinal cords. The acute morphine-induced GFAP expression is transient, peaking at 2 h and declining after 3 h. Acute morphine treatment also increased IL-1β immunoreactivity in SGCs and IL-1β activation in DRGs. MMP-9 and GFAP are expressed in DRG neurons and SGCs, respectively. Confocal analysis revealed a close proximity of MMP-9 and GFAP immunostaining. Importantly, morphine-induced DRG up-regulation of GFAP expression and IL-1β activation was abolished after Mmp9 deletion or naloxone pre-treatment. Finally, intrathecal injections of IL-1β-selective siRNA not only reduced DRG IL-1β expression but also prolonged acute morphine-induced analgesia.Acute morphine induces opioid receptors- and MMP-9-dependent up-regulation of GFAP expression and IL-1β activation in SGCs of DRGs. MMP-9 could mask and shorten morphine analgesia via peripheral neuron-glial interactions. Targeting peripheral glial activation might prolong acute opioid analgesia.Mounting evidence indicates that activation of spinal cord glial cells such as microglia and astrocytes plays a crucial role in the pathogenesis of chronic pain [1-7]. In particular, chronic opioid exposure induces profound changes in spinal cord microglia and astrocytes [8-10]. Upon activation spinal glial cells produce multiple proinflammatory cytokines such as TNF-α, IL-1β, and IL-6 to antagonize morphine analgesia and promote morphine tolerance [11-14], via sensitization of spinal cord dorsal horn neurons [15-17]. For example, IL-1β has been shown to counteract opioid-induced analgesia following both chronic and acute administration of morphine [18]. While intrathecal injection of the inteurleukin-1 receptor (IL-1R) antagonist potentiates acute morphine analgesia [11], intrathecal administration of IL-1β induces heat hyperalgesia [15]. Of interest genetic polymorphism of IL-1R antagon
Acute morphine induces matrix metalloproteinase-9 up-regulation in primary sensory neurons to mask opioid-induced analgesia in mice
Yen-Chin Liu, Temugin Berta, Tong Liu, Ping-Heng Tan, Ru-Rong Ji
Molecular Pain , 2012, DOI: 10.1186/1744-8069-8-19
Abstract: Subcutaneous morphine induced a marked up-regulation of MMP-9 protein in DRGs but not spinal cords. Morphine also increased MMP-9 activity and mRNA expression in DRGs. MMP-9 up-regulation peaked at 2 h but returned to the baseline after 24 h. In DRG tissue sections, MMP-9 is expressed in small and medium-sized neurons that co-express mu opioid receptors (MOR). In DRG cultures, MOR agonists morphine, DAMGO, and remifentanil each increased MMP-9 expression in neurons, whereas the opioid receptor antagonist naloxone and the MOR-selective antagonist D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP) suppressed morphine-induced MMP-9 expression. Notably, subcutaneous morphine-induced analgesia was enhanced and prolonged in Mmp9 knockout mice and also potentiated in wild-type mice receiving intrathecal injection of MMP-9 inhibitors. Consistently, intrathecal injection of specific siRNA targeting MMP-9 reduced MMP-9 expression in DRGs and enhanced and prolonged morphine analgesia. Subcutaneous morphine also produced heat hyperalgesia at 24 h, but this opioid-induced hyperalgesia was not enhanced after MMP-9 deletion or inhibition.Transient MMP-9 up-regulation in DRG neurons can mask opioid analgesia, without modulating opioid-induced hyperalgesia. Distinct molecular mechanisms (MMP-9 dependent and independent) control acute opioid-induced pronociceptive actions (anti-analgesia in the first several hours and hyperalgesia after 24 h). Targeting MMP-9 may improve acute opioid analgesia.Opioids especially mu opioid receptor (MOR) agonists remain to be the most effective treatment for moderate to severe pain. MOR is expressed by primary sensory neurons including small-sized (C-fiber) and medium-sized (Aδ-fiber) neurons in the dorsal root ganglia (DRGs) [1-5]. MOR is also expressed in primary afferent terminals and lamina II interneurons in the spinal cord [1,6-8]. MOR agonist, such as [D-Ala2, N-Me-Phe4, Gly5-ol]-enkephalin (DAMGO) elicits potent presynaptic inhibition via suppress
Large A-fiber activity is required for microglial proliferation and p38 MAPK activation in the spinal cord: different effects of resiniferatoxin and bupivacaine on spinal microglial changes after spared nerve injury
Marc R Suter, Temugin Berta, Yong-Jing Gao, Isabelle Decosterd, Ru-Rong Ji
Molecular Pain , 2009, DOI: 10.1186/1744-8069-5-53
Abstract: SNI induced robust mechanical allodynia and p38 activation in spinal microglia. SNI also induced marked cell proliferation in the spinal cord, and all the proliferating cells (BrdU+) were microglia (Iba1+). Bupivacaine induced a complete sensory and motor blockade and also significantly inhibited p38 activation and microglial proliferation in the spinal cord. In contrast, and although it produced an efficient nociceptive block, RTX failed to inhibit p38 activation and microglial proliferation in the spinal cord.(1) Blocking peripheral input in TRPV1-positive fibers (presumably C-fibers) is not enough to prevent nerve injury-induced spinal microglial activation. (2) Peripheral input from large myelinated fibers is important for microglial activation. (3) Microglial activation is associated with mechanical allodynia.Injuries to peripheral nervous system can result in neuropathic pain and contribute to chronic post-operative pain [1]. Current treatments for persistent post-operative pain are not satisfactory and prevention at early stage might be important for the success [2]. Section of a peripheral nerve induces injury discharges at the time of injury followed by spontaneous activity in the axons and soma of primary sensory neurons. The onset of spontaneous activity is strongly implicated in the generation of neuropathic pain [3-6]. However, the relative contribution of different types of primary afferents to the genesis of spontaneous activity is still under debate. Many studies demonstrated that A-fibers are the principal contributors of ectopic firing from the periphery following nerve injury [7-11]. Some studies also reported spontaneous activity in C-fibers but at different times after nerve injury, either very early during the first 15 minutes [12] or later after a few days [13]. The C-fibers' activity was also found in the neighbouring intact spinal nerve after spinal nerve ligation [5] or after stimulation of a nerve stump with nociceptive mediators [14]. Int
A competência reflexiva processual em servi?o social na a??o profissional junto às popula??es
Granja, Berta;
Cadernos de Pesquisa , 2011, DOI: 10.1590/S0100-15742011000200006
Abstract: this article is the result of ethnographic research that was carried out in portugal, brazil and canada on the professional activities of social assistants. it is centered on aspects relating to the knowledge that is constructed during their interaction with the population. the professional activity of social assistants responds to problems that individuals experience in a singular way; these responses result from the way the social, economic and political structures as well as the systems which influence the lifestyle, life paths and living conditions of individuals, groups and both their individual and collective identities. the answer to these problems in action demands professional knowledge that comes from a specific social and cognitive structure; this knowledge is the basis of the identity form constructed and reconstructed by individual and collective reflection as well as the affirmation of professional autonomy in their actions. the professionals work under constant tension, intrinsic to the action itself, in order to reinvent and adapt procedures that are difficult to codify and formalize when complex social relationships intersect with diverse and at times, antagonistic logics. the tensions, conflicts and limits within the context of the interaction with populations are factors of uncertainty and complexity. to act under these conditions, the professionals need a pattern of regularity and generality that establishes itself as the professional procedures for action, as this article shows.
Georges Banu (dir.), Les cités du théatre d’art – de Stanislavski à Strehle
Berta Teixeira
Revista Crítica de Ciências Sociais , 2012,
Abstract: Les cités du théatre d’art - de Stanislavski à Strehler é uma obra colectiva dirigida por Georges Banu, cuja publica o resulta de uma pesquisa preliminar sobre o conceito de théatre d’art. Esta no o serviu de base a um colóquio europeu co-organizado pela Universidade Paris III e a Académie Expérimentale des Théatres, tendo ainda como associadas diversas institui es teatrais e de pesquisa, entre outras, o Théatre du Rond-Point – Compagnie Marcel Maréchal, o Théatre du Vieux-Colombier, o Pic...
Para romper el ghetto
Berta Hiriart
Política y cultura , 1992,
Sistemas médicos en Mali en zona de inmigración: interacciones pasadas y presentes entre lo local y lo global.
Relaciones Internacionales , 2009,
Tiro à queima-roupa
Berta Waldman
Novos Estudos - CEBRAP , 2007, DOI: 10.1590/s0101-33002007000100014
Informe sobre las "piedras campana" del Arroyo de la Virgen en Uruguay
Mariana Berta
Revista musical chilena , 2008,
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