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Search Results: 1 - 10 of 77507 matches for " Ming-gao Zhao "
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Enhanced quantal release of excitatory transmitter in anterior cingulate cortex of adult mice with chronic pain
Hiroki Toyoda, Ming-Gao Zhao, Min Zhuo
Molecular Pain , 2009, DOI: 10.1186/1744-8069-5-4
Abstract: The ACC is involved in major brain functions including learning, memory, and persist pain [1-9]. Recently, a number of studies consistently suggest that the ACC plays important roles in processing pain-related information in humans and in the behavioral responses to noxious stimuli or tissue injury in animals [3,6,10-14]. As for the mechanisms of pain transmission and modulation, it has been proposed that the enhancement of synaptic transmission contributes to chronic pain. For example, we have shown that excitatory synaptic transmission was enhanced in the ACC of mice with persistent inflammatory pain [15] and neuropathic pain [7]. There are at least two main evidences supporting for presynaptic changes of glutamate release in the ACC after the nerve injury: First, we demonstrated that paired-pulse facilitation (PPF), a phenomenon in which activation of a synapse at shorter intervals results in a presynaptic facilitation of transmitter release in response to the second stimulus [16] was apparently reduced in ACC synapses with chronic pain [7,15]. Second, we showed that the rate of MK-801 (NMDA receptor antagonist) blocking was significantly faster in ACC synapses with chronic pain together with the increase of mEPSCs rate [7,15]. Therefore, it is likely that peripheral inflammation or nerve injury produces increases in mean quantal content in ACC synapses.The quantal content of transmission at a synapse is determined by the number of releasable quanta (N) that corresponds to the number of functional vesicles, and the probability (p) of each quantum to be released. Although our previous studies demonstrated that presynaptic neurotransmitter release was enhanced by peripheral inflammation and neuropathic pain in ACC synapses [7,15], the exact changes in these quantal parameters remains to be investigated. To examine the source of the enhanced presynaptic neurotransmitter release, here we performed quantal analysis of excitatory synaptic transmission with inflammatory
5,12-Dimethylpyrazino[1,2-a:4,5-a′]dibenzimidazole-5,12-diium dichloride dihydrate
Jie Han,Ming-gao Zhao,Jun Zhang,Lan Ma
Acta Crystallographica Section E , 2012, DOI: 10.1107/s1600536812046594
Abstract: The title hydrated salt, C18H18N42+·2Cl ·2H2O, sits about an inversion centre, such that the asymmetric unit contains one half-molecule. In the crystal, hydrogen bonds occur between the water molecules and chloride anions, and there is π–π stacking of the benzene and imidazole rings of inversion-related pairs of molecules, with a centroid–centroid distance of 3.704 (17) .
2-Chloromethyl-1-methyl-1,3-benzimidazole
Jie Han,Jun Zhang,Qi Yang,Ming-gao Zhao
Acta Crystallographica Section E , 2011, DOI: 10.1107/s1600536811028376
Abstract: The title compound, C9H9ClN2, was prepared from the reaction of N-methylbenzene-1,2-diamine and 2-chloroacetic acid in boiling 6 M hydrochloric acid. The benzimidazole unit is approximately planar, the largest deviation from the mean plane being 0.008 (1) . The Cl atom is displaced by 1.667 (2) from this plane. The methyl group is statistically disordered with equal occupancy.
Requirement of extracellular signal-regulated kinase/mitogen-activated protein kinase for long-term potentiation in adult mouse anterior cingulate cortex
Hiroki Toyoda, Ming-Gao Zhao, Hui Xu, Long-Jun Wu, Ming Ren, Min Zhuo
Molecular Pain , 2007, DOI: 10.1186/1744-8069-3-36
Abstract: The prefrontal cortex, including the anterior cingulate cortex (ACC) is believed to play important roles in emotion, learning, memory and persistent pain in the adult brain [1-7]. Long-term potentiation (LTP), known to be involved in learning and memory, is a key synaptic mechanism for cortical synaptic plasticity [8]. Recent studies demonstrate that LTP can be induced in the cingulate slices [3,9,10]. However, several recent studies showed that molecular signaling pathways involved in the synaptic potentiation in the ACC differ from those in the hippocampus. For example, both N-methyl-D-aspartate (NMDA) receptor subunit 2A and 2B (NR2A and NR2B) contribute to cingulate LTP [3], while NR2A is preferentially contributing to hippocampal LTP [11,12]. For calcium-related signaling messengers, calcium-calmodulin (CaM) dependent adenylyl cyclase (AC) type 1 is critical for synaptic LTP in the ACC [9], while AC1 deletion alone did not affect hippocampal LTP [13]. On the other hand, the downstream targets of calcium-stimulated cAMP-dependent signaling pathways underlying LTP in the ACC synapses have been far less investigated compared to hippocampal synapses.As the downstream target of cAMP signaling pathways, mitogen-activated protein kinase (MAPK) is well characterized in the hippocampus [14,15]. The MAPK is a family of serine/threonine protein kinases that transduce extracellular signals from cell surface receptors to the cell nucleus [16,17]. The MAPK cascade includes extracellular signal-regulated (ERK), p38, c-Jun N-terminal kinase (JNK), and ERK5 [17]. The activation of ERK is coupled to stimulation of cell surface receptors via several different upstream signaling pathways, and plays critical roles in the regulation of gene expression and cell proliferation [18]. In neurons, the ERK signaling pathway is activated by synaptic activity such as membrane depolarization, calcium influx and neurotrophins [19-21]. Furthermore, the ERK signaling pathway might regulate synap
Calcium/calmodulin-dependent kinase IV contributes to translation-dependent early synaptic potentiation in the anterior cingulate cortex of adult mice
Hiroki Toyoda, Ming-Gao Zhao, Valentina Mercaldo, Tao Chen, Giannina Descalzi, Satoshi Kida, Min Zhuo
Molecular Brain , 2010, DOI: 10.1186/1756-6606-3-27
Abstract: The long-lasting changes of neural circuitry in forebrain structures including the anterior cingulate cortex (ACC) are believed to contribute to emotion, learning, memory and pain [1-6], and such long-term changes in neural circuitry may require new protein synthesis. Long-term potentiation (LTP) is typically divided into early-phase and late-phase LTP, in which the latter is mainly thought to be dependent on protein synthesis. At the CA1 [7] and CA3 [8] synapses, protein synthesis inhibitors disrupt late-phase but not early-phase LTP. By contrast, other studies reported that early-phase LTP in CA1 [9], CA3 [10], and dentate gyrus [11] was suppressed by protein synthesis inhibitors (see Table 1). Thus, it is likely that protein synthesis-dependent mechanisms play critical roles in not only late-phase but also early-phase LTP, at least in part. However, little is known about whether transcription and translation affects early-phase LTP within ACC synapses.It has been well established that the cyclic AMP-responsive element binding protein (CREB) is a major transcription factor associated with long-term memory [12,13], and calcium-calmodulin-dependent protein kinase IV (CaMKIV) plays an essential role in activity-dependent CREB phosphorylation [14-16]. In the hippocampus, the CaMKIV-CREB pathway is required for protein synthesis-dependent late-phase LTP [17,18]. On the other hand, it is conceivable that CaMKIV is also involved in early-phase LTP, because our previous study has shown that early-phase LTP in the ACC, amygdala, insular cortex and somatosensory cortex was disrupted in CaMKIV knockout mice [19]. Additionally, we previously reported that early-phase LTP in ACC neurons of CaMKIV transgenic mice was significantly enhanced compared with those of wild-type mice [20]. Thus, it is possible that CaMKIV modulates early-phase LTP by regulating transcription and translation in ACC synapses. In our behavioral study, trace fear memory was significantly enhanced in CaMKI
Enhanced synaptic long-term potentiation in the anterior cingulate cortex of adult wild mice as compared with that in laboratory mice
Ming-Gao Zhao, Hiroki Toyoda, Yu-Kun Wang, Min Zhuo
Molecular Brain , 2009, DOI: 10.1186/1756-6606-2-11
Abstract: The NMDA receptor plays a critical role in synaptic plasticity in many brain regions including the hippocampus, amygdala and anterior cingulate cortex (ACC) [1]. In most central synapses, NMDA receptors are composed of NR1, NR2 (A, B, C, and D), and NR3 (A and B) subunits. The formation of functional NMDA receptors requires a combination of NR1 and at least one NR2 subunit [2]. It is known that the NR2A and NR2B subunits predominate in the forebrain neurons, and the NR2A/NR2B subunit composition determines the functional properties of NMDA receptors [3,4]. Moreover, NMDA receptor subunits can undergo plastic changes in different regions of the brain during early development and different physiological/pathological conditions [2,5-8]. For example, enriched animals display better leaning, enhanced hippocampal LTP, increased NMDA receptor NR2B subunit mediated currents in the forebrain [9,10].The importance of NMDA receptor NR2B subunit in hippocampal LTP and behavioral learning has been demonstrated by studies using transgenic mice with forebrain overexpression of NR2B subunits [11]. In these transgenic mice, hippocampal LTP is significantly enhanced, along with enhanced learning ability [11] and persistent pain [12]. In the ACC, NMDA receptor-dependent plasticity including LTP and long-term depression, depend on both NR2B and NR2A subunit-containing NMDA receptors [13,14]. NMDA NR2B receptors contribute to LTP induced by different induction protocols in the ACC [14-16]. Our previous study provides strong evidence that NR2B-containing NMDA receptors in the ACC can contribute to the formation of classical contextual fear memory [2,14].It is well known that experience-dependent neuroanatomical and synaptic plasticity occurs in the brain. Previous studies reported that animals exposure to enriched environments results in increased cognitive and behavioral performances [17-19]. Furthermore, it has also been reported that environmental enrichment delayed the onset of neuro
Elevated interleukin-8 enhances prefrontal synaptic transmission in mice with persistent inflammatory pain
Guang-bin Cui, Jia-ze An, Nan Zhang, Ming-gao Zhao, Shui-bing Liu, Jun Yi
Molecular Pain , 2012, DOI: 10.1186/1744-8069-8-11
Abstract: In the present study, we examined IL-8 expression in the ACC, somatosensory cortex (SSC), and the dorsal horn of lumbar spinal cord following hind-paw administration of complete Freund's adjuvant (CFA) in mice and its effects on the ACC synaptic transmission. Quantification of IL-8 at protein level (by ELISA) revealed enhanced expression in the ACC and spinal cord during the chronic phases of CFA-induced peripheral inflammation. In vitro whole-cell patch-clamp recordings revealed that IL-8 significantly enhanced synaptic transmission through increased probability of neurotransmitter release in the ACC slice. ACC local infusion of repertaxin, a non-competitive allosteric blocker of IL-8 receptors, notably prolonged the paw withdrawal latency to thermal radian heat stimuli bilaterally in mice.Our findings suggest that up-regulation of IL-8 in the ACC partly attributable to the enhanced prefrontal synaptic transmission in the mice with persistent inflammatory pain.Chemokines, a family of proinflammatory cytokines play a role in immune system regulation, cell growth, cell development, and inflammation [1]. Interleukin-8 (IL-8), also known as CXCL8, is an α chemokine and its main function is chemotaxis of neutrophils and T lymphocytes [2]. In the immune system, IL-8 exerts its biological action by binding to seven-transmembrane G-protein-coupled receptors named CXCR1 and CXCR2. In the CNS, CXCR2 receptors have been described on astrocytes, microglia, and neurons [3]. The chemokine IL-8 is known to be synthesized by microglial cells and astrocytes [4]. IL-8 may be an important factor in intercellular communication between glia and neurons by rapidly altering the excitability of neurons, probably through presynaptic mechanisms [5]. Repertaxin is a new non-competitive allosteric blocker of IL-8 receptors (CXCR1/R2), which by locking CXCR1/R2 in an inactive conformation prevents receptor signaling and human polymorphonuclear leukocyte (PMN) chemotaxis [6].Studies using diffe
Interplay of Amygdala and Cingulate Plasticity in Emotional Fear
Hiroki Toyoda,Xiang-Yao Li,Long-Jun Wu,Ming-Gao Zhao,Giannina Descalzi,Tao Chen,Kohei Koga,Min Zhuo
Neural Plasticity , 2011, DOI: 10.1155/2011/813749
Abstract: The amygdala is known to be a critical brain region for emotional fear. It is believed that synaptic plasticity within the amygdala is the cellular basis of fear memory. Recent studies demonstrate that cortical areas such as the prefrontal cortex (PFC) and anterior cingulate cortex (ACC) may also contribute to the formation of fear memory, including trace fear memory and remote fear memory. At synaptic level, fear conditioning also triggers plastic changes within the cortical areas immediately after the condition. These results raise the possibility that certain forms of synaptic plasticity may occur within the cortex while synaptic potentiation takes place within synapses in the hippocampus and amygdala. This hypothesis is supported by electrophysiological evidence obtained from freely moving animals that neurons in the hippocampus/amygdala fire synchronous activities with cortical neurons during the learning. To study fear-related synaptic plasticity in the cortex and its functional connectivity with neurons in the amygdala and hippocampus will help us understand brain mechanisms of fear and improve clinical treatment of emotional disorders in patients. 1. Introduction Fear is an adaptive response to pain or the threat of danger. It is believed that amygdala is a key brain area for fear. As the major cellular model used for understanding this neural mechanism, long-term potentiation (LTP), a type of long-lasting synaptic plasticity, has been predominantly studied in the amygdala. Consequently, much evidence suggests that LTP is required for the establishment and consolidation of fear memory [1]. In addition, the anterior cingulate cortex (ACC) is known as a key structure that contributes to not only the recall of fear memory [2], but also the formation of fear memory [3]. It has been elucidated how recent and remote fear memories are organized in the brain (Figure 1). To date, considerable evidence indicates that fear learning and memory are mediated by changes in synaptic strength in the ACC [4]. Figure 1: Interplay of the cortex and hippocampus/amygdala in fear memory. There are two major hypotheses related to the brain network involved in fear memory. Depending on the different types of conditioning protocols, it is likely that both mechanisms may take place. In model A, early fear memory is formed within the hippocampus and/or amygdala. At some time point after learning (e.g., during sleep), some of this information is replayed and transferred into the cortical synapses. After the formation of remote memory in the cortex, early synaptic changes
Roles of the AMPA receptor subunit GluA1 but not GluA2 in synaptic potentiation and activation of ERK in the anterior cingulate cortex
Hiroki Toyoda, Ming-Gao Zhao, Bettina Ulzh?fer, Long-Jun Wu, Hui Xu, Peter H Seeburg, Rolf Sprengel, Rohini Kuner, Min Zhuo
Molecular Pain , 2009, DOI: 10.1186/1744-8069-5-46
Abstract: Activity-dependent synaptic plasticity in the central nervous system (CNS) has been proposed to contribute to major brain functions, including memory, chronic pain and drug addiction [1-4]. Long-term potentiation (LTP) is a major form of synaptic plasticity, and the enhancement of synaptic transmission in central regions related to sensory transmission and perception is believed to be a key cellular mechanism for chronic pain [2,5]. The anterior cingulate cortex (ACC) is a major cortical area that is believed to contribute to injury-related unpleasantness and memory in animal models of pain and memory [6-9]. Activation of postsynaptic glutamate NMDA receptor by different stimulation protocols triggers LTP in pyramidal neurons of the ACC [10-13]. Calcium-dependent intracellular signaling proteins, including AC1 (adenylyl cyclase subtype 1), ERK (extracellular signal-related kinase) and CaMKIV (calmodulin-dependent protein kinase IV) are found to contribute to ACC LTP [11,14-16].Glutamatergic AMPA (α amino-3-hydroxy-5-methylisoxazole-4-propionic acid) receptors mediate the majority of fast excitatory synaptic transmission in the brain, including the ACC region [17-19]. In the forebrain areas, AMPA receptors are heteromeric complexes assembled from mainly GluA1 and GluA2 [20]. The other two subunits of AMPA receptor, GluA3 and GluA4 express at relative lower levels [21,22]. According to the new subunit nomenclature recommended by the International Union of Basic and Clinical Pharmacology (IUPHAR), these AMPA subunits are renamed as GluA1, GluA2, GluA3 and GluA4 [23]. The requirement of different AMPA subtype receptors for LTP is likely to be regional-, development-dependent [24-27]. For example, in the hippocampal CA1 region, GluA1 is required for LTP in adult but not juvenile animals [25,27]. Furthermore, LTP in the cerebellum require GluA2 subunit [28]. It is also important to note that not all cortical LTP share the similar mechanisms. In the somatosensory cortex, F
Presynaptic regulation of the inhibitory transmission by GluR5-containing kainate receptors in spinal substantia gelatinosa
Hui Xu, Long-Jun Wu, Ming-Gao Zhao, Hiroki Toyoda, Kunjumon I Vadakkan, Yongheng Jia, Raphael Pinaud, Min Zhuo
Molecular Pain , 2006, DOI: 10.1186/1744-8069-2-29
Abstract: Fast excitatory glutamatergic synaptic transmission in the brain involves alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA), N-methyl-D-aspartate (NMDA), and kainate (KA) receptors. Compared with AMPA and NMDA receptors, the functions and physiological roles of KA receptors (KARs) have been discovered recently with the discovery of selective pharmacological tools [1] and the use of KA receptor subunit knockout mice [2,3]. KARs are composed of homomeric and heteromeric associations of five cloned subunits: GluR5-7, KA1 and KA2 [4]. Among KAR subunits, GluR5-7 homomers are functional kainate gated ion channels [5,6]. KA1 and KA2 form functional channels as heteromers [6,7].KARs are present at both postsynaptic and presynaptic locations [8-13]. Generally, postysynaptic KARs mediate a small portion of excitatory synaptic transmission, whereas the presynaptic KARs regulate either glutamatergic or GABAergic transmission [11,13,14]. The modulation of γ-aminobutyric acid (GABA) release by presynaptic GluR5 KARs has been well reported in the hippocampus and cortex [2,15-22]. In the spinal dorsal horn, postsynaptic KARs mediate excitatory synaptic responses by only high intensity stimulation[14], while presynaptic KARs biphasically regulate both the excitatory [23,24] and inhibitory transmission [25,26]. The deletion of GluR5 abolished KAR function in cultured DRG neurons, whereas presynaptic modulation of inhibitory transmission was preserved in cultured dorsal horn neurons [26]. Thus, both GluR5 and GluR6 may regulate presynaptic GABA and glycine release in cultured spinal dorsal horn neurons. However, it is still unknown whether similar modulation exists in the substantia gelatinosa (SG) of the intact spinal slices and which KAR subunits are involved in the modulation in inhibitory transmission in this region.Superficial lamina of the spinal dorsal horn, particularly the SG, receives nociceptive information from fine myelinated Aδ- and unmyelinated C-primary
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