neuronal

Influence of triptolide on neuronal apoptosis in rat with cerebral injury after focal ischemia reperfusion

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Influence of triptolide on neuronal apoptosis in rat with cerebral injury after focal ischemia reperfusion by Deng-ming Wei, Guang-zhao Huang, Yi-gu Zhang, Guang-xun Rao.

Objective: To study effect of triptolide(TL) on neuronal apoptosis in cerebral tissue rat after ischemia-reperfusion. Method: Triptolide at dose 0.2 or 0.4 mg·kg -1was intr aperitoneally injected once a day for 4 d. The focal ischemia-rep erfusion model was established with thread embolism middle artery before trip tolide injection the fourth day. Neurological deficit score rats eval uated; and immunohistochemical techniques were used to count positive cells express MPO TUNEL tissue. Result: Compare d control group, neural function significantly impr oved, number infiltrate neutrophil cere bral remarkably reduced two TL-treated groups. Conclusio n: results suggested that TL can inhibit infiltration decrease degree [

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The role of the insulin receptor substrate-1 in the differentiation of rat hippocampal neuronal cells

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The role of the insulin receptor substrate-1 in the differentiation of rat hippocampal neuronal cells by Andrea Morrione, Magali Navarro, Gaetano Romano, Michael Dews, Krzysztof Reiss, Barbara Valentinis, Barbara Belletti, Renato Baserga.

H19-7/IGF-IR cells are rat hippocampal expressing a human IGF-I receptor, which differentiate to neuronal phenotype when stimulated by at 39 degrees C. have low levels of expression insulin receptor substrate-l (IRS-1), major substrate the IGF-IR. induces serine-phosphorylation and down-regulation endogenous IRS-1 upon differentiation cells. The profound influence on was confirmed transfecting these with plasmid mouse IRS-1. Over-expression wild type in abolishes IGF-I-induced A mutant lacking PTB domain loses ability inhibit program. H19-7/IGF-IR/IRS-1 C show stronger prolonged activation Akt, compared role Akt inhibition program using inhibitor Class I PI3 kinases LY29400, restores strong reduction MAP signaling, is related superactivation Akt. This constitutively active inhibited These experiments confirm importance MAPK mechanism IGF-I-mediated

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Pharmacological reduction of ER stress protects against TDP-43 neuronal toxicity in vivo

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Pharmacological reduction of ER stress protects against TDP-43 neuronal toxicity in vivo by Alexandra Vaccaro, Shunmoogum A. Patten, Dina Aggad, Carl Julien, Claudia Maios, Edor Kabashi, Pierre Drapeau, J. Alex Parker.

C. elegans and D. rerio expressing mutant TAR DNA Binding Protein 43 (TDP-43) are powerful in vivo animal models for the genetics pharmacology of amyotrophic lateral sclerosis (ALS). Using these small-animal ALS, we previously identified methylene blue (MB) as a potent suppressor TDP-43 toxicity. Consequently here investigated how MB might exert its neuroprotective properties found that it acts through reduction endoplasmic reticulum (ER) stress response. We tested other compounds known to be active ER unfolded protein response worms zebrafish human (mTDP-43). three compounds: salubrinal, guanabenz new structurally related compound phenazine, which also reduced paralysis, neurodegeneration oxidative our mTDP-43 models. genetics, showed all four act suppressors toxicity Interestingly, operate different branches pathway achieve common action. Our results indicate protein-folding homeostasis is an important target therapeutic development ALS TDP-43-related neurodegenerative diseases.

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Sex difference and senile change in hypothalamic neuronal response to electrical stimulation of the limbic system in the rat.

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Sex difference and senile change in hypothalamic neuronal response to electrical stimulation of the limbic system in the rat. by Tatsuo Akema, Masazumi Kawakami.

To get an electrophysiological basis for understanding the sexual and age-related changes in brain mechanisms controlling gonadotropin secretion, we studied single unit responses to electrical stimulation preoptico-arcuate, amygdalo-preoptic hippocampo-preoptic neural connections rat. Orthodromic pulse were recorded young mature aged, male female rats by post-stimulus histogram analysis. Electrical of medial preoptic area elicited one-half hypothalamic arcuate neurons tested while induced less than one-third male. The percentage responding did not differ between aged animals. Stimulation amygdala evoked a larger number animals both sexes. There was no difference amygdaloid stimulation. Percentages hippocampal greater females showing regular estrous cycles males or which showed constant vaginal smears. In whose daily treatment with progesterone, more responded hippocampus rats. cycling progesterone-recycling had similar neuronal limbic Stimulus thresholds inducing these almost equivalent among different groups This suggests that alteration observed due change excitability sites animal groups. These results indicate there are sex differences synaptic functions transmit signals impulses neurons. It is also suggested pathways may be functionally modified because absence cycles.

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Notes on renewal processes and neuronal spike trains

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Notes on renewal processes and neuronal spike trains by Shunji Osaki.

Some stochastic models of neuronal spike trains are discussed. First, the equivalence between a model and two-unit standby redundant is shown. Second, modified S. K. Srinivasan G. Rajamannar proposed analyzed.

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Neuronal apoptosis inhibitory protein (NAIP)-like immunoreactivity in brains of adult patients with Down syndrome

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Neuronal apoptosis inhibitory protein (NAIP)-like immunoreactivity in brains of adult patients with Down syndrome by Rainer Seidl, Michal Bajo, K. Böhm, E. C. LaCasse, A. E. MacKenzie, N. Cairns, Gert Lubec.

In Down syndrome (DS), enhanced apoptosis (programmed cell death) may play a role in the pathogenesis of characteristic early mental retardation and precocious neurodegeneration Alzheimer-type. The human IAP (inhibitor proteins) genes (NAIP, c-IAP-2/HIAP-1, c-IAP-1/Hiap-2, XIAP, survivin) are an evolutionary conserved family proteins which prevent death across species, implying that they act at central, highly point cascade. Evidence for downregulation NAIP-mRNA fetal DS (23rd week gestation), as found by subtractive hybridization technique challenged studies protein level adult brain specimen. NAIP-like immunoreactivity was determined four different regions cerebral cortex cerebellum 9 patients with Alzheimer-like neuropathologic lesions, Alzheimer disease (AD) compared to controls. For first time, NAIP-IR could be demonstrated cortical brain. Compared control subjects, western blotting significantly decreased levels parietal occipital frontal AD. While mode NAIP action is unknown, inhibition certain caspases has already been other IAP-family members (c-IAP1, c-IAP2 XIAP). Although AD awaits further confirmation, results suggest alterations regulatory (inhibitory) another feature

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Tat-NOL3 protects against hippocampal neuronal cell death induced by oxidative stress through the regulation of apoptotic pathways

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Tat-NOL3 protects against hippocampal neuronal cell death induced by oxidative stress through the regulation of apoptotic pathways by Eun Jeong Sohn, Min Jea Shin, Won Sik Eum, Dae Won Kim, Ji In Yong, Eun Ji Ryu, Meeyoung Park, Jinseu Park, Yong-Jun Cho, Soo Young Choi, Jung Hwan Park, Su Bin Cho, Hyun Ju Cha, Sang Jin Kim, Hyeon Ji Yeo, Eun Ji Yeo, Yeon Joo Choi, Seung Kwon Im, Hae Young Kweon, Duk-Soo Kim, Yeon Hee Yu, Sung-Woo Cho.

Oxidative stress-induced apoptosis is associated with neuronal cell death and ischemia. The NOL3 [nucleolar protein 3 (apoptosis repressor CARD domain)] protects against oxidative death. However, the protective mechanism responsible for this effect as well effects of stress in ischemia remain unclear. Thus, we examined on hydrogen peroxide (H2O2)-induced these hippocampal HT22 cells an animal model forebrain using Tat-fused (Tat-NOL3). Purified Tat-NOL3 transduced into H2O2-exposed inhibited production reactive oxygen species (ROS), DNA fragmentation reduced mitochondrial membrane potential (ΔΨm). In addition, prevented through regulation apoptotic signaling pathways including Bax, Bcl-2, caspase-2, -3 -8, PARP p53. brains significantly protected CA1 region hippocampus by regulating activation microglia astrocytes. Taken together, findings demonstrate that acting anti-apoptotic protein. suggest represents a therapeutic agent protection ischemic brain injury.

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7-Nitroindazole and Methylene Blue, Inhibitors of Neuronal Nitric Oxide Synthase and NO-Stimulated Guanylate Cyclase, Block MK-801-Elicited Behaviors in Mice

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7-Nitroindazole and Methylene Blue, Inhibitors of Neuronal Nitric Oxide Synthase and NO-Stimulated Guanylate Cyclase, Block MK-801-Elicited Behaviors in Mice by Stephen I. Deutsch, Richard B. Rosse, Steven M. Paul, Vincent Tomasino, Lee Koetzner, Cassandra Morn, John Mastropaolo.

We examined the abilities of 7-nitroindazole and methylene blue, inhibitors neuronal isoform nitric oxide synthase (NOS) oxide-stimulated guanylate cyclase activity respectively, to attenuate explosive episodic jumping behavior(s) (“popping”) elicited by MK-801 in mice. MK-801, like phencyclidine (PCP), is a high-affinity, noncompetitive antagonist N-methyl-D-aspartate (NMDA) subtype glutamate receptor. have postulated that MK-801-elicited popping behavior mice represents an animal model schizophrenia, because markedly inhibited/antagonized both typical atypical antipsychotic drugs. In present study, induced was measured using automated detection system quantifies vertical displacements on testing platform. 7-Nitroindazole (100 mg/kg) blue (32 100 significantly reduced number force behavior. Mouse rotorod performance did not differ between animals receiving 7-nitroindazole, or their respective vehicles, suggesting attenuation due either sedation ataxia caused blue. Our findings suggest may, part, mediate behaviors NMDA receptor antagonists, NOS may actions.

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TRPA1 activation in a human sensory neuronal model: relevance to cough hypersensitivity?

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TRPA1 activation in a human sensory neuronal model: relevance to cough hypersensitivity? by Rebecca Clarke, Kevin Monaghan, Imad About, Caoimhin S. Griffin, Gerard P. Sergeant, Ikhlas El Karim, J. Graham McGeown, Sara Louise Cosby, Tim M. Curtis, Lorcan McGarvey, Fionnuala Lundy.

The cough reflex becomes hyperresponsive in acute and chronic respiratory diseases, but understanding the underlying mechanism is hampered by difficulty accessing human tissue containing both nerve endings neuronal cell bodies. We refined an adult stem sensory model to overcome limited availability of neurones applied study transient receptor potential ankyrin 1 (TRPA1) channel expression activation.Human dental pulp cells (hDPSCs) were differentiated towards a phenotype, termed peripheral equivalents (PNEs). Using molecular immunohistochemical techniques, together with Ca2+ microfluorimetry whole patch clamping, we investigated roles for growth factor (NGF) viral mimic poly I:C TRPA1 activation.PNEs exhibited morphological, functional characteristics neurons expressed channels. PNE treatment NGF 20 min generated significantly larger inward outward currents compared untreated PNEs response agonist cinnamaldehyde (p<0.05). caused similar heightened responses activation cells.Using observed mediated hyperresponsiveness, representing neuro-inflammatory mechanisms associated nociceptive recognised hypersensitivity syndrome.

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Glial protein S100B modulates long-term neuronal synaptic plasticity

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Glial protein S100B modulates long-term neuronal synaptic plasticity by Hiroshi Nishiyama, Thomas Knöpfel, Shogo Endo, Shigeyoshi Itohara.

Glial cells are traditionally regarded as elements for structural support and ionic homeostasis, but have recently attracted attention putative integral of the machinery involved in synaptic transmission plasticity. Here, we demonstrate that calcium-binding protein S100B, which is synthesized considerable amounts astrocytes (a major glial cell subtype), modulates long-term Mutant mice devoid S100B developed normally had no detectable abnormalities cytoarchitecture brain. These mutant mice, however, strengthened plasticity identified by enhanced potentiation (LTP) hippocampal CA1 region. Perfusion slices with recombinant proteins reversed levels LTP to those wild-type slices, indicating might act extracellularly. In addition LTP, spatial memory Morris water maze test fear contextual conditioning. The results indicate a modulator neuronal strengthen notion glial–neuronal interaction important information processing

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