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choline acetyltransferase/necrosis
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Overexpression of tumour necrosis factor alpha in the brain of transgenic mice differentially alters nerve growth factor levels and choline acetyltransferase activity.
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Tumour necrosis factor alpha (TNF-alpha) is a pleiotrophic cytokine synthesized primarily by macrophages and monocytes, which exerts a variety of biological activities during inflammatory responses, immune reactions, and wound healing. Within the central nervous system (CNS), the basal levels of
The toxicity of tumor necrosis factor-alpha upon cholinergic neurons within the nucleus basalis and the role of norepinephrine in the regulation of inflammation: implications for Alzheimer's disease.
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Inflammation and reduced forebrain norepinephrine are features of Alzheimer's disease that may interact to contribute to the degeneration of specific neural systems. We reproduced these conditions within the basal forebrain cholinergic system, a region that is vulnerable to degeneration in
Tumor necrosis factor-alpha triggers cell death of sensitized potassium chloride-stimulated cholinergic neurons.
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Cell death of cholinergic neurons of the basal forebrain plays an important role in neurodegenerative disorders, such as Alzheimer's disease. Inflammatory cytokines, such as, for example, tumor necrosis factor-alpha (TNF-alpha), may be involved in these neurodegenerative processes. The aim of this
Smoke, choline acetyltransferase, muscarinic receptors, and fibroblast proliferation in chronic obstructive pulmonary disease.
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Acetylcholine (ACh), synthesized by choline acetyltransferase (ChAT), and muscarinic M(1), M(2), and M(3) receptors (MRs) are involved in fibroblast proliferation. We evaluated ChAT, MRs, and extracellular signal-regulated kinase (ERK) 1/2 and nuclear factor (NF) kappaB activation in lung
Choline acetyltransferase and the nicotinic acetylcholine receptor AChRα7 in experimental myositis.
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It is not known to what extent a non-neuronal cholinergic system is involved in myositis (muscle inflammation) evoked by marked muscle overuse. Therefore, in the present study, a recently established rabbit myositis model was used and the expression patterns of ChAT and nicotinic acetylcholine
Interleukin-1β and tumor necrosis factor-α co-operatively enhance a novel trophic activity of astrocytes for pontine cholinergic neurons in vitro.
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Insulin and insulin-like growth factors (IGFs) are the only known trophic factors for pontine cholinergic neurons. The present study revealed that astrocyte-extract pretreated with IL-1β and TNF-α significantly enhanced choline acetyltransferase (ChAT) activity of the pontine neurons in the presence
Survival role of locally produced acetylcholine in the bovine corpus luteum.
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The present study was conducted to explore the source of acetylcholine (ACH) in the corpus luteum (CL) and to test our hypothesis of an antiapoptotic role of ACH in the bovine CL and, further, to investigate whether nerve growth factor (NGF), insulin-like growth factor 1 (IGF1), and transforming
Expression and function of NIK- and IKK2-binding protein (NIBP) in mouse enteric nervous system.
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BACKGROUND
NIK- and IKK2-binding protein (NIBP)/TRAPPC9 is expressed in brain neurons, and human NIBP mutations are associated with neurodevelopmental disorders. The cellular distribution and function of NIBP in the enteric nervous system (ENS) remain unknown.
METHODS
Western blot and reverse
Ameliorative effect of deoxyvasicine on scopolamine-induced cognitive dysfunction by restoration of cholinergic function in mice.
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6-Hydroxydopamine induced cardiac malformations and alterations of the autonomic nervous system in the developing chicken embryo.
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6-Hydroxydopamine (6-OHDA) was injected into the air sac of developing chicken embryos on day E3 in order to study its effects on cardiac development both morphologically and biochemically. A dose-dependent teratogenic effect and fetotoxicity were observed in the 6-OHDA-treated embryos. Cardiac
Neural-immune interactions in sympathetic ganglia.
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Effects of immune cytokines on neuronal gene expression have recently been examined in cultured superior cervical (sympathetic) ganglia, a widely used model system for the study of neurotransmitter plasticity. Following deafferentation and explantation into culture, interleukin-1 causes an
Adenoviral gene delivery of pigment epithelium-derived factor protects striatal neurons from quinolinic acid-induced excitotoxicity.
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The 50-kDa secreted glycoprotein pigment epithelium-derived factor (PEDF) is neuroprotective for various types of cultured neurons, but whether it is neuroprotective for neurons in vivo is not known. We examined the effects of adenovirus-mediated gene transfer of PEDF on quinolinic acid (QA)-induced
The presence of the APP(swe) mutation in mice does not increase the vulnerability of cholinergic basal forebrain neurons to neuroinflammation.
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Neuroinflammation, and elevated levels of inflammatory proteins, such as tumor necrosis factor-alpha, and the deposition of beta-amyloid may interact to contribute to the pathogenesis of Alzheimer's disease. We reproduced a component of the neuroinflammatory state within the basal forebrain
Alzheimer's Disease-like Early-phase Brain Pathogenesis: Self-curing Amelioration of Neurodegeneration from Pro-inflammatory 'Wounding' to Anti-inflammatory 'Healing'.
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The etiological initiators of neuroinflammation remain inconclusive, and effective interventions to block neurodegeneration are unavailable. Surprisingly, we found collagen II-combined complete Freund's adjuvant (CC) that usually induces rheumatoid arthritis (RA) also drives Alzheimer's disease
Mechanisms of toxicity and tolerance to diisopropylphosphorofluoridate at the neuromuscular junction of the rat.
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Diisopropylphosphorofluoridate (DFP), an irreversible inhibitor of acetylcholinesterase (AChE) activity, when given as an acute dose (1.5 mg/kg, sc) caused fasciculations and induced necrosis in rat skeletal muscle fibers. No adaptation was seen to daily dosing of DFP (1.5 mg/kg, sc) since all rats
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