(acetylcholine chloride) articles in PubMed
- Acetamiprid Accumulates in Different Amounts in Murine Brain Regions. [Journal Article]
- Int J Environ Res Public Health 2016; 13(10)IJ
- Neonicotinoids such as acetamiprid (ACE) belong to a new and widely used single class of pesticides. Neonicotinoids mimic the chemical structure of nicotine and share agonist activity with the nicoti...
Neonicotinoids such as acetamiprid (ACE) belong to a new and widely used single class of pesticides. Neonicotinoids mimic the chemical structure of nicotine and share agonist activity with the nicotine acetylcholine receptor (nAchR). Neonicotinoids are widely considered to be safe in humans; however, they have recently been implicated in a number of human health disorders. A wide range of musculoskeletal and neuromuscular disorders associated with high doses of neonicotinoids administered to animals have also been reported. Consequently, we used a mouse model to investigate the response of the central nervous system to ACE treatment. Our results show that exposure to ACE-containing water for three or seven days (decuple and centuple of no observable adverse effect level (NOAEL)/day) caused a decrease in body weight in 10-week old A/JJmsSlc (A/J) mice. However, the treatments did not affect brain histology or expression of CD34. ACE concentrations were significantly higher in the midbrain of ACE-treated mice than that of the normal and vehicle groups. Expression levels of α7, α4, and β2 nAChRs were found to be low in the olfactory bulb and midbrain of normal mice. Furthermore, in the experimental group (centuple ACE-containing water for seven days), β2 nAChR expression decreased in many brain regions. Information regarding the amount of accumulated ACE and expression levels of the acetylcholine receptor in each region of the brain is important for understanding any clinical symptoms that may be associated with ACE exposure.
- Altered Satellite Cell Responsiveness and Denervation Implicated in Progression of Rotator-Cuff Injury. [Journal Article]
- PLoS One 2016; 11(9):e0162494Plos
- CONCLUSIONS: Since SS satellite cells can be activated in culture, a NO-donor drug combined with stretching could promote muscle growth and improve functional outcome after RCI. PCAs suggest indices including satellite cell responsiveness, atrogin-1, atrophy, and innervation may predict surgical outcome.
- The tobacco-specific carcinogen-operated calcium channel promotes lung tumorigenesis via IGF2 exocytosis in lung epithelial cells. [Journal Article]
- Nat Commun 2016; 7:12961NC
- Nicotinic acetylcholine receptors (nAChRs) binding to the tobacco-specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) induces Ca(2+) signalling, a mechanism that is implicated in...
Nicotinic acetylcholine receptors (nAChRs) binding to the tobacco-specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) induces Ca(2+) signalling, a mechanism that is implicated in various human cancers. In this study, we investigated the role of NNK-mediated Ca(2+) signalling in lung cancer formation. We show significant overexpression of insulin-like growth factors (IGFs) in association with IGF-1R activation in human preneoplastic lung lesions in smokers. NNK induces voltage-dependent calcium channel (VDCC)-intervened calcium influx in airway epithelial cells, resulting in a rapid IGF2 secretion via the regulated pathway and thus IGF-1R activation. Silencing nAChR, α1 subunit of L-type VDCC, or various vesicular trafficking curators, including synaptotagmins and Rabs, or blockade of nAChR/VDCC-mediated Ca(2+) influx significantly suppresses NNK-induced IGF2 exocytosis, transformation and tumorigenesis of lung epithelial cells. Publicly available database reveals inverse correlation between use of calcium channel blockers and lung cancer diagnosis. Our data indicate that NNK disrupts the regulated pathway of IGF2 exocytosis and promotes lung tumorigenesis.
- Juvenile myasthenia gravis in Norway: A nationwide epidemiological study. [Journal Article]
- Eur J Paediatr Neurol 2016 Sep 10EJ
- CONCLUSIONS: This study confirms the rarity of JMG in Norway, especially among males, and shows a stable incidence rate over the last 25 years.
- Pharmacological Evaluation of Antiasthmatic Activity of Myrica nagi Bark Extracts. [Journal Article]
- Antiinflamm Antiallergy Agents Med Chem 2016 Sep 23AA
- CONCLUSIONS: The results of present investigation suggest that the polar extract of Myrica nagi bark have better antiasthmatic activity than the non polar and methanolic extract.
- The challenges of modulating the 'rest and digest' system: acetylcholine receptors as drug targets. [Review]
- Drug Discov Today 2016 Sep 22DD
- Acetylcholine, a major neurotransmitter of the parasympathetic and sympathetic nervous systems, was discovered in the early 1900s. Over the years, researchers have revealed much about its regulation,...
Acetylcholine, a major neurotransmitter of the parasympathetic and sympathetic nervous systems, was discovered in the early 1900s. Over the years, researchers have revealed much about its regulation, properties of its receptors and features of the downstream signaling that influence its terminal effects. The acetylcholine system, traditionally associated with neuromuscular communication, is now known to play a crucial part in modulation of the immune system and other 'rest and digest' effects. Recent research seeks to elucidate the system's role in brain functions including cognition, sleep, arousal, motivation, reward and pain. We highlight clinically approved and experimental drugs that modulate the acetylcholine receptors. The complexities in targeting the acetylcholine receptors are vast and finding future indications for drug development associated with specific acetylcholine receptors remains a challenge.
- Nerve growth factor-induced plasticity in medial prefrontal cortex interneurons of aged Wistar rats. [Journal Article]
- Exp Gerontol 2016 Sep 21EG
- The medial prefrontal cortex (mPFC) has been identified as a critical center for working and long-term memory. In this study, we have examined the expression of neuropeptide Y (NPY) and vasoactive in...
The medial prefrontal cortex (mPFC) has been identified as a critical center for working and long-term memory. In this study, we have examined the expression of neuropeptide Y (NPY) and vasoactive intestinal polypeptide (VIP) in mPFC interneurons and the density of the mPFC cholinergic and dopaminergic innervation in cognitively-impaired aged Wistar rats. We also tested the possibility that the potential age-related changes might rely on insufficient neurotrophic support. The total number of NPY- and VIP-immunoreactive neurons and the density of vesicular acetylcholine transporter (VAChT)- and tyrosine hydroxylase (TH)-immunoreactive varicosities were estimated using stereological methods. The number of NPY-immunoreactive neurons was significantly reduced in aged rats, whereas the number of VIP-immunoreactive neurons was unaltered. The decreased expression of NPY was fully reversed by intracerebroventricular administration of nerve growth factor. No differences in the density of VAChT- and TH-immunoreactive varicosities were found among all groups. Our results indicate that the reduced expression of NPY in the mPFC of aged rats can be ascribed to the age-associated loss of neurotrophic support, and raise the possibility that these changes might contribute for the cognitive decline that occurs during non-pathological aging.
- A Novel Tobacco Use Phenotype Suggests the 15q25 and 19q13 Loci May Be Differentially Associated with Cigarettes per Day and Tobacco-Related Problems. [Journal Article]
- Nicotine Tob Res 2016 Sep 23NT
- CONCLUSIONS: CPD captures variation at 15q25. Although strong conclusions cannot be drawn, these finding suggest measuring additional dimensions of problems may detect genetic variation not accounted for by smoking quantity. Replication in independent samples will help further refine phenotype definition efforts.Different facets of tobacco-related problems may index unique genetic risk. Cigarettes per day, a simple measure of tobacco consumption, is associated with variants at the 15q25 gene cluster. Additional dimensions of tobacco problems may help to capture variation at 19q13. Results demonstrate the utility of adopting a data-driven approach to defining phenotypes for genetic association studies of tobacco involvement and provide results that can inform replication efforts.
- Association of CYP2C19 variants and epoxyeicosatrienoic acids on patients with microvascular angina. [Journal Article]
- Am J Physiol Heart Circ Physiol 2016 Sep 23; :ajpheart.00473.2016AJ
- CONCLUSIONS: CYP2C19 variants is associated with MVA. The decline of EET-based defensive mechanisms owing to CYP2C19 variants may affect coronary microvascular dysfunction.
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- Polo-like Kinase 1 Regulates Vimentin Phosphorylation at Ser-56 and Contraction in Smooth Muscle. [Journal Article]
- J Biol Chem 2016 Sep 23JB
- Polo-like kinase 1 (Plk1) is a serine/threonine protein kinase that has been implicated in mitosis, cytokinesis and smooth muscle cell proliferation. The role of Plk1 in smooth muscle contraction has...
Polo-like kinase 1 (Plk1) is a serine/threonine protein kinase that has been implicated in mitosis, cytokinesis and smooth muscle cell proliferation. The role of Plk1 in smooth muscle contraction has not been investigated. Here, stimulation with acetylcholine induced Plk1 phosphorylation at Thr-210 (an indication of Plk1 activation) in smooth muscle. Contractile stimulation also activated Plk1 in live smooth muscle cells as evidenced by changes in fluorescence resonance energy transfer signal of a Plk1 sensor. Moreover, knockdown of Plk1 in smooth muscle attenuated force development. Smooth muscle conditional knockout of Plk1 also diminished contraction of mouse tracheal rings. Plk1 knockdown inhibited acetylcholine induced vimentin phosphorylation at Ser-56 without affecting myosin light chain phosphorylation. Expression of T210A Plk1 inhibited the agonist-induced vimentin phosphorylation at Ser-56 and contraction in smooth muscle. However, myosin light chain phosphorylation was not affected by T210A Plk1. Ste20-like kinase (SLK) is a serine/threonine protein kinase that has been implicated in spindle orientation and microtubule organization during mitosis. In this study, knockdown of SLK inhibited Plk1 phosphorylation at Thr-210 and activation. Finally, asthma is characterized by airway hyperresponsiveness, which largely stems from airway smooth muscle hyperreactivity. Here, smooth muscle conditional knockout of Plk1 attenuated airway resistance and airway smooth muscle hyperreactivty in a murine model of asthma. Taken together, these findings suggest that Plk1 regulates smooth muscle contraction by modulating vimentin phosphorylation at Ser-56. Plk1 activation is regulated by SLK during contractile activation. Plk1 contributes to the pathogenesis of asthma.