scholarly journals Cholinergic anti-inflammatory pathway ameliorates murine experimental Th2-type colitis by suppressing the migration of plasmacytoid dendritic cells

2022 ◽  
Vol 12 (1) ◽  
Author(s):  
Yuya Kanauchi ◽  
Takeshi Yamamoto ◽  
Minako Yoshida ◽  
Yue Zhang ◽  
Jaemin Lee ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Therapeutic Potential ◽  
Plasmacytoid Dendritic Cells ◽  
Nerve Fibers ◽  
Chronic Inflammatory Bowel Disease ◽  
Jak2 Inhibitor ◽  
Cholinergic Pathway ◽  
Anti Inflammatory

AbstractUlcerative colitis (UC) is a chronic inflammatory bowel disease. Several studies have demonstrated that α7 nicotinic acetylcholine receptors (α7nAChRs) exert anti-inflammatory effects on immune cells and nicotine suppress UC onset and relapse. Plasmacytoid dendritic cells (pDCs) reportedly accumulate in the colon of UC patients. Therefore, we investigated the pathophysiological roles of α7nAChRs on pDCs in the pathology of UC using oxazolone (OXZ)-induced Th2-type colitis with BALB/c mice. 2-deoxy-D-glucose, a central vagal stimulant suppressed OXZ colitis, and nicotine also ameliorated OXZ colitis with suppressing Th2 cytokines, which was reversed by α7nAChR antagonist methyllycaconitine. Additionally, α7nAChRs were expressed on pDCs, which were located very close to cholinergic nerve fibers in the colon of OXZ mice. Furthermore, nicotine suppressed CCL21-induced bone marrow-derived pDC migration due to Rac 1 inactivation, which was reversed by methyllycaconitine, a JAK2 inhibitor AG490 or caspase-3 inhibitor AZ-10417808. CCL21 was mainly expressed in the isolated lymphoid follicles (ILFs) of the colon during OXZ colitis. The therapeutic effect of cholinergic pathway on OXZ colitis probably through α7nAChRs on pDCs were attributed to the suppression of pDC migration toward the ILFs. Therefore, the activation of α7nAChRs has innovative therapeutic potential for the treatment of UC.

scholarly journals Nicotine Induces Polyspermy in Sea Urchin Eggs through a Non-Cholinergic Pathway Modulating Actin Dynamics

Cells ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 63 ◽  
Author(s):  
Nunzia Limatola ◽  
Filip Vasilev ◽  
Luigia Santella ◽  
Jong Tai Chun
Keyword(s):  
Sea Urchin ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Molecular Mechanisms ◽  
Actin Dynamics ◽  
Dependent Manner ◽  
Animal Cells ◽  
Sea Urchin Eggs ◽  
Cholinergic Pathway ◽  
Dose Dependent

While alkaloids often exert unique pharmacological effects on animal cells, exposure of sea urchin eggs to nicotine causes polyspermy at fertilization in a dose-dependent manner. Here, we studied molecular mechanisms underlying the phenomenon. Although nicotine is an agonist of ionotropic acetylcholine receptors, we found that nicotine-induced polyspermy was neither mimicked by acetylcholine and carbachol nor inhibited by specific antagonists of nicotinic acetylcholine receptors. Unlike acetylcholine and carbachol, nicotine uniquely induced drastic rearrangement of egg cortical microfilaments in a dose-dependent way. Such cytoskeletal changes appeared to render the eggs more receptive to sperm, as judged by the significant alleviation of polyspermy by latrunculin-A and mycalolide-B. In addition, our fluorimetric assay provided the first evidence that nicotine directly accelerates polymerization kinetics of G-actin and attenuates depolymerization of preassembled F-actin. Furthermore, nicotine inhibited cofilin-induced disassembly of F-actin. Unexpectedly, our results suggest that effects of nicotine can also be mediated in some non-cholinergic pathways.

[3H]nicotine binding sites are associated with mammalian optic nerve terminals

1988 ◽  
Vol 1 (2) ◽  
pp. 245-248 ◽  
Author(s):  
Glen T. Prusky ◽  
Max S. Cynader
Keyword(s):  
Optic Nerve ◽  
Visual System ◽  
Nicotinic Acetylcholine Receptors ◽  
Binding Sites ◽  
Acetylcholine Receptors ◽  
Optic Tract ◽  
Nerve Fibers ◽  
Nerve Terminals ◽  
Nicotinic Acetylcholine ◽  
Retinotectal Transmission

AbstractThe autoradiographic distribution of [3H]nicotine binding sites was examined in the superior colliculus in normal rats and cats, and in animals in which one or both eyes were removed. [3H]Nicotine binding sites in normal animals were densely concentrated in the superficial layers of the colliculus corresponding to the zone of termination of optic nerve fibers. Following bilateral enucleation, [3H]nicotine binding in the superficial collicular layers was drastically reduced. Unilateral enucleation markedly reduced [3H]nicotine binding sites in the colliculus contralateral to the removed eye, with little effect on the ipsilateral colliculus. These results provide further evidence that nicotinic acetylcholine receptors have a presynaptic location on optic tract terminals and may therefore modulate retinotectal transmission in both the rat and cat visual system.

scholarly journals Revisiting nicotine’s role in the ageing brain and cognitive impairment

2017 ◽  
Vol 28 (7) ◽  
pp. 767-781 ◽  
Author(s):  
Alireza Majdi ◽  
Farzin Kamari ◽  
Manouchehr Seyedi Vafaee ◽  
Saeed Sadigh-Eteghad
Keyword(s):  
Cognitive Impairment ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Therapeutic Potential ◽  
Amyloid Β ◽  
Therapeutic Effects ◽  
Molecular Pathways ◽  
Pharmacological Chaperone ◽  
Age Related ◽  
Brain Ageing

AbstractBrain ageing is a complex process which in its pathologic form is associated with learning and memory dysfunction or cognitive impairment. During ageing, changes in cholinergic innervations and reduced acetylcholinergic tonus may trigger a series of molecular pathways participating in oxidative stress, excitotoxicity, amyloid-β toxicity, apoptosis, neuroinflammation, and perturb neurotrophic factors in the brain. Nicotine is an exogenous agonist of nicotinic acetylcholine receptors (nAChRs) and acts as a pharmacological chaperone in the regulation of nAChR expression, potentially intervening in age-related changes in diverse molecular pathways leading to pathology. Although nicotine has therapeutic potential, paradoxical effects have been reported, possibly due to its inverted U-shape dose-response effects or pharmacokinetic factors. Additionally, nicotine administration should result in optimum therapeutic effects without imparting abuse potential or toxicity. Overall, this review aims to compile the previous and most recent data on nicotine and its effects on cognition-related mechanisms and age-related cognitive impairment.

scholarly journals The anti-inflammatory pathway regulated via nicotinic acetylcholine receptors in rat intestinal mesothelial cells

2017 ◽  
Vol 79 (11) ◽  
pp. 1795-1802 ◽  
Author(s):  
Taiki MIHARA ◽  
Wataru OTSUBO ◽  
Kazuhide HORIGUCHI ◽  
Shoma MIKAWA ◽  
Noriyuki KAJI ◽  
...  
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Mesothelial Cells ◽  
Nicotinic Acetylcholine ◽  
Inflammatory Pathway ◽  
Anti Inflammatory

scholarly journals Activation of Alpha7 Nicotinic Acetylcholine Receptors Reduce Chronic Pain-induced Anxiety and Depression-Like Behaviors via WNT/β-Catenin Pathway

2021 ◽  
Author(s):  
Xingrui Gong ◽  
Yongmei Chen ◽  
Rongmei Fan ◽  
Meihua Cai ◽  
Mazhong Zhang
Keyword(s):  
Chronic Pain ◽  
Inflammatory Response ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Brain Inflammation ◽  
Anxiety And Depression ◽  
Common Mechanism ◽  
Cold Response ◽  
Nicotinic Acetylcholine ◽  
Anti Inflammatory

Abstract Chronic pain frequently leads to anxiety, depression and microglia-related inflammation is the common mechanism for chronic pain and psychiatric disorders. Activation of alpha 7 nicotinic acetylcholine (α7 nAch) receptor suppresses microglia-related inflammation. Thus, we evaluated the activation of α7 nAch receptors on chronic pain-induced anxiety- and depression-like behaviors and explored the potential mechanisms. Open field, sucrose preference, and pain behavior tests (paw withdrawal threshold, and cold response to acetone) were evaluated in male Wistar rats that received spared nerve injury (SNI) and complete Freund’s adjuvant (CFA) into the unilateral ankle articular cavity. The effect of intracerebroventricular (ICV) injection of α7 nAch receptor agonist PHA and α7 nAch receptor antagonist on anxiety and depression-like behaviors and cytokines expression were examined. Cytokines in medial prefrontal cortex (mPFC), basolateral amygdala (BA), and ventral hippocampus (VH) were measured using enzyme-linked immune absorbent assay. SNI surgery and CFA injection induced anxiety- and depression-like behaviors, and ICV injection of PHA reduced that anxiety- and depression-like behaviors. SNI surgery and CFA injection skewed the mPFC, BA, and VH to a pro-inflammatory response and ICV injection of PHA shift brain to an anti-inflammatory response in those sites. The anti-depressive effect and anti-inflammatory effect of PHA were reversed by WNT/β-catenin inhibitor. Activation of alpha7 nicotinic acetylcholine receptors reduces chronic pain-induced anxiety- and depression-like behaviors, the mechanisms may be attributed to the activation of WNT/β-catenin pathway and suppression of brain inflammation.

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