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Case 3.16
Published in Monica Fawzy, Plastic Surgery Vivas for the FRCS(Plast), 2023
How does chemodenervation work, and how would you apply this to facial palsy patients?Purified Botulinum toxin causes a neuromuscular blocking effect by binding presynaptically to cholinergic nerve terminals and preventing the release of acetylcholine.It can thus be used to improve symmetry by selectively weakening:contralateral normal muscles, oripsilateral muscles affected by hypertonicity and synkinesis – in patients with a post-paralytic picture.
Cosmetic Facial Interventions
Published in R James A England, Eamon Shamil, Rajeev Mathew, Manohar Bance, Pavol Surda, Jemy Jose, Omar Hilmi, Adam J Donne, Scott-Brown's Essential Otorhinolaryngology, 2022
Botulinum toxin type A (BTX-A) is a zinc-dependent endopeptidase produced by Clostridium botulinum. It acts on cholinergic nerve endings to produce muscle paresis that lasts for around 3 months, and then starts to wear off. When the muscle relaxes, it stops pulling on the skin and the wrinkle caused by the muscle pull fades away. Botulinum toxin has been the most revolutionary anti-aging treatment in recent years. It has an excellent safety profile and has been used extensively for facial rejuvenation with a focus on hyperkinetic wrinkles. It is also used in the dysfunctional paralyzed face to improve facial symmetry or in the scarred face to improve dermal contour with the use of fillers. Generally, an appropriate amount of Botulinum toxin is injected and the patient is reviewed after 2 weeks for further injections if required. This helps to avoid creating an unnatural appearance and a frozen face. Botulinum toxin is contraindicated in patients with underlying neuromuscular junction disorder, allergy to any of its components (human albumin, botulinum toxin), pregnancy and breastfeeding.
Adrenergic Agonists
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
Adrenaline acts directly causing smooth muscle dilation by its interaction with the β2 receptors and indirectly relaxes gut by decreasing the release of acetylcholine from the cholinergic nerve terminals because of its action on α2 adrenoceptors seen in the ganglionic cells thereby decreasing electrolyte and water secretion to lumen of intestine (Cellek et al., 2007; Quinson et al., 2001; Schemann et al., 2010).
Gastroparesis syndromes: emerging drug targets and potential therapeutic opportunities
Published in Expert Opinion on Investigational Drugs, 2023
Le Yu Naing, Matthew Heckroth, Prateek Mathur, Thomas L Abell
The 5-HT4 receptor is a G-protein linked receptor that promotes the activation of the adenyl cyclase/cyclic adenosine monophosphate (cAMP)/protein kinase A pathway enhancing cell excitability[29]. Activation of these receptors on myenteric cholinergic nerve terminals induces the release of several neurotransmitters that promote propulsive motility and produce coordinated contraction and relaxation of gastrointestinal smooth muscle[32]. They have also been shown to play a role in inhibiting visceral pain and suppressing intestinal hypersensitivity in response to distension. 5-HT4 receptor agonists are used clinically as a prokinetic agent for patients with gastroparesis. Cisapride, a potent 5-HT4 agonist, and tegaserod, a partial 5-HT4 agonist, were both shown to be effective at relieving Gp symptoms as well as accelerating gastric emptying and colonic transit. However, both were withdrawn from the US market secondary to reports of serious cardiac arrhythmias related to QT interval prolongation. Tegaserod is now available with limited access in the US[33].
Investigation of the toxicological and inhibitory effects of some benzimidazole agents on acetylcholinesterase and butyrylcholinesterase enzymes
Published in Archives of Physiology and Biochemistry, 2021
The central cholinergic system is a complex component of cell bodies and dendrites. Cerebral blood flow, cortical plasticity and cognitive performance, and learning-memory processes such as activity, sleep-wake cycle (Pfaller et al.2017). It has an important role in controlling many different functions such as modulation. Cholinergic is basal anterior brain. The presence of neurons was first reported by Shute and Lewis in 1967 and then by other researchers, confirmed by (Gonca Koçancı and Aslım 2016). Anatomically, the central cholinergic system represents a wide range neuronal network in the nervous system. The central and peripheral nervous system of adults transport intracellular alerts. Cholinacyltransferase (ChAT), acetylcholine (ACh), cholinesterases (Acetylcholinesterase (AChE) and butyrylcholinesterase (BChE)), cholinergic receptors (muscarinic receptors (MR) and nicotinic receptors (NR)) are components of the cholinergic system (Aslan et al.2018). AChE, neurotransmitter acetylcholine (ACh) in cholinergic synapses and neuromuscular synapses which rapidly hydrolyze into choline and acetate playing an important role in the transmission of cholinergic nerve and is one of the most effective enzymes in the nervous system (Weinreb et al.2004).
Nicotine lowers TNF-α, IL-1b secretion and leukocyte accumulation via nAChR in rat stomach
Published in Toxin Reviews, 2021
Servet Kizildag, Ferda Hosgorler, Güven Güvendi, Talha Basar Koc, Sevim Kandis, Asuman Argon, Mehmet Ates, Nazan Uysal
Nicotine may exert both local effects where it is applied regionally and systemic effects where it passes into blood circulation. Nicotine is absorbed locally by parasympathetic ganglia and cholinergic nerve endings in the digestive tract, which affects hormone and mediator secretion (Massarrat 2008). The effect of nicotine in gastric tissue is due to its local activity rather than the effects of passing through the systemic circulation. The absorption of nicotine from biological membranes is influenced by environmental pH. Since it is highly ionized in acidic environments, it is difficult for it to pass through biological membranes, so local absorption from the stomach is lower than the small intestine (National Center for Chronic Disease et al., 2014). In the experimental rodent study, it was shown that 83% of nicotine was absorbed from the digestive system, and only 10% was absorbed by the stomach by the 60th minute (Ahdaya and Guthrie 1981). In our experience, regarding the average nicotine dose of each rat, it can be said that 0,13 mg from 1.34 mg show these effects in the stomach.