Release of non-neuronal acetylcholine from the isolated human placenta is affected by antidepressants

Wessler, Ignaz; Herschel, Sabine; Bittinger, Fernando; Kirkpatrick, Charles James

doi:10.1016/j.lfs.2007.01.004

Cited by 12 publications

(6 citation statements)

References 18 publications

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“…There is no evidence as to whether these lymphocytes have appropriate access to supply ACh for the renal function, but it is thought that this might be one of possible mechanism by which ACh is delivered to tissues. It is known that various types of epithelial cells, including urinary bladder, airway, and skin cells, produce ACh in animals, including humans (Wessler et al, 2007;Kawashima and Fujii, 2008). In this study, ChAT immunoreactivity was observed in CCD principal cells, suggesting the existence of an autocrine/paracrine ACh system in non-neuronal cells.…”

Section: Discussionsupporting

confidence: 49%

Non-neuronal expression of choline acetyltransferase in the rat kidney

et al. 2011

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Section: Discussionsupporting

confidence: 49%

Non-neuronal expression of choline acetyltransferase in the rat kidney

et al. 2011

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“…It is now known that cells other than neurons express the proteins required for acetylcholine metabolism. Acetylcholine is synthesized, amongst others, by immune cells (lymphocytes, dendritic cells, neutrophils) [81–83], keratinocytes [84], endothelial cells [85], and epithelial cells of placenta [86], urinary bladder [87] and airways [88]. Acting through muscarinic and nicotinic receptors, acetylcholine participates in a wide range of physiological processes including keratinocyte proliferation and differentiation, ciliary beat frequency in airway epithelial cells and relaxation of smooth muscle in vessels [89].…”

Section: Acetylcholine and Its Role In Inflammationmentioning

confidence: 99%

Cholinergic control of inflammation

Rosas-Ballina¹,

Tracey

2009

Journal of Internal Medicine

481

347

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Cytokine production is necessary to protect against pathogens and promote tissue repair, but excessive cytokine release can lead to systemic inflammation, organ failure and death. Inflammatory responses are finely regulated to effectively guard from noxious stimuli. The central nervous system interacts dynamically with the immune system to modulate inflammation through humoral and neural pathways. The effect of glucocorticoids and other humoral mediators on inflammatory responses has been studied extensively in the past decades. In contrast, neural control of inflammation has only been recently described. We summarize autonomic regulation of local and systemic inflammation through the ‘cholinergic anti-inflammatory pathway’, a mechanism consisting of the vagus nerve and its major neurotransmitter, acetylcholine, a process dependent on the nicotinic acetylcholine receptor α7 subunit. We recapitulate additional sources of acetylcholine and their contribution to the inflammatory response, as well as acetylcholine regulation by acetylcholinesterase as a means to attenuate inflammation. We discuss potential therapeutic applications to treat diseases characterized by acute or chronic inflammation, including autoimmune diseases, and propose future research directions.

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“…Ex vivo experimentation on human placentas revealed that a high concentration of doxepin, which possess both transporter antagonism as well as potent receptor antagonism at multiple targets (e.g., adrenergic, muscarinic, and histaminergic), decreases nonneuronal acetylcholine release. Although the clinical relevancy of the concentrations used are not clear, this has been speculated to be a possible mechanism for some clinical findings reporting low birth weight due to prenatal antidepressant exposure, because acetylcholine may control vascularization and alter energy availability to the fetus (Wessler et al, 2007). However, similar studies have not been performed using other antidepressants.…”

Section: B Role Of Serotonin In Developmentmentioning

confidence: 99%