Alpha subunit composition of nicotinic acetylcholine receptors in the rat autonomic ganglia neurons as determined with subunit-specific anti-α(181–192) peptide antibodies

Skok, Maryna; Voitenko, L. P.; Voitenko, S. V.; Lykhmus, Elena Y; Kalashnik, E.N.; Litvin, T.I.; Tzartos, Socrates J.; Skok, V. I.

doi:10.1016/s0306-4522(99)00160-8

Cited by 115 publications

(67 citation statements)

References 50 publications

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“…6,16,17 This argument is supported by evidence that the ␣3 nAChR subunit is abundant in autonomic ganglia, located on postganglionic neurons, and ␣3 nAChR antibodies block ganglionic transmission in animal models. 7,18 Progressive elevation in ␣3 nAChR antibody levels resulted in increased postganglionic but not preganglionic sudomotor dysfunction. A similar finding with ganglionic ␣3 nAChR antibody levels and progressive mixed ganglionic sudomotor dysfunction was also described.…”

Section: Figure 1 Elevated Ganglionic Antibody Levels Results In Highementioning

confidence: 99%

Sudomotor dysfunction in autoimmune autonomic ganglionopathy

Kimpinski¹,

Iodice²,

Sandroni³

et al. 2009

Neurology

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Section: Figure 1 Elevated Ganglionic Antibody Levels Results In Highementioning

confidence: 99%

Sudomotor dysfunction in autoimmune autonomic ganglionopathy

Kimpinski¹,

Iodice²,

Sandroni³

et al. 2009

Neurology

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“…␣5 subunits are coexpressed with approximately 70 to 80% of ␣3-containing receptors in the chick ciliary ganglion neurons (Conroy and Berg, 1995) and human neuroblastoma cells (Wang et al, 1996), approximately 30% of rat cardiac parasympathetic neurons (Poth et al, 1997), and nearly all rat SCG neurons (Skok et al, 1999). It is well known that ␣5 subunits participate in the formation of ion channels but do not form ACh binding sites (Ramirez-Latorre et al, 1996;Wang et al, 1996;Gerzanich et al, 1998;Nelson and Lindstrom, 1999).…”

Section: Discussionmentioning

confidence: 99%

Deficiency of Nicotinic Acetylcholine Receptor β4 Subunit Causes Autonomic Cardiac and Intestinal Dysfunction

Wang

Orr-Urtreger

Chapman

et al. 2003

Molecular Pharmacology

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Neuronal nicotinic acetylcholine receptors (nAChR) are composed of 12 subunits (␣2-␣10 and ␤2-␤4), which play the central role in autonomic transmission. ␤4 subunits are abundantly expressed in autonomic ganglia, forming acetylcholine binding sites and ion channels with ␣3 or ␣3 and ␣5 subunits as pentameric receptors. To investigate the physiological and pharmacological properties of ␤4 subunits in autonomic ganglia, we measured autonomic functions in knockout mice lacking nAChR subunit ␤4 (␤4 Ϫ/Ϫ ) and wild-type mice. ␤4 Ϫ/Ϫ mice had an attenuated bradycardiac response to high frequency (60 pulse/s) vagal stimulation, as well as an increased sensitivity to hexamethonium blockade at low dose (3 mg/kg) and a reduced ileal contractile response to the nicotinic agonists cytisine, dimethylphenylpiperazinium iodide, nicotine (10 mg/kg each), and epibatidine (0.1 mg/kg). The results suggest that ␤4 subunits are important components of nAChRs in autonomic ganglia. Deficiency of ␤4 subunits altered ion channel properties, conductance, and sensitivity and affinity of receptors to agonists and antagonists, affecting ganglionic transmission.

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“…Other studies by Tracey have focused on the α7 nicotinic acetylcholine receptor as a primary mediator of the anti-inflammatory signal conveyed by the efferent vagus nerve (Wang et al, 2003). However, nicotinic receptors, including the α7 subunit, mediate the communication between the spinal 'cholinergic' sympathetic preganglionic neurons and the catecholamine-producing neurons located in sympathetic ganglia and the adrenal medulla (Skok et al, 1999). Also, nicotine administration stimulates catecholamine release by activation of nicotinic receptors localized on peripheral postganglionic sympathetic neurons and the adrenal medulla (Haass and Kubler, 1997).…”

Section: Role Of the Vagus Nerve And Parasympathetic Nervous Systemmentioning

confidence: 99%

Autonomic innervation and regulation of the immune system (1987–2007)

Nance¹,

Sanders²

2007

Brain, Behavior, and Immunity

754

580

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Since 1987, only a few neuroanatomical studies have been conducted to identify the origin of innervation for the immune system. These studies demonstrated that all primary and secondary immune organs receive a substantial sympathetic innervation from sympathetic postganglionic neurons. Neither the thymus nor spleen receive any sensory neural innervation; however, there is evidence that lymph nodes and bone marrow may be innervated by sensory neurons located in dorsal root ganglia. There is no neuroanatomical evidence for a parasympathetic or vagal nerve supply to any immune organ. Thus, the primary pathway for the neural regulation of immune function is provided by the sympathetic nervous system (SNS) and its main neurotransmitter, norepinephrine (NE). Activation of the SNS primarily inhibits the activity of cells associated with the innate immune system, while it either enhances or inhibits the activity of cells associated with the acquired/adaptive immune system. Innate immune cells express both alpha and beta-adrenergic receptor subtypes, while T and B lymphocytes express adrenergic receptors of the beta2 subtype exclusively, except for murine Th2 cells that lack expression of any subtype. Via these adrenergic receptors, NE is able to regulate the level of immune cell activity by initiating a change in the level of cellular activity, which often involves a change in the level of gene expression for cytokines and antibodies.

show abstract

Alpha subunit composition of nicotinic acetylcholine receptors in the rat autonomic ganglia neurons as determined with subunit-specific anti-α(181–192) peptide antibodies

Cited by 115 publications

References 50 publications

Sudomotor dysfunction in autoimmune autonomic ganglionopathy

Sudomotor dysfunction in autoimmune autonomic ganglionopathy

Deficiency of Nicotinic Acetylcholine Receptor β4 Subunit Causes Autonomic Cardiac and Intestinal Dysfunction

Autonomic innervation and regulation of the immune system (1987–2007)

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