Nicotine and sympathetic neurotransmission

Haass, Markus; Kübler, W.

doi:10.1007/bf00053022

Cited by 245 publications

(169 citation statements)

References 53 publications

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“…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). Finally, α7 nicotine receptor-deficient mice do not show functional deficits in parasympathetic autonomic function (Franceschini et al, 2000), as might be predicted by the cholinergic anti-inflammatory hypothesis (Wang et al, 2003).…”

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

746

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.

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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

746

580

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“…The actions of nicotine on sympathetic nerve terminals mediate, at least in part, its acute cardiovascular actions (Nedergaard and Schrold, 1977;Richardt et al, 1988;Haass and Kubler, 1997). Nicotine is known to increase the release of neurotransmitter following nerve stimulation in the rodent vas deferens (von Ku « gelgen and Starke, 1991;Todorov et al, 1991).…”

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confidence: 99%

Nicotine induces calcium spikes in single nerve terminal varicosities: a role for intracellular calcium stores

et al. 2001

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AbstractöWhile nicotine is known to act at neuronal nicotinic acetylcholine receptors (nAChRs) to facilitate neurotransmitter release, the mechanisms underlying this action are poorly understood. Some of its e¡ects are known to be mediated by presynaptic receptors. In the mouse vas deferens nicotine (10^30 WM) transiently increased the force of neurogenic contraction by 135 þ 25%, increased the amplitude of excitatory junction potentials by 74 þ 6% and increased the frequency of spontaneous excitatory junction potentials in four out of six preparations. Confocal microscopy and the calcium indicator Oregon Green 488 BAPTA-1 dextran were used to measure calcium concentration changes in the nerve terminals. Nicotine did not a¡ect the action potential-evoked calcium transient but instead triggered small, random £uctuations (`calcium spikes') in intra-varicosity calcium concentrations at an average frequency of 0.09 þ 0.02 Hz. These were insensitive to tetrodotoxin at a concentration that blocked action-potential evoked calcium transients (300 nM). They were abolished by the nAChR blocker hexamethonium (100 WM) and by both ryanodine (100 WM) and ca¡eine (3 mM), agents that modify calcium release from intracellular stores.We propose a novel mechanism whereby nicotine's action at nAChRs triggers calcium-induced calcium release from a ryanodine-sensitive calcium store in nerve terminals. This primes neurotransmitter release mechanisms and enhances both spontaneous and action potential-evoked neurotransmitter release. ß

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“…The first is a direct effect on the central nervous system; and the second is a stimulatory effect on the ganglionic sympathetic transmission that leads to a subsequent increase in the postganglionic efferent sympathetic activity; and the third, is an effect on the sympathetic peripheral nervous terminations 34,37 . For Grassi et al 38 , in addition to the peripheral adrenergic stimulation, there is a partial loss by baroreflex capacity to contain it.…”

Section: Discussionmentioning

confidence: 99%