Prejunctional nicotinic receptors involved in facilitation of stimulation‐evoked noradrenaline release from the vas deferens of the guinea‐pig

Todorov, Latchezar D.; Windisch, K.; Shersen, H.; Lajtha, Ábel; Papasova, M; Vizi, E.S.

doi:10.1111/j.1476-5381.1991.tb12151.x

Cited by 49 publications

(19 citation statements)

References 24 publications

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“…The increase in the amplitude of EJPs and the increase in the frequency of SEJPs suggest that nicotine also acts on prejunctional sympathetic terminals to increase the release of the co-transmitter ATP, which is the neurotransmitter generating EJPs in the mouse vas deferens (Stja «rne and A î strand, 1984). Similar conclusions were reached from transmitter release studies in guinea-pig vas deferens (von Ku « gelgen and Starke, 1991;Todorov et al, 1991).…”

Section: Discussionsupporting

confidence: 70%

“…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). The mouse vas deferens has a rich sympathetic innervation and has been successfully used in the past to measure changes in the intra-terminal calcium concentration (Brain and Bennett, 1997).…”

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confidence: 99%

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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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Section: Discussionsupporting

confidence: 70%

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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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“…Prejunctional muscarinic receptors block the release of norepinephrine and ATP [13,17,30,32]. Similarly, prejunctional nicotinic receptors reduce norepinephrine release [49]. Therefore, acetylcholine released from cholinergic nerves modulates adrenergic transmission to the vas deferens.…”

Section: Cholinergic Mechanismsmentioning

confidence: 99%

Physiology of the vas deferens

Steers

1994

World J Urol

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Seminal emission occurs in response to rhythmic contractions of male secondary sex organs, including the vas deferens. Although contraction of the vas is directly due to adrenergic mechanisms, numerous substances modulate the release of norepinephrine from sympathetic pathways. These substances include local endogenous factors and neurotransmitters such as acetylcholine and NPY. Many substances are capable of altering the contractility of the vas deferens by modulating neural transmitter release or the basal tone of this smooth muscle. Because multiple pathways and substrates are capable of affecting its contractility, it is not surprising that drugs and metabolic disorders influence the function of the vas deferens and, ultimately, male fertility.

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“…), is the non-specific agonist of nicotinic acetylcholine receptors (nAChRs) (Newman et al, 2002). Nicotinic receptors are located in both the central and peripheral nervous systems (Newman et al, 2002;McGehee et al, 1995;Todorov et al, 1991). These receptors belong to a superfamily of ligand-gated ion channels and 17 subunits have been identified.…”

Section: Introductionmentioning

confidence: 99%

Nicotine potentiates the neurogenic contractile response of rabbit bladder tissue via nicotinic acetylcholine receptors: Nitric oxide and prostaglandins have no role in this process

et al. 2007

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Prejunctional nicotinic receptors involved in facilitation of stimulation‐evoked noradrenaline release from the vas deferens of the guinea‐pig

Cited by 49 publications

References 24 publications

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

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

Physiology of the vas deferens

Nicotine potentiates the neurogenic contractile response of rabbit bladder tissue via nicotinic acetylcholine receptors: Nitric oxide and prostaglandins have no role in this process

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