Modulation of Neurotransmitter Release from Airways Nerves

Barnes, Peter J.

doi:10.1007/978-3-0348-7558-5_9

Cited by 8 publications

(3 citation statements)

References 283 publications

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“…The parasympathetic innervation provides the primary means by which airways tone is regulated in guinea‐pigs and man (Taylor et al , 1984; Barnes, 1993). In the airways, cholinergic neurotransmission is modulated by a number of different prejunctional receptors, the activation of which can facilitate or inhibit the release of acetylcholine (ACh) (Barnes, 1994).…”

Section: Introductionmentioning

confidence: 99%

Prostaglandin E₂ suppression of acetylcholine release from parasympathetic nerves innervating guinea‐pig trachea by interacting with prostanoid receptors of the EP₃‐subtype

Spicuzza

Giembycz

Barnes

et al. 1998

British J Pharmacology

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1 We have demonstrated recently that exogenous prostaglandin E 2 (PGE 2 ) inhibits electrical ®eld stimulation (EFS)-induced acetylcholine (ACh) release from parasympathetic nerve terminals innervating guinea-pig trachea. In the present study, we have attempted to characterize the pre-junctional prostanoid receptor(s) responsible for the inhibitory action of PGE 2 and to assess whether other prostanoids modulate, at a prejunctional level, cholinergic neurotransmission in guinea-pig trachea. 3 H]-ACh release when compared to receptors of the EP 3 -subtype. However, the relative importance of the dierent receptors will depend not only on the sensitivity of guinea-pig trachea to prostanoids but on the nature of the endogenous ligands released locally that have activity on parasympathetic nerves.

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Section: Introductionmentioning

confidence: 99%

Prostaglandin E₂ suppression of acetylcholine release from parasympathetic nerves innervating guinea‐pig trachea by interacting with prostanoid receptors of the EP₃‐subtype

Spicuzza

Giembycz

Barnes

et al. 1998

British J Pharmacology

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“…adrenoceptors (Barnes, 1994). In fact, even in species that lack a direct sympathetic supply to the airways smooth muscle, cholinergic and noradrenergic varicosities lie in close apposition which has lead to the suggestion that there may be crosstalk between the two nervous systems (Jones et al, 1980b).…”

Section: Introductionmentioning

confidence: 99%

“…Although noradrenergic nerves do not directly control airways smooth muscle tone they may influence cholinergic neurotransmission via activation of pre-junctional aor fl-1 Author for correspondence. adrenoceptors (Barnes, 1994). In fact, even in species that lack a direct sympathetic supply to the airways smooth muscle, cholinergic and noradrenergic varicosities lie in close apposition which has lead to the suggestion that there may be crosstalk between the two nervous systems (Jones et al, 1980b).…”

Section: Introductionmentioning

confidence: 99%

Paradoxical facilitation of acetylcholine release from parasympathetic nerves innervating guinea‐pig trachea by isoprenaline

Belvisi

Patel

Takahashi

et al. 1996

British J Pharmacology

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1 Previous studies have provided evidence that activation of fl-adrenoceptors on cholinergic nerve terminals can inhibit neurotransmission in the airways. However, in most cases, this conclusion has been based on indirect evidence obtained from mechanical experiments where changes in airways smooth muscle tone were measured.2 We have assessed whether modulation of cholinergic neurotransmission by fl-adrenoceptor agonists is due to a pre-or post-junctional action by investigating the effect of isoprenaline on contractile responses evoked by exogenous acetylcholine (ACh) and electrical field stimulation (EFS; 4 Hz, 40 V, 0.5 ms pulse width every 15 s), and on EFS-induced ACh release from cholinergic nerves innervating guinea-pig and human trachea. Furthermore, the subtype of /3-adrenoceptor which modulates neurotransmission and the potential role of cyclic AMP in this response were evaluated. 3 In guinea-pig trachea, isoprenaline (1 nM-1 -IM) inhibited the contractile response evoked by exogenous ACh (1 gM) to a similar extent to that evoked by EFS (EC50 = 19.9 and 23 nM, respectively). 4 In epithelium-denuded guinea-pig strips treated with indomethacin (10 gM), isoprenaline significantly enhanced EFS-induced ACh release from cholinergic nerve terminals (by 36% at 0.3 gM). This effect was blocked by propranolol and ICI 118, 551 (each 0.1 gM). In contrast, isoprenaline failed to affect EFSinduced ACh release from parasympathetic nerves innervating human trachea. 5 To evaluate the role of cyclic AMP in the /3-adrenoceptor-induced facilitation of cholinergic neurotransmission, the effects of various cyclic AMP elevating drugs on ACh release were studied.Forskolin (10 gM) significantly augmented (by 17%) EFS-induced ACh release, an effect which was not reproduced by 1,9-dideoxyforskolin (10 gM) which does not activate adenylyl cyclase. Similarly, the cyclic AMP analogue, 8-bromo-cyclic AMP (1 mM) and cholera toxin (1 Mg ml-') facilitated ACh output by 22 and 47% respectively, whereas prostaglandin E2 (PGE2, 0.1 nM-I gM) inhibited this response (by 67% at 1 Mm).6 Zardaverine (10 gM), a dual inhibitor of the phosphodiesterase (PDE)3 and PDE4 isoenzyme families, did not affect EFS-induced ACh release and failed to facilitate the actions of either isoprenaline or PGE2. Similarly, neither SK&F 94120 (10 uM) nor rolipram (10 gM), selective inhibitors of PDE3 and PDE4 respectively, significantly affected the release of ACh in response to EFS. 7 The result of this study suggests that isoprenaline facilitates cholinergic neurotransmission in guineapig, but not human, trachea by activation of pre-junctional /32-adrenoceptors, an effect that may be mediated via activation of the cyclic AMP/cyclic AMP-dependent protein kinase cascade. Furthermore, the data presented herein illustrate the need to undertake direct measurements of neurotransmitter release when examining the effect of agents purported to act pre-junctionally.

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Epithelium-Dependent Inhibition of Cholinergic Transmission in Rat Isolated Trachea by Potassium Channel Openers

Fabiani

1996

Pharmacological Research

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Modulation of Neurotransmitter Release from Airways Nerves

Cited by 8 publications

References 283 publications

Prostaglandin E₂ suppression of acetylcholine release from parasympathetic nerves innervating guinea‐pig trachea by interacting with prostanoid receptors of the EP₃‐subtype

Prostaglandin E₂ suppression of acetylcholine release from parasympathetic nerves innervating guinea‐pig trachea by interacting with prostanoid receptors of the EP₃‐subtype

Paradoxical facilitation of acetylcholine release from parasympathetic nerves innervating guinea‐pig trachea by isoprenaline

Epithelium-Dependent Inhibition of Cholinergic Transmission in Rat Isolated Trachea by Potassium Channel Openers

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Modulation of Neurotransmitter Release from Airways Nerves

Cited by 8 publications

References 283 publications

Prostaglandin E2 suppression of acetylcholine release from parasympathetic nerves innervating guinea‐pig trachea by interacting with prostanoid receptors of the EP3‐subtype

Prostaglandin E2 suppression of acetylcholine release from parasympathetic nerves innervating guinea‐pig trachea by interacting with prostanoid receptors of the EP3‐subtype

Paradoxical facilitation of acetylcholine release from parasympathetic nerves innervating guinea‐pig trachea by isoprenaline

Epithelium-Dependent Inhibition of Cholinergic Transmission in Rat Isolated Trachea by Potassium Channel Openers

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Prostaglandin E₂ suppression of acetylcholine release from parasympathetic nerves innervating guinea‐pig trachea by interacting with prostanoid receptors of the EP₃‐subtype

Prostaglandin E₂ suppression of acetylcholine release from parasympathetic nerves innervating guinea‐pig trachea by interacting with prostanoid receptors of the EP₃‐subtype