Prejunctional GABA-B inhibition of cholinergic, neurally-mediated airway contractions in guinea-pigs
References (35)
- et al.
Prejunctional alpha-2-adrenoreceptors inhibit contraction of tracheal smooth muscle by inhibiting cholinergic neurotransmission
Life Sci
(1981) γ-Aminobutyric acid in peripheral tissues
Life Sci
(1985)- et al.
Bicucullineinsensitive GABA receptors on peripheral autonomic nerve terminals
Eur J Pharmacol
(1981) GABA-B receptors and their significance in mammalian pharmacology
Trends Pharmacol Sci
(1989)- et al.
2-Hydroxysaclofen: an improved antagonist at central and peripheral GABA-B receptors
Neurosci Lett
(1988) The GABA-A receptor gated ion channel: biochemical and pharmacological studies of structure and function
Biochem Pharmacol
(1988)- et al.
Effect of prostaglandin F2α on pulmonary rapidly-adapting receptors in the guinea pig
Prostaglandins
(1984) - et al.
Bronchial hyperreactivity
Am Rev Respir Dis
(1980) Neural control of human airways in health and disease
Am Rev Respir Dis
(1986)- et al.
Prejunctional inhibitory muscarinic receptors on cholinergic nerves in human and guinea pig airways
J Appl Physiol
(1988)
Inhibition of cholinergic neurotransmission in human airways by β2-adrenoreceptors
J Appl Physiol
Modulation of cholinergic neurotransmission in airways by enkephalin
J Appl Physiol
Control of neurotransmission by prostaglandins in canine trachealis smooth muscle
J Appl Physiol
Mechanism of substance P-induced contraction of rabbit airway smooth muscle
J Appl Physiol
Potentiation of vagal contractile response by thromboxane mimetic U-46619
J Appl Physiol
Interaction of serotonin with vagal and acetylcholine induced bronchoconstriction in canine lungs
J Appl Physiol
Chemical nature of synaptic transmission in vertebrates
Physiol Rev
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2016, Pharmacology and TherapeuticsCitation Excerpt :Alternatively, GABAA receptors are ion channels, composed of multiple subunits, that conduct inward chloride currents that serve to hyperpolarize the cell and limit depolarization. GABAA channels in the brainstem regulate cholinergic transmisson to the lung (Haxhui et al., 1986; Moore et al., 2004), and both GABAA channels and GABAB receptors reside on lung postganglionic parasympathetic nerves of the lung and serve to regulate cholinergic nerve activity (Chapman et al., 1991; Tamaoki et al., 1987; Tohda and Kubo, 1998). The Emala lab has demonstrated the GABAA receptors are expressed in ASM (Mizuta et al., 2008), that selective GABAA activation with muscimol can relax contracted ASM (Gleason et al., 2009), and also potentiate the relaxant effect of beta-agonists on ASM (Gallos et al., 2008).
2-hydroxysaclofen
2007, xPharm: The Comprehensive Pharmacology ReferenceBronchial epilepsy or broncho-pulmonary hyper-excitability as a model of asthma pathogenesis
2006, Medical HypothesesSite of action of GABAB receptor for vagal motor control of the lower esophageal sphincter in ferrets and rats
2001, GastroenterologyCitation Excerpt :A post-synaptic function of GBR in vagal motor neurons is shown in whole cell patch clamp experiments in the DMN, where a baclofen-mediated outward current was not affected by the synaptic blocker, tetrodotoxin, indicating a direct effect at GBR receptors on DMN neurons.36 A presynaptic site of action of GBR at cholinergic vagal terminals is supported by the fact that both electrical field stimulation of tracheal strips and vagal nerve stimulation in guinea pigs caused cholinergic-dependent bronchospasms that were inhibited by baclofen.13 Indeed, Andrews and colleagues37 concluded that systemic baclofen increased gastric pressure because of a reduction in the tonic vagal drive to the NANC inhibitory neurons in the stomach.
Effect of the GABA-agonist baclofen on bronchial responsiveness in asthmatics
1999, Pulmonary Pharmacology and Therapeutics