Acetylcholine modulation of high‐voltage‐activated calcium channels in the neurones acutely dissociated from rat paratracheal ganglia

Murai, Yoshinaka; Ishibashi, Hiroyuki; Akaike, Norio; Ito, Yushi

doi:10.1038/sj.bjp.0701753

Cited by 23 publications

(14 citation statements)

References 45 publications

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“…However, blocking ganglion M 1 receptors does not reduce smooth muscle contraction induced by electrically stimulating vagal preganglionic nerves in guinea pigs (Undem et al 1990). Similarly, no functional role for M 1 receptors has been identified in rat tracheal ganglia (Murai et al 1998). This contrasts with rabbit, where blocking M 1 receptors in the bronchi reduces smooth muscle contraction following vagal stimulation (Bloom et al 1988).…”

Section: Muscarinic Receptors In the Lungsmentioning

confidence: 99%

Muscarinic Receptor Antagonists: Effects on Pulmonary Function

Buels

Fryer

2011

Handbook of Experimental Pharmacology

110

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In healthy lungs, muscarinic receptors control smooth muscle tone, mucus secretion, vasodilation, and inflammation. In chronic obstructive pulmonary disease (COPD) and asthma, cholinergic mechanisms contribute to increased bronchoconstriction and mucus secretion that limit airflow. This chapter reviews neuronal and nonneuronal sources of acetylcholine in the lung and the expression and role of M1, M2, and M3 muscarinic receptor subtypes in lung physiology. It also discusses the evidence for and against the role of parasympathetic nerves in asthma, and the current use and therapeutic potential of muscarinic receptor antagonists in COPD and asthma.

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Section: Muscarinic Receptors In the Lungsmentioning

confidence: 99%

Muscarinic Receptor Antagonists: Effects on Pulmonary Function

Buels

Fryer

2011

Handbook of Experimental Pharmacology

110

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“…The direct way to study the presynaptic actions of Z‐338 would be to observe the action of Z‐338 on the cholinegic auto‐inhibitory responses in the prejunctional nerve terminals, but, these experiments are not technically feasible. Therefore, we observed the effects of Z‐338 on cholinergic responses of isolated rat paratracheal ganglion cells, since this was used as the model to study the prejunctional modulations of excitatory neuro‐effector transmission (Murai et al ., 1998; Ito et al ., 2000). In the present experiments, firstly we observed the effects of ACh on isolated paratracheal ganglion cells and then studied the effects of Z‐338 on these responses of the ganglion cells to ACh.…”

Section: Introductionmentioning

confidence: 99%

An electrophysiological study of muscarinic and nicotinic receptors of rat paratracheal ganglion neurons and their inhibition by Z‐338

Kanemoto

Ishibashi

Doi

et al. 2002

British J Pharmacology

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1 To study the mechanisms involved in the action of Z-338, a newly synthesized gastroprokinetic agent, experiments were performed with the paratracheal ganglion cells acutely dissociated from 2-week-old Wistar rats. The e ects of Z-338 on both nicotinic and muscarinic responses of the ganglion cells were studied by nystatin perforated patch recording con®guration under the currentand voltage-clamp conditions. 2 Acetylcholine (ACh) or nicotine, and muscarine or oxotremorine-M (OX-M) induced membrane depolarization with rapid and slow time courses respectively, followed by repetitive generation of action potentials in the ganglion cell. Corresponding to the membrane depolarization induced by cholinergic agents, ACh induced biphasic inward currents with rapid and slow time courses under the voltage-clamp condition. Nicotine and muscarine or OX-M evoked inward currents with rapid and slow time courses, respectively. The rapid and slow inward currents were accompanied by increase and decrease in the membrane conductance, respectively. In addition, OX-M dosedependently suppressed the M-type K + current evoked in response to hyperpolarizing voltage-steps from V H of 725 mV to 750 mV, indicating that the activation of muscarinic acetylcholine receptors inhibits M-type K + current, thus inducing inward current in the ganglion cell. 3 Z-338 competitively suppressed the inward currents induced by OX-M through M 1 ACh receptor, and uncompetitively suppressed the currents induced by nicotine. 4 The inhibitory actions of Z-338 on the membrane depolarization and corresponding inward currents mediated by M 1 -muscarinic and neuronal nicotinic ACh receptors in the isolated ganglion cells were discussed in relation to the inhibitory actions on autoreceptors in the parasympathetic nerve terminals, which would explain the gastroprokinetic actions of Z-338.

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“…At the paratracheal ganglion synapses, nicotinic cholinergic receptors are responsible for the fast excitatory postsynaptic potential (EPSP), and this is followed by a slow EPSP which is mediated by muscarinic receptors ( Barnes, 1992 ; Barnes et al ., 1988 ). ACh elicits the inward currents via nicotinic receptors with a threshold concentration of 3 μ M in the isolated rat paratracheal neurones ( Aibara & Akaike, 1991 ), while the muscarinic receptor mediated response is activated by nanomolar concentrations of ACh ( Murai et al ., 1998 ). In the present study, the depolarizing response induced by low concentration of ACh (0.3 μ M ) was inhibited by pirenzepine, thus suggesting that the ACh‐response observed in the present study may be regulated by muscarinic receptors.…”

Section: Discussionmentioning

confidence: 99%

“…Experiments were performed on paratracheal neurones freshly dissociated from 2‐week‐old Wistar rats. The procedure for obtaining dissociated paratracheal ganglion neurones is similar to that described elsewhere ( Murai et al ., 1998 ). Briefly, the paratracheal ganglia were rapidly removed from the trachea of rats under pentobarbital anaesthesia, and the rats were subsequently killed by exsanguination.…”

Section: Methodsmentioning

confidence: 99%

Activation of potassium conductance by ophiopogonin‐D in acutely dissociated rat paratracheal neurones

Ishibashi

Mochidome

Okai

et al. 2001

British J Pharmacology

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1 The e ect of ophiopogonin-D (OP-D), a steroidal glycoside and an active component of Bakumondo-to, a Chinese herbal antitussive, on neurones acutely dissociated from paratracheal ganglia of 2-week-old Wistar rats was investigated using the nystatin-perforated patch recording con®guration. 2 Under current-clamp conditions, OP-D (10 mM) hyperpolarized the paratracheal neurones from a resting membrane potential of 765.7 to 773.5 mV.3 At the concentration of 1 mM and above, OP-D concentration-dependently activated an outward current accompanied by an increase in the membrane conductance under voltage-clamp conditions at a holding potential of 740 mV. 4 The reversal potential of the OP-D-induced current (I OP-D ) was 779.4 mV, which is close to the K + equilibrium potential of 786.4 mV. The changes in the reversal potential for a 10 fold change in extracellular K + concentration was 53.1 mV, indicating that the current was carried by K + . 5 The I OP-D was blocked by an extracellular application of 1 mM Ba 2+ by 59.0%, but other K + channel blockers, including 4-aminopyridine (3 mM), apamin (1 mM), charybdotoxin (0.3 mM), glibenclamide (1 mM), tolbutamide (0.3 mM) and tetraethylammonium (10 mM), did not inhibit the I OP-D . 6 OP-D also inhibited the ACh-and bradykinin-induced depolarizing responses which were accompanied with ®ring of action potentials. 7 The results suggest that OP-D may be of bene®t in reducing the excitability of airway parasympathetic ganglion neurones and consequently cholinergic control of airway function and further, that the hyperpolarizing e ect of OP-D on paratracheal neurones via an activation of K + channels might explain a part of mechanisms of the antitussive action of the agent.

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Acetylcholine modulation of high‐voltage‐activated calcium channels in the neurones acutely dissociated from rat paratracheal ganglia

Cited by 23 publications

References 45 publications

Muscarinic Receptor Antagonists: Effects on Pulmonary Function

Muscarinic Receptor Antagonists: Effects on Pulmonary Function

An electrophysiological study of muscarinic and nicotinic receptors of rat paratracheal ganglion neurons and their inhibition by Z‐338

Activation of potassium conductance by ophiopogonin‐D in acutely dissociated rat paratracheal neurones

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