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At least 55 records · Page 3Linked to original sources
PubMed1996

The roles of muscarinic receptor subtypes in modulation of nasal ciliary action.

Muscarinic receptors are believed to play an important role in modulation of ciliary action in respiratory system. We studied the in vitro effect of methacholine, a beta-methyl ester of acetylcholine, on the ciliary beat frequency (CBF). Adenoid explants were cultured in Minimum Essential Medium Eagle (MEM). CBF was determined using microphotometry. Methacholine (10(-6) M) increased CBF a maximum of 10.34 +/- 0.42% (p < 0.001). The non-selective muscarinic antagonist atropine (10(-6) M) significantly inhibited the ciliostimulatory effects of methacholine (p < 0.001). To characterize the muscarinic receptor subtypes in nasal mucosa, the selective M1-, M2- and M3-muscarinic antagonists pirenzepine dihydrochloride (PZ), gallamine triethiodide (gallamine), and 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP) were used prior to addition of methacholine, PZ and 4-DAMP, at concentrations of 10(-6) to 10(-8) M, significantly inhibited the ciliostimulatory effects of methacholine (p < 0.0001). There was no significant inhibition of methacholine-induced ciliostimulation by gallamine (p > 0.3). Our study showed that ciliostimulation by methacholine in human upper airway mucosa involves M1- and M3- muscarinic receptor subtypes, but not the M2-receptor subtype. The identification of the muscarinic receptor subtypes and intracellular signalling mechanisms involved in CBF modulation will permit the selection appropriate of pharmacological agents for treating the cholinergic symptoms of rhinitis.

Atropine↗
PubMed1982

Gallamine triethiodide-induced modifications of sodium conductance in Myxicola giant axons.

1. Internal gallamine triethiodide (Flaxedil) modifies Na+ channel kinetics in Myxicola axons but does not alter K+ conductance. The drug has no effect externally. 2. Gallamine initially increases the leakage-conductance, but this effect completely reverses within 30 min despite the maintained presence of drug. 3. During step depolarizations to membrane potentials less than -10 mV, gallamine slows the rate of Na+ inactivation, but all channels which have opened can still inactivate. During depolarizations to more positive potentials, gallamine-modified Na+ currents show a biphasic decline, and at VM greater than -10 mV, Na+ inactivation is incomplete as evidenced by the large Na+ tail currents which follow pulses sufficiently long to have allowed complete inactivation of normal Na+ channels. The tail currents are slower than normal Na+ tails, and exhibit a pronounced hook. With gallamine, the fraction of Na+ channels which do not inactivate increases sigmoidally over the range 0 mV to +80 mV. 4. For VM greater than ENa, gallamine almost completely blocks outward Na+ currents. The block is determined by the direction of Na+ current, rather than the absolute membrane potential. 5. Gallamine has no effect upon the rate of Na+ channel activation, the maximum Na+ conductance, the steady-state Na+ inactivation curve, or the rate of development or removal of inactivation by prepulses. 6. Gallamine eliminated physiological immobilization of intramembrane charge movements (QOFF and QON) and does not itself induce immobilization. Thus, in the presence of gallamine, QOFF following long pulses is the same as QOFF following short pulses.

Animals↗
PubMed1989

Determination of gallamine and its impurities by reversed-phase ion-pair high-performance liquid chromatography and comparison with thin-layer chromatography.

A reversed-phase, ion-pair high-performance liquid chromatographic (HPLC) method for the determination of gallamine and its impurities is described. The separation is achieved on a Nucleosil C18 column with acetonitrile-aqueous phosphate buffer (pH 3.0) (31:69, v/v) containing 0.1 M sodium perchlorate as eluent and on-line UV detection at 200 nm. The method is sensitive (the detection limit is 0.7 ng injected) and reproducible, with a peak area coefficient of variation of 0.19% (n = 15; 3 micrograms injected) and 1.65% (n = 15; 10 ng injected) for a gallamine assay; the detector response is linear over the concentration range 0.5-250 micrograms/ml of gallamine triethiodide with a correlation coefficient of 0.9997. The method has been used to isolate the two main impurities contained in gallamine triethiodide batches; their structures have been determined by NMR and fast atom bombardment mass spectrometry. Various gallamine triethiodide batches have been analysed and the HPLC results compared with those obtained by thin-layer chromatography.

Chromatography, High Pressure Liquid↗
PubMed1995

Control of locomotion in marine mollusc Clione limacina. X. Effects of acetylcholine antagonists.

The swimming central pattern generator (CPG) of the pteropod mollusc Clione limacina is located in the pedal ganglia. It consists of three groups of interneurons (7, 8, and 12) which generate the rhythmical activity and determine the temporal pattern of the motor output, that is, phasic relations between different groups of motor neurons supplying dorsal (group 1 and 3 motor neurons) and ventral (group 2 and 4 motor neurons) muscles of the wings. In this work peripheral and central effects of acetylcholine (ACh) antagonists on the swimming control in C. limacina has been studied. The ACh antagonist atropine blocked transmission from the wing nerves to wing muscles, while gallamine triethiodide (Flaxedil), d-tubocurarine, and alpha-bungarotoxin did not affect the neuromuscular transmission. In the pedal ganglia, the ACh antagonists atropine and gallamine triethiodide blocked inhibitory postsynaptic potentials (IPSPs) produced by group 8 interneurons onto group 7 interneurons and motor neurons of groups 1 and 3. d-Tubocurarine and alpha-bungarotoxin did not affect IPSPs produced by group 8 interneurons. Although atropine and gallamine triethiodide blocked IPSPs produced by group 8 interneurons in antagonistic neurons, these drugs did not influence excitatory postsynaptic potentials (EPSPs) produced by group 8 interneurons onto group 12 interneurons. The main pattern of the swimming rhythm with an alternation of two phases of the swimming cycle persisted after elimination of inhibitory connections from group 8 interneurons to antagonistic neurons by the ACh antagonists. This suggests that there are redundant mechanisms in the system controlling C. limacina's swimming. This redundancy ensures reliable operation of the system and contributes to its flexibility.

Acetylcholine↗
PubMed1984

The effects of acetylcholine on bulbar respiratory related neurones. Consequences of anaesthesia by pentobarbital.

The effects of cholinergic agonists and antagonists applied by microiontophoresis to bulbar respiratory neurones were determined in different preparations: cats anaesthetized by pentobarbital and immobilized by gallamine triethiodide, intercollicular decerebrate cats either not immobilized or immobilized by gallamine triethiodide. Respiratory neurones located at the bulbar level exhibited a muscarinic cholinergic sensitivity in all preparations. Muscarinic responses were either excitatory or inhibitory. The number of neurones showing excitatory responses was lower under pentobarbital anaesthesia than in decerebrate cats.

Acetylcholine↗