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Nervous Control of Membrane Conductance in Mouse Lacrimal Acinar Cells

Overview
Journal Pflugers Arch
Specialty Physiology
Date 1984 Jan 1
PMID 6709489
Citations 3
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Abstract

Intracellular microelectrode recordings were made from superfused in vitro preparations of mouse lacrimal gland. The lacrimal acinar cell had a mean resting membrane potential of -44.1 +/- 0.5 mV and a mean input resistance of 3.5 +/- 0.15 M omega. Electrical field stimulation (FS) had similar effects to ACh applied by microionophoresis, both evoking a biphasic membrane hyperpolarization (up to 15 mV) accompanied by a reduction in input resistance. The equilibrium potential values (EFS and EACh) for the responses to brief duration FS and ACh ionophoresis ranged between -45 and -75 mV and depended on the time at which measurements were made following the onset of stimulation. Superfusion of ACh or adrenaline also caused membrane hyperpolarization and increased membrane conductance. Estimations of EFS and EACh made during prolonged periods of FS and ACh superfusion yielded mean values of -53.9 +/- 1.9 mV and -53.4 +/- 1.5 mV respectively. FS evoked a response in all preparations tested with maximal effects seen at 40 Hz frequency. The mean latency of the FS-evoked hyperpolarization (40 Hz) was 270 +/- 21 ms and that for the ACh ionophoretic response was 400 +/- 65 ms. Low frequency FS (0.5-5 Hz) also induced membrane hyperpolarization and responses to single shock stimuli were occasionally observed. The FS-evoked hyperpolarization was abolished following the blockade of nerve conduction by superfusion of either Na-free or tetrodotoxin-containing media. Effects of FS were not seen in the presence of atropine. Neostigmine potentiated the FS- and ACh-evoked hyperpolarizations.(ABSTRACT TRUNCATED AT 250 WORDS)

Citing Articles

Acetylcholine-induced change in intracellular Cl- activity of the mouse lacrimal acinar cells.

Saito Y, Ozawa T, Hayashi H, Nishiyama A Pflugers Arch. 1985; 405(2):108-11.

PMID: 4059033 DOI: 10.1007/BF00584530.


Acetylcholine stimulates a Ca2+-dependent C1- conductance in mouse lacrimal acinar cells.

Findlay I, Petersen O Pflugers Arch. 1985; 403(3):328-30.

PMID: 3921938 DOI: 10.1007/BF00583609.


The effect of acetylcholine on chloride transport across the mouse lacrimal gland acinar cell membranes.

Saito Y, Ozawa T, Hayashi H, Nishiyama A Pflugers Arch. 1987; 409(3):280-8.

PMID: 3627948 DOI: 10.1007/BF00583477.

References
1.
Greger R, Schlatter E . Properties of the basolateral membrane of the cortical thick ascending limb of Henle's loop of rabbit kidney. A model for secondary active chloride transport. Pflugers Arch. 1983; 396(4):325-34. DOI: 10.1007/BF01063938. View

2.
Petersen O, Poulsen J . Secretory potentials, potassium transport and secretion in the cat submandibular gland during perfusion with sulphate Locke's solution. Experientia. 1968; 24(9):919-20. DOI: 10.1007/BF02138654. View

3.
Parod R, Putney Jr J . An alpha-adrenergic receptor mechanism controlling potassium permeability in the rat lacrimal gland acinar cell. J Physiol. 1978; 281:359-69. PMC: 1282702. DOI: 10.1113/jphysiol.1978.sp012427. View

4.
Greger R, Schlatter E . Presence of luminal K+, a prerequisite for active NaCl transport in the cortical thick ascending limb of Henle's loop of rabbit kidney. Pflugers Arch. 1981; 392(1):92-4. DOI: 10.1007/BF00584588. View

5.
DEAN P, Matthews E . Pancreatic acinar cells: measurement of membrane potential and miniature depolarization potentials. J Physiol. 1972; 225(1):1-13. PMC: 1331091. DOI: 10.1113/jphysiol.1972.sp009926. View