Suppression of carbachol-induced oscillatory Cl− secretion by forskolin in rat parotid and submandibular acinar cells

2008 ◽  
Vol 294 (3) ◽  
pp. G738-G747 ◽  
Author(s):  
Takahide Shintani ◽  
Chikara Hirono ◽  
Makoto Sugita ◽  
Yoshiko Iwasa ◽  
Yoshiki Shiba
Keyword(s):  
Membrane Potential ◽  
Salivary Glands ◽  
Acinar Cells ◽  
Fluid Secretion ◽  
Sympathetic Stimulation ◽  
Current Clamp ◽  
Inward Current ◽  
Parotid Acinar Cells ◽  
Current Clamp Mode ◽  
Rat Parotid

Sympathetic stimulation induces weak salivation compared with parasympathetic stimulation. To clarify this phenomenon in salivary glands, we investigated cAMP-induced modulation of Ca2+-activated Cl− secretion from rat parotid and submandibular acinar cells because fluid secretion from salivary glands depends on the Cl− secretion. Carbachol (Cch), a Ca2+-increasing agent, induced hyperpolarization of the cells with oscillatory depolarization in the current clamp mode of the gramicidin-perforated patch recording. In the voltage clamp mode at −80 mV, Cch induced a bumetanide-sensitive oscillatory inward current, which was larger in rat submandibular acinar cells than in parotid acinar cells. Forskolin and IBMX, cAMP-increasing agents, did not induce any marked current, but they evoked a small nonoscillatory inward current in the presence of Cch and suppressed the Cch-induced oscillatory inward current in all parotid acinar cells and half (56%) of submandibular acinar cells. In the current clamp mode, forskolin + IBMX evoked a small nonoscillatory depolarization in the presence of Cch and reduced the amplitude of Cch-induced oscillatory depolarization in both acinar cells. The oscillatory inward current estimated at the depolarized membrane potential was suppressed by forskolin + IBMX. These results indicate that cAMP suppresses Ca2+-activated oscillatory Cl− secretion of parotid and submandibular acinar cells at −80 mV and possibly at the membrane potential during Cch stimulation. The suppression may result in the weak salivation induced by sympathetic stimulation.

ATP activates a cation-permeable pathway in rat parotid acinar cells

1992 ◽  
Vol 262 (4) ◽  
pp. C934-C940 ◽  
Author(s):  
S. P. Soltoff ◽  
M. K. McMillian ◽  
B. R. Talamo
Keyword(s):  
Membrane Potential ◽  
Uptake Rate ◽  
Purinergic Receptor ◽  
Acinar Cells ◽  
Muscarinic Agonist ◽  
Tetraacetic Acid ◽  
Nucleotide Analogues ◽  
Parotid Acinar Cells ◽  
Biphasic Effect ◽  
Rat Parotid

Effects of several purinergic receptor agonists were examined on rat parotid acinar cells. Extracellular ATP stimulated 45Ca2+ uptake into isolated rat parotid acinar cells in a concentration-dependent fashion (EC50 approximately 125 microM ATP) at a maximum rate of approximately 6 nmol.mg protein-1.min-1. In the absence of extracellular Na+, ATP increased the uptake rate by greater than 100%. Increasing concentrations of extracellular Na+ reduced the ATP-stimulated rate of 45Ca2+ entry in a graded fashion (IC50 16.6 mM), suggesting that Ca2+ and Na+ compete for entry. Uptake rate was not reduced when intracellular Ca2+ was buffered with 1,2-bis(2-aminophenoxy)ethane-N,N,N'N'-tetraacetic acid, indicating that the effects of ATP were not initiated by an elevation in intracellular free Ca2+ concentration. 3-O-(4'-benzoyl)benzoyl-ATP was much more potent (EC50 approximately 4 microM) and stimulated Ca2+ influx at a greater rate (approximately 12 nmol.mg protein-1.min-1) than ATP. Other nucleotide analogues, including adenosine 5'-O-(3-thiotriphosphate), 2-methylthio-ATP, and 5'-adenylylimidodiphosphate, were much less effective than ATP. ATP produced a biphasic effect on membrane potential: an initial hyperpolarization was followed by a rapid depolarization. The depolarization was greatly reduced in the absence of extracellular Na+, but not in the absence of extracellular Ca2+, indicating that the majority of the depolarizing current was due to Na+ entry. Effects of ATP on the membrane potential were distinguishable from those of the Ca2+ ionophore ionomycin and the muscarinic agonist carbachol. Depolarization of the cells by gramicidin or K+ did not produce an increase in 45Ca2+ uptake.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals β-Adrenergic stimulation alters oligosaccharide pyrophosphoryl dolichol metabolism in rat parotid acinar cells

1985 ◽  
Vol 231 (2) ◽  
pp. 431-438 ◽  
Author(s):  
S R Grant ◽  
E E Kousvelari ◽  
D K Banerjee ◽  
B J Baum
Keyword(s):  
Half Life ◽  
Specific Radioactivity ◽  
Acinar Cells ◽  
Protein Glycosylation ◽  
Significant Enhancement ◽  
Adrenergic Stimulation ◽  
Parotid Acinar Cells ◽  
Secretory Glycoproteins ◽  
Rat Parotid ◽  
Stimulation Of

beta-Adrenergic stimulation of rat parotid acinar cells markedly increases [3H]mannose incorporation into N-linked glycoproteins [Kousvelari, Grant, Banerjee, Newby & Baum (1984) Biochem. J. 222, 17-24]. More than 90% of this protein-bound [3H]mannose was preferentially incorporated into four secretory glycoproteins. The ratio of [3H]mannose/[14C]leucine present in these individual proteins was 1.7-4-fold greater with isoproterenol-treated cells than with untreated controls. In isoproterenol-stimulated cells, [3H]mannose incorporation into mannosylphosphoryl dolichol and oligosaccharide-PP-dolichol was increased 2-3-fold over that observed in unstimulated cells. Similarly, formation of mannosylated oligosaccharide-PP-dolichol was increased approx. 4-fold in microsomes prepared from isoproterenol-treated cells. Also, turnover of oligosaccharide-PP-dolichol was significantly increased (5-fold) by β-adrenergic stimulation; the half-life for oligosaccharide-PP-dolichol decreased from 6 min in control cells to 1.2 min in isoproterenol-stimulated cells. By 15 min after isoproterenol addition to acinar cells, the specific radioactivity of parotid oligosaccharide moieties increased about 3-fold over the value observed in the absence of the agonist. Taken together, these results strongly suggest that elevation of N-linked protein glycosylation in rat parotid acinar cells after β-adrenoreceptor stimulation resulted from significant enhancement in the synthesis of mannosylphosphoryl dolichol and oligosaccharide-PP-dolichol and the turnover of oligosaccharide-PP-dolichol.

Hyperpolarization-Activated Inward Current in Neurons of the Rat's Dorsal Nucleus of the Lateral Lemniscus In Vitro

1997 ◽  
Vol 78 (5) ◽  
pp. 2235-2245 ◽  
Author(s):  
Xiao Wen Fu ◽  
Borys L. Brezden ◽  
Shu Hui Wu
Keyword(s):  
Membrane Potential ◽  
Input Resistance ◽  
Resting Potential ◽  
Extracellular Potassium ◽  
Current Clamp ◽  
Lateral Lemniscus ◽  
Inward Current ◽  
Dorsal Nucleus ◽  
Maximal Activation

Fu, Xiao Wen, Borys L. Brezden, and Shu Hui Wu. Hyperpolarization-activated inward current in neurons of the rat's dorsal nucleus of the lateral lemniscus in vitro. J. Neurophysiol. 78: 2235–2245, 1997. The hyperpolarization-activated current ( I h) underlying inward rectification in neurons of the rat's dorsal nucleus of the lateral lemniscus (DNLL) was investigated using whole cell patch-clamp techniques. Patch recordings were made from DNLL neurons of young rats (21–30 days old) in 400 μm tissue slices. Under current clamp, injection of negative current produced a graded hyperpolarization of the cell membrane, often with a gradual sag in the membrane potential toward the resting value. The rate and magnitude of the sag depended on the amount of hyperpolarizing current. Larger current resulted in a larger and faster decay of the voltage. Under voltage clamp, hyperpolarizing voltage steps elicited a slowly activating inward current that was presumably responsible for the sag observed in the voltage response to a steady hyperpolarizing current recorded under current clamp. Activation of the inward current ( I h) was voltage and time dependent. The current just was seen at a membrane potential of −70 mV and was activated fully at −140 mV. The voltage value of half-maximal activation of I h was −78.0 ± 6.0 (SE) mV. The rate of I h activation was best approximated by a single exponential function with a time constant that was voltage dependent, ranging from 276 ± 27 ms at −100 mV to 186 ± 11 ms at −140 mV. Reversal potential ( E h) of I h current was more positive than the resting potential. Raising the extracellular potassium concentration shifted E h to a more depolarized value, whereas lowering the extracellular sodium concentration shifted E h in a more negative direction. I h was sensitive to extracellular cesium but relatively insensitive to extracellular barium. The current amplitude near maximal-activation (about −140 mV) was reduced to 40% of control by 1 mM cesium but was reduced to only 71% of control by 2 mM barium. When the membrane potential was near the resting potential (about −60 mV), cesium had no effect on the membrane potential, current-evoked firing rate and input resistance but reduced the spontaneous firing. When the membrane potential was more negative than −70 mV, cesium hyperpolarized the cell, decreased current-evoked firing and increased the input resistance. I h in DNLL neurons does not contribute to the normal resting potential but may enhance the extent of excitation, thereby making the DNLL a consistently powerful inhibitory source to upper levels of the auditory system.

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