scholarly journals Cholinergic Agonist

2020 ◽  
Author(s):  
Keyword(s):  
Cholinergic Agonist

La3+ and pH sensitivity of Ca2+ entry and intracellular store filling in gastric parietal cells

1995 ◽  
Vol 269 (5) ◽  
pp. G770-G778 ◽  
Author(s):  
P. A. Negulescu ◽  
T. E. Machen
Keyword(s):  
Positive Feedback ◽  
Low Ph ◽  
Parietal Cells ◽  
Additional Increase ◽  
Cholinergic Agonist ◽  
Intracellular Store ◽  
Entry Pathway ◽  
Signaling Function ◽  
Previously Treated ◽  
Gastric Parietal Cells

The fluorescent Ca2+ indicator fura 2 was used to measure cytosolic free [Ca2+] ([Ca2+]i) in order to obtain information about relative rates of Ca2+ influx into parietal cells during treatment with carbachol (a cholinergic agonist) or thapsigargin (TG, a Ca(2+)-mobilizing agent) or during reloading of the internal Ca2+ stores. In Ca(2+)-containing solutions, carbachol-, TG-, and reloading-stimulated Ca2+ entry exhibited nearly identical sensitivity to La3+ [inhibition constant (Ki) approximately 10 microM] or low pH (pKi approximately 7.0). In experiments in which carbachol and TG were used, there was no additional increase in [Ca2+]i when TG was added to carbachol-treated cells or when carbachol was added to cells previously treated with TG. Thus it is likely that a single Ca2+ entry pathway serves a signaling function as well as a role in refilling the Ca2+ store during reloading. Because the Ca2+ pathway is exquisitely sensitive to pH and serosal pH increases during stimulant-induced H+ secretion (which is activated by increases in [Ca2+]i), this mechanism will exert positive feedback on parietal cells in the intact stomach. When parietal cells were pretreated with carbachol in Ca(2+)-free solutions, reloading was independent of pH and La3+, suggesting that Ca(2+)-containing solutions should be used to determine the properties of the influx pathway.

scholarly journals Induction of long-lasting depolarization in medioventral medulla neurons by cholinergic input from the pedunculopontine nucleus

2005 ◽  
Vol 99 (3) ◽  
pp. 1127-1137 ◽  
Author(s):  
Keiko Mamiya ◽  
Kevin Bay ◽  
R. D. Skinner ◽  
E. Garcia-Rill
Keyword(s):  
Action Potential ◽  
Pedunculopontine Nucleus ◽  
Intracellular Recordings ◽  
Stable States ◽  
Cholinergic Agonist ◽  
Firing Rates ◽  
Cholinergic Antagonist ◽  
Muscarinic Cholinergic ◽  
Stimulation Of

Stimulation of the pedunculopontine nucleus (PPN) is known to induce changes in arousal and postural/locomotor states by activation of such descending targets as the caudal pons and the medioventral medulla (MED). Previously, PPN stimulation was reported to induce prolonged responses (PRs) in intracellularly recorded caudal pontine neurons in vitro. The present study used intracellular recordings in semihorizontal slices from rat brain stem (postnatal days 12–21) to determine responses in MED neurons following PPN stimulation. One-half (40/81) of MED neurons showed PRs after PPN stimulation. MED neurons with PRs had shorter duration action potential, longer duration afterhyperpolarization, and higher amplitude afterhyperpolarization than non-PR MED neurons. PR MED neurons were significantly larger (568 ± 44 μm2) than non-PR MED neurons (387 ± 32 μm2). The longest mean duration PRs and maximal firing rates during PRs were induced by PPN stimulation at 60 Hz compared with 10, 30, or 90 Hz. The muscarinic cholinergic agonist carbachol induced depolarization in all PR neurons tested, and the muscarinic cholinergic antagonist scopolamine reduced or blocked carbachol- and PPN stimulation-induced PRs in all MED neurons tested. These findings suggest that PPN stimulation-induced PRs may be due to activation of muscarinic receptor-sensitive channels, allowing MED neurons to respond to a transient, frequency-dependent depolarization with long-lasting stable states. PPN stimulation appears to induce PRs in large MED neurons using parameters known best to induce locomotion.

An "epithelial" preparation from the canine gastric mucosa: responses to secretagogues

1989 ◽  
Vol 257 (1) ◽  
pp. G46-G51 ◽  
Author(s):  
P. K. Rangachari ◽  
D. McWade
Keyword(s):  
Gastric Mucosa ◽  
Acid Output ◽  
The Other ◽  
Muscularis Mucosa ◽  
Muscularis Mucosae ◽  
Cholinergic Agonist ◽  
Sustained Responses

Isolated mucosal preparations from the stomach are generally obtained by removing the external muscle layers, leaving intact the muscularis mucosae. By carefully dissecting off the muscularis mucosa, we have obtained "epithelial" preparations from the canine stomach. Such preparations responded to secretagogues, histamine, pentagastrin, and a cholinergic agonist (cis-2-methyl 4-dimethylaminomethyl 1,3-dioxolane methiodide). Epithelial preparations were, in general, more sensitive than mucosal preparations. Of the three secretagogues tested, histamine was the most consistent stimulant, with well-sustained responses being noted. Responses to the other agonists were more variable. Pentagastrin produced brief but explosive increases in acid output.

Release and reloading of intracellular Ca stores after cholinergic stimulation of the parietal cell

1988 ◽  
Vol 254 (4) ◽  
pp. C498-C504 ◽  
Author(s):  
P. A. Negulescu ◽  
T. E. Machen
Keyword(s):  
Plasma Membrane ◽  
Parietal Cell ◽  
Base Line ◽  
Cholinergic Stimulation ◽  
Gastric Glands ◽  
Cholinergic Agonist ◽  
Intracellular Ca ◽  
Lanthanum Ion ◽  
Intact Rabbit ◽  
Stimulation Of

Microspectrofluorimetry was used to measure cytosolic free Ca, Cai, in single parietal cells of intact rabbit gastric glands loaded with the Ca-sensitive fluorescent dye, fura-2. Cells were repeatedly stimulated with the cholinergic agonist carbachol to gain insights into the membrane mechanisms involved in hormonally stimulated Ca metabolism. In either Ca-containing or Ca-free solutions, carbachol (100 microM) caused a rapid (within 30 s) elevation of Cai from a resting level of 100 nM to greater than 600 nM. After the spike, Cai decreased within 3 min to a lower level that was somewhat elevated (greater than 200 nM) over base line. This plateau was dependent on both carbachol and extracellular Ca (Cao) and could be blocked by the addition of atropine (1 microM) or lanthanum ion (La, 50 microM). The spike is due to the release of Ca from internal stores, whereas the plateau is due to Ca entry across the plasma membrane through agonist-controlled, La-inhibitable channels. After a carbachol stimulation of 3 min or longer, reloading of the internal store was absolutely dependent on Cao. Under these conditions, reloading occurred through a La-sensitive (but nifedipine- and verapamil-insensitive) pathway in the plasma membrane. No significant change in Cai was detectable during the reloading. In contrast to the longer treatments, if carbachol stimulation was terminated with atropine while Cai was still elevated, significant reloading occurred from the cytosol.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of carbachol on extracellular Na-dependent AIB uptake in rat parotid gland

1980 ◽  
Vol 239 (3) ◽  
pp. G183-G189 ◽  
Author(s):  
G. Keryer ◽  
B. Rossignol
Keyword(s):  
Amino Acid Uptake ◽  
Ionophore A23187 ◽  
Acid Uptake ◽  
Parotid Glands ◽  
Extracellular Medium ◽  
Cholinergic Agonist ◽  
Rat Parotid ◽  
Cholinergic Effect ◽  
Ionophore Monensin

In rat parotid glands the uptake of 2-[1-14C]aminoisobutyric acid (AIB), in vitro, depends on a Na concentration gradient between the intra- and extracellular medium. Ouabain (1 mM) which inhibits the Na+-K+-ATPase and a Na+ ionophore, monensin (which dissipates the Na+ gradient), both suppress this amino acid uptake. Carbachol (5 microM) (through muscarinic receptors) evokes a decrease in AIB uptake, and in the presence of 0.1 mM ouabain the cholinergic effect is enhanced. Ouabain alone (0.1 mM) very slightly depresses the [14C]AIB uptake. Neither 1 microM isoproterenol, nor 1 microM Ca2+ ionophore A23187, which affect the membrane potential in rat parotid acinar cells, modifies the AIB uptake. When the Ca is removed from the incubation medium, carbachol still evokes a small decreasing effect on AIB uptake. From these data we can suggest that the reduced AIB uptake (induced by the cholinergic agonist) appears to be related to a process dependent on variation of intracellular Na concentration that may be triggered by the cholinergic agonist.

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