Presynaptic muscarinic receptors and the release of acetylcholine from cerebrocortical prisms: roles of Ca2+ and K+ concentrations

1993 ◽  
Vol 348 (3) ◽  
pp. 228-233 ◽  
Author(s):  
Vladimír Doležal ◽  
Stanislav Tuček
Keyword(s):  
Muscarinic Receptors ◽  
Release Of Acetylcholine ◽  
Presynaptic Muscarinic Receptors

Roles of M2 and M4 Muscarinic Receptors in Regulating Acetylcholine Release From Myenteric Neurons of Mouse Ileum

2005 ◽  
Vol 93 (5) ◽  
pp. 2841-2848 ◽  
Author(s):  
Tadayoshi Takeuchi ◽  
Kaori Fujinami ◽  
Hiroto Goto ◽  
Akikazu Fujita ◽  
Makoto M. Taketo ◽  
...  
Keyword(s):  
Muscarinic Receptors ◽  
Wild Type Mouse ◽  
Electrical Field Stimulation ◽  
Enteric Neurons ◽  
Wild Type ◽  
Ach Release ◽  
Mouse Small Intestine ◽  
Presynaptic Muscarinic Receptors ◽  
In The Wild ◽  
Mouse Ileum

We investigated the subtype of presynaptic muscarinic receptors associated with inhibition of acetylcholine (ACh) release in the mouse small intestine. We measured endogenous ACh released from longitudinal muscle with myenteric plexus (LMMP) preparations obtained from M1–M5 receptor knockout (KO) mice. Electrical field stimulation (EFS) increased ACh release in all LMMP preparations obtained from M1–M5 receptor single KO mice. The amounts of ACh released in all preparations were equal to that in the wild-type mice. Atropine further increased EFS-induced ACh release in the wild-type mice. Unexpectedly, atropine also increased, to a similar extent, EFS-induced ACh release to the wild-type mice in all M1–M5 receptor single KO mice. In M2 and M4 receptor double KO mice, the amount of EFS-induced ACh release was equivalent to an atropine-evoked level in the wild-type mouse, and further addition of atropine had no effect. M2 receptor immunoreactivity was located in both smooth muscle cells and enteric neurons. M4 receptor immunoreactivity was located in the enteric neurons, being in co-localization with M2 receptor immunoreactivity. These results indicate that both M2 and M4 receptors mediate the muscarinic autoinhibition in ACh release in the LMMP preparation of the mouse ileum, and loss of one of these subtypes can be compensated functionally by a receptor that remained. M1, M3, and M5 receptors do not seem to be involved in this mechanism.

Ozone-induced airway hyperresponsiveness and loss of neuronal M2 muscarinic receptor function

1994 ◽  
Vol 76 (3) ◽  
pp. 1088-1097 ◽  
Author(s):  
A. H. Schultheis ◽  
D. J. Bassett ◽  
A. D. Fryer
Keyword(s):  
Muscarinic Receptor ◽  
Muscarinic Receptors ◽  
Ozone Exposure ◽  
Muscarinic Agonist ◽  
Receptor Function ◽  
Vagus Nerves ◽  
Parasympathetic Nerves ◽  
M2 Muscarinic Receptor ◽  
Release Of Acetylcholine ◽  
M2 Muscarinic Receptors

The effect of acute ozone exposure on the function of efferent parasympathetic nerves, M3 muscarinic receptors on airway smooth muscle, and inhibitory M2 muscarinic receptors on the parasympathetic nerves was studied. Immediately after exposure to 2.0 ppm ozone for 4 h, guinea pigs became hyperresponsive to electrical stimulation of the vagus nerves. The normal airway response to intravenous cholinergic agonists at this time demonstrates normal M3 receptor function. M2 muscarinic receptors on the nerves, which normally inhibit release of acetylcholine, were dysfunctional after ozone exposure, as demonstrated by the failure of the muscarinic agonist pilocarpine to inhibit, and the failure of the M2 antagonist gallamine to potentiate, vagally mediated bronchoconstriction. Thus, loss of inhibitory M2 muscarinic receptor function after ozone exposure potentiates release of acetylcholine from the vagus nerves, increasing vagally mediated bronchoconstriction. By 14 days, postozone responses to vagal nerve stimulation were not different from those of air-exposed animals and the function of the neuronal M2 muscarinic receptor was normal, confirming that ozone-induced hyperresponsiveness is reversible.

scholarly journals Presynaptic muscarinic receptors mediating inhibition of neurogenic contractions in rabbit vas deferens are of the ganglionic M1-type

1988 ◽  
Vol 158 (3) ◽  
pp. 233-242 ◽  
Author(s):  
Manfrid Eltze ◽  
Gernot Gmelin ◽  
Jürgen Wess ◽  
Carsten Strohmann ◽  
Reinhold Tacke ◽  
...  
Keyword(s):  
Muscarinic Receptors ◽  
Vas Deferens ◽  
Presynaptic Muscarinic Receptors ◽  
Rabbit Vas Deferens ◽  
M1 Type

Interaction of enkephalin and caerulein on guinea pig small intestine

1983 ◽  
Vol 244 (1) ◽  
pp. G65-G70
Author(s):  
W. M. Yau ◽  
P. F. Lingle ◽  
M. L. Youther
Keyword(s):  
Small Intestine ◽  
Guinea Pig ◽  
Muscarinic Receptors ◽  
Dose Response ◽  
Response Curve ◽  
Acetylcholine Release ◽  
Control Level ◽  
Release Studies ◽  
Release Of Acetylcholine

This is a report on the effect of caerulein and methionine-enkephalin interaction on mechanical contraction and acetylcholine release in vitro. The ability of enkephalin to relax caerulein-induced contractions and the manner in which the caerulein dose-response curve was shifted in the presence of enkephalin strongly suggest that enkephalin and caerulein are functional antagonists in this system. The failure of enkephalin to alter the action of exogenous acetylcholine implies that such an antagonism is not mediated through a competition with postsynaptic muscarinic receptors on the muscle. Data from acetylcholine-release studies indicate that caerulein stimulation was dose related. As with the mechanical contractions, the release of acetylcholine in response to caerulein was inhibited by enkephalin. However, naloxone was capable of blocking this inhibition and restoring the release to its control level without interfering with caerulein stimulation. These data provide evidence for the modulatory roles of neuronal peptides in the cholinergic control of gut motility.

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