Linopirdine (DuP 996) selectively enhances acetylcholine release induced by high potassium, but not electrical stimulation, in rat brain slices and guinea pig ileum

1993 ◽  
Vol 29 (4) ◽  
pp. 262-270 ◽  
Author(s):  
Craig P. Smith ◽  
Linda R. Brougham ◽  
Hugo M. Vargas
Keyword(s):  
Electrical Stimulation ◽  
Guinea Pig ◽  
Rat Brain ◽  
Acetylcholine Release ◽  
Brain Slices ◽  
Guinea Pig Ileum ◽  
High Potassium

The identification of acetyl-l-carnitylcholine in rat brain extracts and the comparison of its cholinomimetic properties with acetylcholine

1970 ◽  
Vol 48 (10) ◽  
pp. 709-722 ◽  
Author(s):  
E. A. Hosein ◽  
A. Kato ◽  
E. Vine ◽  
A. M. Hill
Keyword(s):  
Guinea Pig ◽  
Rat Brain ◽  
Total Activity ◽  
Guinea Pig Ileum ◽  
Molar Basis ◽  
Choline Esters ◽  
Brain Extracts

Acetyl-l-carnitylcholine (l-ACCh) was identified in rat brain extracts on paper chromatograms developed in butanol–water for 138 h. l-ACCh was also identified in brain extracts fractionated on t.l.c. plates and on Sephadex G-10 columns. In every instance l-ACCh was separated from the acetylcholine (ACh) present and the ACh-like activity of l-ACCh was about 20% of the total activity in the extract. Both l-ACCh and ACh were found to be inseparable in a variety of chromatographic systems including electrophoresis. Treatment of these choline esters with cholinesterases showed that while true acetylcholinesterase hydrolyzed both l-ACCh and ACh, pseudocholinesterase destroyed only ACh. On a molar basis, the ACh-like activity of ACCh is one-half that of ACh on both the guinea pig ileum and frog rectus preparations. Like ACh, the ratio of the nicotinic to muscarinic potency of l-ACCh is unity. Mixtures of l-ACCh and ACh show summation of ACh-like activity on both the guinea pig ileum and frog rectus preparations.

Functional evidence that acetylcholine release from Auerbach's plexus of guinea-pig ileum is modulated by α2A-adrenoceptor subtype

1991 ◽  
Vol 205 (3) ◽  
pp. 311-313 ◽  
Author(s):  
Corrado Blandizzi ◽  
Margit Doda ◽  
Gabor Tarkovács ◽  
Mario Del Tacca ◽  
E.Sylvester Vizi
Keyword(s):  
Guinea Pig ◽  
Acetylcholine Release ◽  
Guinea Pig Ileum ◽  
Auerbach’S Plexus ◽  
Auerbach's Plexus

Somatostatin modulation of peptide-induced acetylcholine release in guinea pig ileum

1984 ◽  
Vol 246 (5) ◽  
pp. G509-G514 ◽  
Author(s):  
D. H. Teitelbaum ◽  
T. M. O'Dorisio ◽  
W. E. Perkins ◽  
T. S. Gaginella
Keyword(s):  
Substance P ◽  
Guinea Pig ◽  
Myenteric Plexus ◽  
Acetylcholine Release ◽  
Longitudinal Muscle ◽  
Guinea Pig Ileum ◽  
Gut Motility ◽  
Release Of Acetylcholine

The peptides caerulein, neurotensin, somatostatin, and substance P modulate the activity of intestinal neurons and alter gut motility. We examined the effects of these peptides on acetylcholine release from the myenteric plexus and intestinal contractility in vitro. Caerulein (1 X 10(-9) M), neurotensin (1.5 X 10(-6) M), and substance P (1 X 10(-7) M) significantly enhanced the release of [3H]acetylcholine from the myenteric plexus of the guinea pig ileum. This effect was inhibited by tetrodotoxin (1.6 X 10(-6) M). Somatostatin (10(-6) M) inhibited caerulein- and neurotensin-evoked release of acetylcholine but did not inhibit release induced by substance P. Caerulein, neurotensin, and substance P caused contraction of the guinea pig ileal longitudinal muscle. Somatostatin inhibited the contractions induced by caerulein and neurotensin. In contrast, substance P-induced contraction was not inhibited significantly by somatostatin. Thus, in the guinea pig ileum, caerulein-, neurotensin-, and substance P-induced contractility is due, at least in part, to acetylcholine release from the myenteric plexus. The ability of somatostatin to inhibit peptide-induced contractility is selective, and its mechanism may be attributed to inhibition of acetylcholine release.

Acetylcholine release from canine isolated airway is not modulated by norepinephrine

1986 ◽  
Vol 61 (3) ◽  
pp. 1025-1030 ◽  
Author(s):  
J. G. Martin ◽  
B. Collier
Keyword(s):  
Guinea Pig ◽  
Acetylcholine Release ◽  
Electrical Field Stimulation ◽  
Output Pulse ◽  
Physiological Salt Solution ◽  
Guinea Pig Ileum ◽  
Cholinergic Nerves ◽  
Ach Release ◽  
Electrical Field ◽  
Neural Origin

We measured acetylcholine (ACh) release from canine isolated tracheal smooth muscle (TSM) and bronchial spirals using a radioenzymic assay technique. Tissue was incubated in physiological salt solution containing physostigmine (3.10(-5) M), atropine (10(-7) M), and choline (5.10(-6) M), and bath fluid was collected every 15 min for assay. There was a resting release of ACh of 209 +/- 44 pmol/g tissue (mean +/- SE) from 53 to 77 specimens of TSM. Electrical field stimulation (ES) increased ACh release, which was blocked by tetrodotoxin (10(-6) g/ml), confirming the neural origin of ACh. The ACh output during ES (2-ms pulses) at 10 Hz increased linearly from 188 +/- 50 pmol/g tissue (mean +/- SE) for a 1-min volley, to 323 +/- 57 for three volleys, and 544 +/- 128 for five volleys. The ACh output/pulse was constant during ES at 20, 15, 10, and 5 Hz, but it was significantly higher at 2 than at 5 Hz (P less than 0.005). Incubation of TSM with norepinephrine (NE, 10(-5) M) did not affect ACh output either at 2 or 10 Hz. Likewise, ACh output from bronchial spirals during ES and 2 Hz was unaffected by NE. In contrast, NE treatment of isolated guinea pig ileum reduced the ACh released by ES at 2 Hz to 40 +/- 7% (P less than 0.001) of the control ACh output. It is concluded that evoked release of ACh (output/pulse) from cholinergic nerves in canine airway is frequency dependent, as in guinea pig ileum, but that, unlike guinea pig ileum, NE does not modulate its release.

Sign in / Sign up

Export Citation Format

Share Document