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PubMed1970

The release of acetylcholine by acetylcholine in the cat's superior cervical ganglion.

1. The experiments described in this paper tested the effect of acetylcholine (ACh), carbachol or preganglionic nerve stimulation on the release of ACh from the cat's perfused superior cervical ganglion; radioactive tracer methods were used.2. When the ganglion's transmitter store of ACh had been labelled, radioactive ACh was released by nerve stimulation (5 Hz for 2 min), but there was no release by ACh (0.15-15 mug) or by carbachol (1-10 mug) when these drugs were injected close to the ganglion. Perfusion with low or moderate concentrations of ACh (0.15-5 mug/ml) also failed to release ACh, but high concentrations (15-50 mug/ml) released a small amount of labelled material. There was no correlation between ganglion stimulation by ACh and release of radioactivity.3. Ganglion-blocking concentrations of ACh did not reduce the release of ACh during continuous nerve stimulation.4. When resting (unstimulated) ganglia were perfused with (3)H-choline and eserine, the extra ACh synthesized and stored by such ganglia (surplus ACh) was labelled. Preganglionic nerve stimulation (5 Hz for 2 min) did not release surplus ACh, but perfusion with ACh (0.5-15 mug/ml), or injection of carbachol (0.5-2.5 mug) did.5. Surplus ACh released by ACh or by carbachol did not contribute to the ganglion stimulating effect of either drug.6. It is concluded that the presynaptic effects of ACh are not of physiological importance.

Acetylcholine↗
PubMed1975

Studies upon the mechanism by which acetylcholine releases surplus acetylcholine in a sympathetic ganglion.

1. Acetylcholine (ACh) releases surplus ACh from the superior cervical ganglion of the cat and the experiments described in this paper tested whether this results from exchange of endogenous ACh with exogenous ACh; the experiments also attempted to characterize pharmacologically the mechanism of this action of ACh. 2. The surplus ACh in the ganglion was radioactively labelled by perfusion of the ganglion with [3H]-choline-Krebs solution containing diisopropylphosphofluoridate, and the release of surplus [3H]-ACh by [14C]-ACh injected close arterially to the ganglion measured. The amount of [3H]-ACh released by [14C]-ACh was 33 +/- 5 times greater than was the amount of [14C]-ACh accumulated by ganglia. The amount of exogenous ACh accumulated by ganglia that had first formed surplus ACh was not different from exogenous ACh accumulation by ganglia that had not formed surplus ACh. Thus, it is concluded that surplus ACh release by ACh is not the result of ACh exchange. 3. In other experiments, surplus [3H]-ACh was accumulated in ganglia exposed to physostigmine. Nicotine, pilocarpine or ACh released surplus ACh; the effect of both nicotine and ACh was blocked by hexamethonium; atropine blocked the effect of ACh but not that of nicotine. It is concluded that both nicotinic and muscarinic receptors can be involved in the release of surplus ACh by cholinomimetic agonists.

Acetylcholine↗
PubMed1980

Modulation by acetylcholine of the electrically-evoked release of [3H]-acetylcholine from the ileum of the guinea-pig.

1 Acetylcholine (ACh) stores within neurones of the myenteric plexus of the guinea-pig were labelled with [3H]-choline and the influence of unlabelled ACh, atropine, or atropine and unlabelled ACh on the electrically-evoked output of [3H]-ACh was evaluated. 2 Electrical transmural stimulation (5 Hz) of the ileum led to an increase in the output of [3H]-ACh over that released spontaneously. Superfusion with unlabelled ACh (6.8 microM) caused a marked reduction in the release of [3H]-ACh which was reversed by atropine (3.5 microM). Atropine itself had no effect on the electrically-evoked [3H]-ACh. 3 These experiments provide further evidence for the existence in the guinea-pig ileum of neuronal muscarinic receptors for ACh subserving an inhibitory role on transmitter release.

Acetylcholine↗
PubMed2004

Novel aspects in cutaneous biology of acetylcholine synthesis and acetylcholine receptors.

Extraneuronal acetylcholine (ACh) has been demonstrated to influence a plethora of cutaneous cell functions in an autocrine, paracrine and endocrine fashion. Through the differentiation-specific expression of its different nicotinic (nACh-R) and muscarinic (mACh-R) receptors, ACh acts upon keratinocyte proliferation and migration, terminal differentiation and barrier formation, sweat and sebum secretion as well as microcirculation and angiogenesis. Only very recently it has been recognized that acetylcholinesterase, but not cholineacetyltransferase, activity is regulated by hydrogen peroxide. Considering that the outer layer of the human skin can be a target for UV-generated H2O2 in the millimolar range, this mechanism needs to be taken into account for the regulation of ACh homeostasis in skin biology. Consequently, ACh can accumulate, as shown, for example, in the depigmentation process in vitiligo. There is a highly regulated distribution of ACh-R in human epidermis and adnexal structures, supporting previously observed effects of cholinergic compounds on keratinocyte biology. Most significantly, the regulated expression of ACh-R in sebaceous glands advocates a role for ACh in sebum production and as a promoter of sebocyte differentiation, thus offering an explanation for skin diseases associated with altered sebum production after chronic nicotine exposure. So far, ACh-induced sweat production has been thought to be under the exclusive control of mACh-R. However, recently, the presence of both different nACh-R and mACh-R in myoepithelial and acinar cells of eccrine sweat glands has been documented, indicating a more complex regulation of sweat production and expulsion.

Acetylcholine↗
PubMed1981

Antibodies to the nicotinic acetylcholine receptor, obtained from serum of myasthenic patients, may decrease acetylcholine release from rat hippocampal nerve endings in vitro.

Release of [3H]-ACh from [3H]-Ch loaded nerve endings from rat hippocampus is dependent on Ca2+ and K+-concentration. [3H]-ACh release, evoked by a depolarizing K+ concentration is decreased in the presence of IgG isolated from the serum of some myasthenic patients but not in that of IgG from controls. Myasthenic IgG contains antibodies to the nicotinic acetylcholine receptor (nAChR). Isolated nerve endings were shown not to be leaky. Curare-sensitive alpha-bgt receptor was found at a concentration of 60-90 fmol/mg protein. It is discussed if a presynaptic nAChR exists in the membrane of hippocampal nerve endings and is involved in an autoregulation of ACh-release or if myasthenic IgG in a manner independent of the receptor.

Acetylcholine↗
PubMed1975

Increased extrajunctional acetylcholine sensitivity produced by chronic acetylcholine sensitivity produced by chronic post-synaptic neuromuscular blockade.

1. Anaesthetized rats were paralysed for periods of up to 3 days by chronic administration of D-tubocurarine (DTC), succinylcholine or alpha-bungarotoxin. 2. After 3 days of treatment with DTC, the phrenic nerve remained active. Neuromuscular transmission and spontaneous miniature end-plate potentials (m.e.p.p.s) were restored after removal of the DTC. Resting potentials and input resistances of muscle fibres that had been paralysed for 3 days were similar to those in denervated fibers. 3. Chronic neuromuscular blockade increased the binding of [125-I]-alpha-bungarotoxin by extrajunctional regions of muscle. The time course of the increase was similar to that seen after denervation. Binding to muscles from animals that were anaesthetized and respirated, but not paralysed, was not increased. 4. Three days of paralysis increased the sensitivity of the extrajunctional muscle membrane to acetylcholine (ACh) applied by iontophoresis. 5. Approximately the same proportion of muscle fibres from muscles paralysed for 3 days gave overshooting action potentials in the presence of tetrodotoxin 10-minus 6 g/ml. as did fibres form muscles denervated for 3 days. 6. Chronic paralysis did not change the accumulation of acetylcholinesterase above a ligation in the sciatic nerve. 7. These results are consistent with the idea that extrajunctional ACh sensitivity is normally controlled by muscle activity.

Acetylcholine↗
PubMed1977

Acetylcholine receptor distribution on myotubes in culture correlated to acetylcholine sensitivity.

1. A linear relation, with a slope of 0-9 +/- 0-2 on a log-log plot, was obtained between acetylcholine (ACh) sensitivity and alpha-bungarotoxin (alpha-BTX) binding site density in developing L6 and rat primary myotubes. ACh sensitivity was defined as g/Qn where g is conductance, Q is ACh charge and n is the Hill coefficient. Experimentally we found n approximately 1-7 for our myotubes, which is similar in value to that reported for adult systems. 2. The linear relationship is compatible with an organization whereby each ion channel is always complexed with a fixed number of ACh receptors such that the dose-response characteristics of each such complex are independent of average ACh receptor density. 3. Light microscope autoradiography showed that the alpha-bungarotoxin binding sites on L6 myotubes are uniformly distributed over the surface, while primary rat myotubes exhibit gradients and hot spots. Electron microscope autoradiography indicated that about 70% of the [125I]alpha-bungarotoxin label was on the surface of the myotubes. The alpha-bungarotoxin site density, after subtracting myoblast background, varied from 5 to 400 sites/micrometer2 on different L6 myotubes, and from 54 to 900 sites/micrometer2 on primary rat myotubes, with occasional hot spots of 3000-4000 sites/micrometer2. The conductance sensitivities varied from 10(-4) to 2 X 10(-2) Momega-1/nC1-7.

Acetylcholine↗
PubMed1987

Surplus acetylcholine and acetylcholine release in the rat diaphragm.

1. Skeletal muscles from rat, mouse and frog were incubated under different conditions and the amounts of acetylcholine (ACh) extractable from the tissue and released into the medium were determined by mass fragmentography. In some experiments measurements were made of the amounts of ACh ('bound' ACh) surviving in a muscle homogenate to which an excess of acetylcholinesterase had been added. In other experiments the membrane potentials, end-plate potentials (e.p.p.s), and miniature end-plate potentials (m.e.p.p.s) were studied. 2. During incubation in Ringer medium the ACh content of the rat hemidiaphragm usually did not change, but after inhibition of cholinesterase by soman the ACh content rose gradually from about 100 to 150 pmol to a plateau of about 400 pmol after 4 h. A similar formation of 'surplus ACh' after cholinesterase inhibition was found in the mouse diaphragm, but not in the frog sartorius muscle. 3. Surplus ACh accumulated predominantly in the end-plate region of the rat diaphragm. In muscles, 16-18 h after in vivo denervation, the capacity to form surplus ACh was decreased by more than 80%. 4. The amount of ACh diffusing from the resting hemidiaphragm into the incubation medium ('resting release') varied between 0.5 and 0.9 pmol min-1 in different experiments; it remained at the same level during accumulation of surplus ACh. It was reduced by more than 80% 16-18 h after denervation. 5. The amplitude of m.e.p.p.s and e.p.p.s did not increase while surplus ACh was accumulating. 6. Incubation of hemidiaphragms in Ringer solution containing [3H]choline caused the formation of [3H]ACh. Additional amounts of [3H]choline were incorporated into ACh when the nerve was stimulated for 60 min. However, incubation in the presence of soman (3,3-dimethyl-2-butylmethylphosphonofluoridate), in the absence of stimulation, did not cause an increase of the [3H]ACh content of the muscles. 7. From hemidiaphragms with active cholinesterase about 120 pmol ACh was lost after prolonged nerve stimulation or incubation with 50 mM-KCl in the presence of hemicholinium-3, and about 35 pmol remained in the tissue. In soman-treated muscles, containing surplus ACh, about as much ACh was released by nervous stimulation as from untreated hemidiaphragms, and much more ACh remained unreleased. 8. Transection of the muscle at both sides of the end-plate or incubation of intact muscles in the presence of 50 mM-KCl depolarized the muscle fibres to -35 and -31 mV, respectively. Surplus ACh was partially released by 50 mM-KCl, but not by muscle transection.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗
PubMed1975

Endogenous acetylcholine release and labelled acetylcholine formation from [3H]choline in the myenteric plexus of the guinea-pig ileum.

The spontaneous release of acetylcholine (ACh) from the guinea-pig myenteric plexus - longitudinal muscle preparation superfused at a constant rate in the presence of physostigmine was 10 nmol-g-1-h-1. This release was decreased to one-third by tetradotoxin or by MnCl2 and increased 2.5 times by 0.1 Hz and 20 times by 16 Hz stimulation. The formation of [3H]ACh from [3H]choline increased from 3 to 33 nmol-g(-1)-h(-1) when the concentration of [3H]choline was increased from 1 muM to 50 muM. The rate of [3H]ACh formation was not affected by tetrodotoxin, MnCl2, or physostigmine in the absence of stimulation. It was increased by 50% by 0.1 Hz and by 100% by 16 Hz stimulation during the first 9 min of exposure to [3H]choline but not subsequently. The myenteric plexus - longitudinal muscle preparation contains 200 nmol/g choline. Results suggest that the apparent small [3H]ACh formation from low concentrations of [3H]choline is due to the dilution of [3H]choline by endogenous choline. The major part of [3H]ACh formation appears to be due to the intracellular turnover of ACh while the evoked release of [3H]ACh appears to originate from a small pool.

Acetylcholine↗
PubMed1995

Acetylcholine potentiates acetylcholine-induced increases in K+ current in cat atrial myocytes.

A nystatin-perforated patch whole cell recording method was used to study the effects of acetylcholine (ACh) on ACh-induced K+ currents in atrial myocytes isolated from cat hearts. The general protocol involved an initial 4-min exposure to ACh (ACh1), followed by a 4-min washout in ACh-free Tyrode solution and then a second 4-min ACh exposure (ACh2). Voltage ramps (40 mV/s) between -130 and +30 mV were used to assess changes in total membrane conductance. ACh2 (10 microM) induced an increase in K+ conductance that was significantly larger than that induced by ACh1 (10 microM) at voltages both negative and positive to the reversal potential. The potentiated current induced by ACh2 reversed at about -80 mV and inwardly rectified at voltages positive to the reversal potential. External Ba2+ (5 mM) or tetraethylammonium (10 mM) abolished all ACh2-induced increases in membrane conductance. The sensitivity to K+ channel blockers, reversal potential, and the rectifying properties indicate that the current potentiated by ACh2 is a K+ current. Atropine (1 microM) blocked all effects of ACh on K+ currents. Potentiation of K+ current by ACh2 required 1) ACh1 concentrations > or = 1 microM, 2) ACh1 duration > or = 2 min, and 3) recovery interval > or = 2 min. We conclude that an initial exposure to ACh potentiates subsequent ACh-induced increases in K+ current. ACh-induced potentiation depends on the concentration and duration of the initial ACh exposure and the recovery interval between consecutive ACh exposures.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1986

Interaction of acetylcholine and gastric inhibitory polypeptide on endocrine and exocrine rat pancreatic secretion: augmentation of acetylcholine-induced amylase and volume secretion by the insulinotropic action of gastric inhibitory polypeptide.

Exocrine pancreatic secretion is under partial control of endocrine pancreatic hormones. We studied the interaction of three doses of acetylcholine (Ach), a stimulator of exocrine and endocrine pancreatic secretion, with one dose of gastric inhibitory polypeptide (GIP) which is strongly insulinotropic, but has no effect on exocrine pancreatic secretion. The effects of Ach and GIP on insulin secretion from the rat pancreas were additive at 0.05 X 10(-6) M Ach and slightly, but not significantly less than additive at 0.25 or 2.5 X 10(-6) M Ach. GIP had an augmenting effect on amylase and volume secretion from the pancreas, when pancreatic secretion was stimulated by 2.5 X 10(-6) M Ach, but not by 0.05 or 0.25 X 10(-6) M. Exogenous rat insulin could exert an effect similar to that of GIP, although a higher dose was required. Atropine inhibited the effect of Ach on exocrine and endocrine pancreatic secretion, but not the insulinotropic action of GIP. It is hypothesized that GIP could play a role in regulating exocrine pancreatic secretion by its insulinotropic action.

Acetylcholine↗
PubMed2005

Galantamine activates muscle-type nicotinic acetylcholine receptors without binding to the acetylcholine-binding site.

Galantamine (Reminyl; Janssen Pharmaceutica, Titusville, NJ) belongs to a class of acetylcholinesterase inhibitors approved for symptomatic treatment of Alzheimer's disease. The drug presumably acts by raising and prolonging the profile of acetylcholine (ACh) via an inhibitory effect on the esterase. However, there is also evidence demonstrating that galantamine can activate the nicotinic ACh receptor or modulate its activation by ACh. In this study, we have examined the ability of galantamine to directly activate the muscle-type nicotinic ACh receptor or to modulate receptor activation by selected nicotinic agonists. Studies of direct activation by galantamine demonstrated that this ligand is a low-efficacy agonist of the muscle-type ACh receptor. Point mutations in the M2-M3 linker (alphaS269I) and the M2 transmembrane domain (epsilonT264P) had similar effects on receptor activation by galantamine and nicotinic agonists, suggesting that the general features of receptor activation by galantamine are similar to that in the presence of ACh. Experiments performed in the simultaneous presence of galantamine and various nicotinic ligands showed that channel activation by the nicotinic ligands studied (ACh, carbachol, and choline) was not affected by the presence of galantamine at concentrations up to 100 microm. In addition, galantamine did not reduce the initial rate of binding for 125I-alpha-bungarotoxin. These results demonstrate that galantamine does not interfere with the occupation of the nicotinic agonist binding site by ACh, carbachol, or choline. We conclude that galantamine activates the muscle-type ACh receptor by interacting with a binding site that is distinct from the site for nicotinic agonists.

Acetylcholine↗
PubMed1992

[Effects of "non-quantal" acetylcholine on the sensitivity of the postsynaptic membrane: action of ouabain and imitation of these effects by exogenous acetylcholine].

Development of postsynaptic potentiation (PSP) and desensitization (DS) caused by "non-quantal" acetylcholine after acetylcholinesterase inhibition was studied by means of ouabain, an agent known to modulate (initially increase and then decrease) the level of non-quantal secretion of ACh. Ouabain had no effect on the MEPC parameters when AChE was active. After AChE inhibition ouabain initially increased the decay time constant of MEPC (tau), i.e. caused postsynaptic potentiation (PSP). This effect of ouabain grew with time between inhibition of AChE and application of ouabain. The PSP stage was followed by shortening of MEPCs decay, due to the development of desensitization (DS), and that process was more pronounced than in control. Applied before AChE inhibition, ouabain had no effect on tau. Thus neither PSP nor DS developed under those conditions. Exogenous ACh (20 nmol/l) applied simultaneously with inhibitor of AChE partially prevented the shortening of MEPCs decay, but decreased the amplitude of MEPC. Applied after MEPCs shortening, exogenous ACh (50 nmol/l) tended to return the initial value of tau. It is concluded that nonquantal ACh produces PSP and DS on the postsynaptic membrane after inhibition of ACh and that the DS persists after cessation of nonquantal secretion for a long time.

Acetylcholine↗
PubMed1975

Correlation between drug induced changes of acetylcholine release and acetylcholine fractions in rat brain.

After administration of eserine, a new acetylcholine (ACh) subfraction called f+ is formed in rat brain tissue. References and methods are given for the calculation of this subfraction, which can be isolated and determined only together with the so-called "free" ACh fraction. Alterations of the f+-ACh subfraction caused by barbital, urethane, pentetrazol, arecoline and scopolamine in telencephalon, cortex and striatum of rat brain are connected with changes of ACh concentrations determined in comparable releasing tests.

Acetylcholine↗
PubMed1990

[Acetylcholine and the primary input of acupuncture sensation--influence of peripheral acetylcholine on the role of electroacupuncture analgesia].

In order to investigate the correlation between the peripheral ACh and the primary input of acupuncture sensation, in the paper the cholinesterase inhibitor--Neostigmine and the ACh synthesis blocker--Hemicholine, which are unable to pass through blood brain barrier, and ACh were used as tools to increase or decrease the level of ACh in peripheral nerve system of rats. The results indicated that: 1) The effect of electroacupuncture analgesia can be enhanced by subcutaneous injection of neostigmine which related to the dosage used. 2) The influence of electroacupuncture analgesia can be markedly inhibited by intraperitoneal injection of Hemicholine. 3) This influence of suppression by Hemicholine can be reversed at once when acetylcholine in combination with neostigmine was injected. But could not reverse by neostigmine alone. It suggested that the effect of electroacupuncture analgesia and the primary input of acupuncture sensation were significantly related to the level and content of ACh in periphery.

Acetylcholine↗
PubMed1989

Inhibition of acetylcholine storage by acetylcholine analogs in vitro.

Forty-five acetylcholine (AcCh) analogs were chemically synthesized and characterized. They and two commercially available analogs were tested for the ability to inhibit active transport of AcCh by synaptic vesicles purified from the electric organ of Torpedo californica. A range of potencies greater than 4 orders of magnitude was found. A quaternary nitrogen and the presence of the carbonyl group are important to potency. The addition of hydrophobic groups to both ends of isonipecotic acid yielded the most potent analogs, which exhibited a nearly 1000-fold increase in potency relative to AcCh. The probable conformation of AcCh bound by the transporter has been deduced and confirmed by the synthesis of a potent rigid analog based on 2-amino-9-fluorenone. A potent analog was shown to be a competitive inhibitor with respect to AcCh, thus confirming that its site of action is the transporter active site. The structure-activity data clearly distinguish the binding site for AcCh from the site for vesamicol [(--)-(trans)-2-(4-phenylpiperidino)cyclohexanol], which is a noncompetitive inhibitor.

Acetylcholine↗
PubMed1988

A possible role for the acetylcholine transport system in non-quantal release of acetylcholine at the rodent myoneural junction.

The effects on the spontaneous, non-quantal release of acetylcholine (ACh) from motor nerve terminals of substances known to inhibit the ACh transport system present in cholinergic synaptic vesicles have been investigated. In mouse diaphragms, the hyperpolarization normally produced by d-tubocurarine (dTC) in muscle endplates that had been treated by an anticholinesterase was partly or completely abolished by 2-(4-phenylpiperidino) cyclohexanol (AH5183, 10(-7)-10(-6)M), quinacrine (10(-7)M) and tetraphenylborate (10(-6) M). Since the sensitivity of the endplate to ACh was not changed, the block of the dTC induced hyperpolarization indicated an inhibition of the spontaneous, non-quantal release of ACh. This was confirmed by direct measurement of the ACh released by rat diaphragm. The release of ACh from the innervated diaphragm was decreased by about 50% by AH5183 (10(-8)-10(-6) M) and by 42% by quinacrine (10(-7)-10(-6) M). The ACh released was presumably neural, since the release of ACh from 4-day denervated diaphragms was not diminished by either AH5183 or quinacrine. The results indicate that the spontaneous release of ACh from the motor nerve terminals is probably mediated by a carrier which may be the vesicular transport system responsible for moving ACh into the vesicle. The transport system is likely incorporated into the membrane of the nerve terminal during exocytosis.

Acetylcholine↗
PubMed1987

Effects of cannabinoids on levels of acetylcholine and choline and on turnover rate of acetylcholine in various regions of the mouse brain.

The psychoactive cannabinoids, delta 9-tetrahydrocannabinol (delta 9-THC), delta 8-tetrahydrocannabinol (delta 8-THC), 11-hydroxy-delta 9-tetrahydrocannabinol (11-OH-delta 9-THC) and 9-nor-9 beta-hydroxyhexahydrocannabinol (beta-HHC), as well as the nonpsychoactive cannabinoids, cannabinol (CBN), cannabidiol (CBD), abnormal CBD, delta 8-THC methyl ether (1-OCH3-delta 8-THC) and 9-nor-9 alpha-hydroxyhexahydrocannabinol (alpha-HHC), were used to assess the role of cholinergic mechanisms in the different behavioral actions of these cannabinoids. Their effects on mouse brain choline and acetylcholine (ACh) levels and on ACh turnover were determined in cortex, hippocampus, striatum, midbrain and medulla-pons. delta 9-THC (30 mg/kg) caused a significant elevation of ACh in all five brain areas. 11-OH-delta 9-THC (30 mg/kg) increased ACh in hippocampus, striatum and midbrain. delta 8-THC (30 mg/kg) increased ACh in cortex and hippocampus. delta 9-THC and 11-OH-delta 9-THC increased choline in midbrain and cortex, whereas beta-HHC increased choline in all areas, except hippocampus, at a dose of 30 mg/kg. Also at this dose, delta 9-THC, 11-OH-delta 9-THC, delta 8-THC and beta-HHC decreased ACh turnover in the hippocampus, as did CBN (10-30 mg/kg), 1-OCH3-delta 8-THC (100 mg/kg) and alpha-HHC (100 mg/kg). ACh turnover was also decreased in midbrain by 1-OCH3-delta 8-THC and in the striatum by alpha-HHC. Thus, the most consistent effects of cannabinoids, both psychotomimetic and nonpsychotomimetic, were to increase ACh and decrease ACh turnover in the hippocampus.(ABSTRACT TRUNCATED AT 250 WORDS)

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