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J C Szerb

Publications and source records attributed to J C Szerb.

54 records · Page 3Linked to original sources
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↗
PubMed1974

The release of labelled acetylcholine and choline from cerebral cortical slices stimulated electrically.

1 In order to establish the origin of the increased efflux of radioactivity caused by electrical stimulation of cerebral cortical slices which had been incubated with [(3)H]-choline, labelled choline and acetylcholine (ACh) collected by superfusion were separated by gold precipitation.2 In the presence of physostigmine electrical stimulation (1 Hz, 10 min) increased the release of only [(3)H]-ACh which was greatly enhanced by the addition of atropine.3 Continuous stimulation in the presence of physostigmine resulted in an evoked release of [(3)H]-ACh which declined asymptotically. This evoked release appeared to follow first-order kinetics with a rate constant which remained stable over the course of prolonged stimulation.4 The rate constant for the evoked release of [(3)H]-ACh with 1 Hz stimulation was three times greater in the presence of physostigmine and atropine than in the presence of physostigmine alone, while the size of the store from which [(3)H]-ACh was released was nearly identical under these two conditions.5 In the absence of physostigmine and atropine, stimulation caused the appearance of only [(3)H]-choline in the samples.6 Reduction of [(3)H]-ACh stores before the application of physostigmine resulted in a reduced evoked release of total radioactivity, both in the absence or presence of physostigmine and atropine, and decreased the evoked release of [(3)H]-ACh without affecting the release of [(3)H]-choline.7 Results suggest that electrical stimulation of cortical slices which had been incubated with [(3)H]-choline causes the release of only [(3)H]-ACh, both in the presence or absence of an anticholinesterase. The evoked increase in the efflux of total radioactivity is therefore a good measure of the release of [(3)H]-ACh.

Acetylcholine↗
PubMed1974

The output per stimulus of acetylcholine from cerebral cortical slices in the presence or absence of cholinesterase inhibition.

1 The release of endogenous acetylcholine (ACh) from cerebral cortical slices stimulated at 0.25, 1, 4, 16 and 64 Hz was measured in the presence either of physostigmine or of physostigmine and atropine.2 Atropine potentiated the evoked release of endogenous ACh especially at low frequencies resulting in an output per stimulus which sharply declined with increasing frequency of stimulation, while in the absence of atropine the output of ACh per stimulus was low and fairly constant.3 The evoked release of [(3)H]-ACh per stimulus following the incubation of the slices with [(3)H]-choline, as estimated by means of rate constants of the evoked release of total radioactivity, showed a frequency dependence similar to endogenous ACh when the two were tested under identical conditions.4 In the absence of an anticholinesterase the evoked release of [(3)H]-ACh per stimulus was dependent on frequency of stimulation in a similar way to that in the presence of physostigmine and atropine.5 Results suggest that under physiological conditions, i.e. in the absence of an anti-cholinesterase, the release of ACh per stimulus decreases with increasing frequency of stimulation and that this decrease is due to a lag in the mobilization of stored ACh rather than in the synthesis of new ACh.

Acetylcholine↗
PubMed1969

The effect of topically applied atropine on resting and evoked cortical acetylcholine release.

1. Cortical acetylcholine (ACh) output was measured in cats anaesthetized either with Dial compound (0.6 ml./kg) or with halothane-N(2)O. ACh output was found to be 1.67 ng/cm(2).min under Dial anaesthesia, and 0.30 ng/cm(2).min under halothane-N(2)O.2. Addition of atropine sulphate (1 mug/ml.) to the collection fluid increased ACh output fourfold under Dial anaesthesia but had no effect under halothane-N(2)O anaesthesia.3. Isolation of the cortex, lesions in the mesencephalon and topical application of tetrodotoxin (TTX) reduced ACh output under Dial anaesthesia to about 0.8 ng/cm(2).min. The effect of atropine on ACh output was somewhat reduced by isolation and completely abolished by mesencephalic lesions or TTX.4. ACh release evoked by reticular formation stimulation under halothane-N(2)O anaesthesia was increased fourfold by atropine but evoked release due to direct stimulation of the cortex was increased only twofold.5. ACh release due to depolarization of the cortex with KCl was not increased by atropine.6. Dihydro-beta-erythroidine (DHE) or D-tubocurarine failed to affect ACh output even in a concentration of 100 mug/ml.7. It is concluded that atropine does not increase spontaneous ACh release and only ACh release evoked by trans-synaptic stimulation of cholinergic neurones is potentiated by atropine.8. These findings are fully consistent with the hypothesis that atropine increases ACh output by blocking cortical cholinergic synapses which are a part of a circuit inhibiting cholinergic neurones.

Acetylcholine↗
PubMed1967

Cortical acetylcholine release and electroencephalographic arousal.

1. In cats anaesthetized with N(2)O-halothane acetylcholine (ACh) release from the parietal cortex was measured. In addition, low and high-frequency electroencephalographic (e.e.g.) activity was recorded quantitatively.2. Stimulation of the mesencephalic reticular formation at 30, 60 and 100/sec produced an identical increase in cortical ACh output, while 300/sec stimulation was about (1/3) as effective and 10/sec stimulation failed to increase ACh output.3. Reticular formation stimulation at 60 and 100/sec reduced the low-frequency and increased the high-frequency e.e.g. activity. Stimulation at 30 and 300/sec was less effective, while 10/sec stimulation had no effect on e.e.g.4. Acute undercutting of the cortex did not affect the resting output of ACh but greatly reduced the increase due to reticular formation stimulation as compared to the contralateral intact side. Cutting the cortex around the collection area did not affect the increase in ACh output due to reticular formation stimulation.5. Stimulation of the hypothalamus, medial thalamus and septum at 100/sec also increased cortical ACh output while stimulation of the dorsal hippocampus and caudate nucleus failed to do so.6. Low frequency cortical e.e.g. activity was reduced by stimulating the reticular formation, the hypothalamus, the medial thalamus and slightly by septum stimulation. High-frequency e.e.g. activity was increased by stimulating the reticular formation and the hypothalamus.7. It is concluded that the ACh measured originates from the neural tissue underlying the collection area. The increased release is concomitant to e.e.g. activation but the pathways involved in cortical e.e.g. activation and increased ACh release are distinct, since the two phenomena do not vary in a parallel fashion when the reticular formation is stimulated at different frequencies or when different subcortical areas are stimulated.8. The effectiveness of septal stimulation in increasing ACh release indicates that at least part of the cortical cholinergic fibres traverse this area on their way to the cortex.

Acetylcholine↗