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Biomedical subjects

H W Kosterlitz

Publications and source records attributed to H W Kosterlitz.

At least 127 records · Page 7Linked to original sources
PubMed1971

Impulse transmission in the myenteric plexus-longitudinal muscle preparation of the guinea-pig ileum.

1. In a preparation consisting of the myenteric plexus and the longitudinal muscle layer removed from a segment of guinea-pig ileum, spontaneous action potentials occurred which were unaffected by tetrodotoxin but suppressed by Mn(2+) and were therefore myogenic.2. A single current pulse of 0.1 ms duration evoked a response consisting of an early action potential followed after a delay of about 200 ms by a complex of biphasic spikes. The first action potential was conducted for no more than 15 mm and the second complex for 30-70 mm.3. Since the first action potential was unaffected by hyoscine or Mn(2+) but abolished by tetrodotoxin, it was due to excitation of nerve fibres. The later complex of spikes was suppressed by hyoscine and Mn(2+) and therefore due to excitation of smooth muscle. It was also inhibited by adrenaline or morphine, compounds which depress acetylcholine release. The evoked smooth muscle response was followed by absence of spontaneous electrical activity for 2-4 seconds.4. The nerves travelling in a longitudinal direction had a mean maximum conduction velocity of 0.65 m/s, an absolute refractory period of 2.8 ms and a relative refractory period of about 20 ms.5. The conduction velocity of the smooth muscle response evoked by stimulation of the nerve with a single pulse was 0.16 m/second. After a single pulse the muscle was inexcitable for 0.7-1.3 s; the delay of transmission from nerve to muscle was 210 ms. When instead of a single pulse a train of two-five pulses at 20 ms intervals was applied, the size, conduction distance and conduction velocity of the evoked smooth muscle response were increased.

Action Potentials↗
PubMed1970

Synaptic potentials recorded by the sucrose-gap method from the rabbit superior cervical ganglion.

1. Compound ganglionic potentials evoked by stimulation of the preganglionic nerves to the superior cervical ganglion of the rabbit were recorded by the sucrose-gap method.2. When the distal part of the ganglion was bathed in flowing isotonic sucrose solution or sodium-deficient solutions, ganglionic action potentials were no longer evoked, only large synaptic potentials.3. The compound synaptic potential, which remained unaltered for more than 1 h, originated in a population of cells at the interface between the Krebs and sucrose solutions. Hexamethonium reduced the size but did not alter the time course of the synaptic potential.4. It is suggested that a higher concentration of sodium ions is required for the generation of ganglionic action potentials than for either conduction in the postganglionic axons or production of synaptic potentials.5. When lithium replaced sodium in the solution bathing the distal part of the ganglion, the synaptic potential was greatly reduced in amplitude. Impulse propagation in the postganglionic axons was only slightly impaired when lithium replaced sodium in the solution bathing the axons.6. A quantitative assessment of the potency of the ganglion-blocking drugs nicotine, pentolinium, hexamethonium and pempidine was made by measuring the depression of the synaptic potentials produced by bathing the distal part of the ganglion in flowing isotonic sucrose solution. The concentrations which produced a 50% depression were 8.1 muM nicotine, 26.5 muM pentolinium, 111 muM hexamethonium and 22.2 muM pempidine.

Animals↗
PubMed1970

The effects of adrenaline, noradrenaline and isoprenaline on inhibitory alpha- and beta-adrenoceptors in the longitudinal muscle of the guinea-pig ileum.

1. Two preparations, a segment of the ileum and the myenteric plexuslongitudinal muscle preparation, have been used for an analysis of the inhibitory effects of adrenaline, noradrenaline and isoprenaline on the contractor responses of the longitudinal muscle to acetylcholine or to electrical, coaxial or field, stimulation.2. Since the inhibitory effects of adrenaline, noradrenaline and isoprenaline on the acetylcholine-induced contractions were not affected by phenoxybenzamine but were antagonized by propranolol, it is concluded that beta-adrenoceptors are present on the muscle cells.3. The responses to electrical stimulation were suppressed by adrenaline or noradrenaline but only partly inhibited by isoprenaline. Propranolol antagonized the effect of isoprenaline and, to some extent, that of noradrenaline, but scarcely affected the action of adrenaline. Phenoxybenzamine, on the other hand, antagonized most of the effect of adrenaline and, to some extent, that of noradrenaline; it usually potentiated the effect of isoprenaline.4. The output of acetylcholine evoked by electrical stimulation was diminished by adrenaline or noradrenaline but was not affected by isoprenaline. The depressant effect on acetylcholine release was antagonized by phenoxybenzamine but not affected by propranolol; therefore these effects of adrenaline and noradrenaline are mediated by alpha-adrenoceptors.5. It may be assumed that alpha-adrenoceptors in situ are stimulated mainly by circulating adrenaline and possibly noradrenaline and thus cause a prejunctional inhibition at the nerve-smooth muscle junction.

Acetylcholine↗
PubMed1968

Resting and action potentials recorded by the sucrose-gap method in the superior cervical ganglion of the rabbit.

1. Evoked ganglionic action potentials and drug-induced changes in resting potential were recorded by the sucrose-gap method. The height of the action potential was 10-20 mV.2. Since the amplitude of the P wave is inversely proportional to the external potassium concentration between 0.5 and 12 mM, the P wave is probably caused by a phase of increased permeability to K(+).3. In the absence of an anticholinesterase, the depolarizing actions of choline and acetylcholine on the ganglion are almost equal, whereas acetylcholine is 2-3 times more potent than choline on the fibres of the internal carotid nerve. In the presence of eserine, acetylcholine induces a depolarization of the ganglion of up to 14 mV, while increase in [K(+)](o) causes a depolarization of up to 55 mV.4. Although the post-ganglionic fibres in the distal pole of the ganglion are depolarized by drugs, for example, acetylcholine, they contribute little to drug-induced potential changes and probably little to evoked action potentials.5. The hyperpolarization which occurs after exposure of the ganglion to acetylcholine is not due to a phase of increased permeability to K(+).

Acetylcholine↗