1. Segments of rabbit ileum incubated with (3)H-DOPA or (3)H-dopamine and perfused with McEwen solution spontaneously release (3)H-dopamine; this basal release is doubled when the sympathetic nerves are stimulated. Evidence is presented to show that the release is probably from the sympathetic nerve terminals.2. Both cocaine and bretylium reduce the spontaneous release of (3)H-dopamine as well as the increased release resulting from sympathetic nerve stimulation. Guanethidine depresses the release during nerve stimulation but increases the spontaneous release of the amine. Phenoxybenzamine potentiates both the spontaneous release and that during nerve stimulation.3. Tyramine releases (3)H-dopamine from the preparation but tachyphylaxis to the drug rapidly develops.4. It is concluded that the release of (3)H-dopamine from the sympathetic nerves of the isolated perfused rabbit ileum possesses many of the characteristics of that of noradrenaline from other sympathetically innervated structures.

Animals↗

PubMed1965

Inhibition of dopamine-beta-oxidase by diethyldithiocarbamate.

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Amino Acid Oxidoreductases↗

PubMedDate not supplied

Pharmacological evidence that protein kinase C modulates monosynaptic excitations in the olfactory cortex.

The possible occurrence and role of protein kinase C at the lateral olfactory tract (LOT)-pyramidal cell synapse of the rat olfactory cortex slice has been investigated by determining the effects of both activators (4-beta-phorbol-12,13,diacetate [PDAc] and 1,2-dioctanoyl-sn-glycerol) and inhibitors (5-isoquinolinylsulphonyl)-2-methylpiperazine [H-7], sangivamycin and polymyxin B) of the enzyme on the surface field potential known as the N-wave. PDAc (0.3 to 20 mumol/l) and 1,2-dioctanoyl-sn-glycerol (25 to 250 mumol/l) increased the area and amplitude of the potential. In control slices in which a population spike was recorded, PDAc also triggered the appearance of multiple spikes. In a series of input-output experiments, PDAc (2.5 or 5 mumol/l) increased the area and amplitude of the N-wave relative to that of the action potential but did not significantly affect pyramidal cell excitability. The effects of PDAc on the N-wave were antagonised by all three protein kinase C inhibitors but not by the calmodulin antagonist calmidazolium and were greater in slices perfused with solution containing 10 rather than 1 mmol/l Mg2+ or 1.25 rather than 5 mmol/l Ca2+. The effect of PDAc on the amplitude but not area of the N-wave was blocked by the potassium channel blocker tetraethylammonium (10 mmol/l) but not by 4-aminopyridine (0.25 mmol/l). In a series of conditioning experiments, PDAc (1 to 5 mumol/l) reduced the amplitude of the N-wave evoked by a second stimulus compared to that evoked by the first conditioning pulse.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

PubMedDate not supplied

Effects of barbiturates on responses evoked by excitatory amino acids in slices of rat olfactory cortex.

A study has been made of the effects of ranges of concentrations of phenobarbitone, pentobarbitone and thiopentone on responses evoked by gamma-aminobutyric acid (GABA), L-glutamate, L-aspartate, N-methyl-D-aspartate, kainate and quisqualate in slices of olfactory cortex of the rat. All three barbiturates affected GABA-evoked depolarizations similarly in that responses were potentiated by small doses but markedly inhibited at greater concentrations. Responses to L-aspartate and L-glutamate were little affected except at the largest dose of phenobarbitone tested (10 mM). The responses evoked by the selective agonists of excitatory amino acid receptors were inhibited by the barbiturates, the relative sensitivities being quisqualate greater than or equal to N-methyl-D-aspartate greater than or equal to kainate with phenobarbitone, quisqualate greater than or equal to kainate greater than N-methyl-D-aspartate with pentobarbitone and quisqualate greater than kainate = N-methyl-D-aspartate with thiopentone. The possible significance of these findings is discussed.

Amino Acids↗