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Biomedical subjects

M Vogt

Publications and source records attributed to M Vogt.

At least 253 records · Page 14Linked to original sources
PubMed1972

Loss of simian virus 40 DNA-RNA hybrids from nitrocellulose membranes; implications for the study of virus--host DNA interactions.

Complete hybrids of simian virus 40 (SV40)DNA and its complementary RNA (cRNA) are not retained on nitrocellulose membranes. At saturating cRNA concentrations, retention of the hybrids indicates incomplete homology between DNA and RNA, probably due to incorporation of host DNA in the viral DNA; this effect is most pronounced when DNA is produced in cells infected at high multiplicity. Hybrids between DNA of Chinese hamster cells transformed by SV40 and cRNA are retained if the DNA fragments are long, but they are lost if the DNA is sheared to less than the length of an SV40 DNA molecule. Hence, in cells examined with about six SV40 genomes per cell, each genome is individually integrated. The results may explain previous discrepancies in the estimation of the number of viral genomes in transformed cells.

Animals↗
PubMed1972

Influence of age and of testosterone on the response of male rats to parachlorophenylalanine.

1. Castrated male rats and male rats that had been castrated as well as adrenalectomized, showed hypersexual behaviour 24 h after treatment with parachlorophenylalanine (PCPA), as did intact rats.2. A dose of PCPA 100 mg/kg was sufficient to induce mounting behaviour; this dose lowered the cerebral 5-hydroxytryptamine (5-HT) to about 50% in 24 h and further to 40% in 72 hours.3. Groups of juvenile male rats treated chronically with PCPA 100 mg/kg or 50 mg/kg, or with testosterone propionate 1.25 mg, showed hair loss after three weeks of treatment (6 injections), because of increased social interaction.4. Groups of intact male rats 9-11 weeks old given testosterone propionate 1.25 mg subcutaneously, showed mounting behaviour 3-5 h after the injection which was indistinguishable from the behaviour seen 24 h after treatment with PCPA 100 mg/kg. The 5-HT content of the brain was not altered by testosterone.5. The number of rats which showed mounting after PCPA treatment did not change with age, but the younger rats made more mounts in the observation time than rats more than three months old.6. The age of castration (3 weeks or 4 months) did not influence the results.

Adrenalectomy↗
PubMed1972

Release of 5-hydroxytryptamine from caudate nucleus and septum.

1. The anterior horn of one lateral ventricle was perfused in anaesthetized cats treated with inhibitors of monoamine oxidase, and the effluent was tested for 5-hydroxytryptamine (5-HT).2. The basal release of 5-HT varied from 0.25 to 4 ng in 25 min, and was usually about 1 ng.3. The basal release rose and fell with body temperature.4. Electrical stimulation for 15 min of the nucleus linearis intermedius or of the nucleus linearis rostralis caused a release of 5-HT which rarely outlasted the collection period of 25 min.5. Low frequencies (0.5/sec) were, per stimulus, more effective than high frequencies in releasing 5-HT. Over a 15 min period of stimulation, however, the highest total yield was at 20/sec; it fell abruptly at still greater frequencies.6. No release was obtained if the stimulating electrode was positioned in a variety of brain structures outside the two linear nuclei.7. The experiments indicate that 5-HT acts as a transmitter of impulses in neurones originating in the linear nuclei and terminating in caudate nucleus and septum.

Animals↗
PubMed1972

Release of transmitters on stimulation of the nucleus linearis raphe in the cat.

The nucleus linearis intermedius raphe and the nucleus linearis rostralis were stimulated during the perfusion of the anterior horn of the right lateral ventricle of anaesthetized cats. Whereas release of 5-hydroxytryptamine (5-HT) was consistently obtained, there was no release of acetylcholine (ACh). The independence of the release of 5-HT from that of ACh was seen both during low basal release of ACh (rising base line), and during the period when a plateau of resting release had been reached. It was also demonstrated in experiments in which the same perfusate was examined for both compounds.

Acetylcholine↗
PubMed1971

Sleep produced by clonidine (2-(2,6-dichlorophenylamino)-2-imidazoline hydrochloride).

1. The dose of clonidine (given intravenously) required to elicit sleep in the young chick is 1/25th to 1/50th of an equiactive dose of noradrenaline. The approximate ED50 is 0.01 mumol/kg. Phentolamine (10-15 mg/kg, but not 5 mg/kg) antagonizes the action of both clonidine and noradrenaline.2. Intensive treatment with p-chlorophenylalnine (700 mg/kg for 3-4 days) does not prevent the hypnotic effect of clonidine in the chick, although brain 5-HT is reduced to 15% of normal. Neither is natural sleep modified.3. Sleep after clonidine is not affected by methysergide (0.1-1 mumol/kg, i.m.), but prevented by LSD (0.1-0.3 mumol/kg). The effect of LSD is interpreted as a physiological antagonism.4. Clonidine (50 mg/kg) injected intravenously into adult rats causes sleep which is not abolished by phentolamine (5 mg/kg) or by p-chlorophenylalanine in doses which interfere with natural sleep.5. When, per kg body weight, the same dose of clonidine is injected into the lateral cerebral ventricle of rats, sleep ensues in more than half the animals, and persistent eating in about a third; only one of seventeen rats showed no change in behaviour. Eating and sleeping remained unaltered after p-chlorophenylalanine. The actual dose of clonidine injected into the lateral ventricle was 0.037 mumol, amounting to about 0.15 mumol/kg or 15 times the dose required intravenously in the chick. Noradrenaline 0.15 mumol per (intraventricular) injection caused eating but no sleep, whereas higher doses produced ataxia and paresis.6. The work suggests that clonidine does not elicit sleep by an action requiring the integrity of the 5-HT-containing neurones arising in the raphé nuclei, and that its action is not on tryptamine receptors. In the chick, sleep appears to be produced by a central sympathomimetic effect; it is possible, but not certain, that this also holds for the rat.7. The intravenous hypnotic dose of clonidine for the cat is about the same as that for the rat, but injection is not accompanied by signs of peripheral sympathetic stimulation.

Animals↗
PubMed1971

Noradrenaline release from isolated muscles of the nictitating membrane of the cat.

1. When the splanchnic nerves were stimulated in the cat for periods of up to 2 hr, the amount of adrenaline taken up by the nictitating membrane was very small; the highest figure was 0.37 mug/g, corrected for losses.2. The noradrenaline (NA) stores of the isolated medial muscle of the nictitating membrane were labelled with [(3)H]NA, and field stimulation of single muscles was carried out in a small organ bath. A stimulation period of 5 min with supramaximal shocks delivered at a frequency of 25/sec produced a mean release of NA into the bath fluid of 0.46 +/- 0.13 mug/g (uncorrected). Phenoxybenzamine, 10 mug/ml., increased this figure by a factor of 2-3.6. When corrections were made for the amount of transmitter metabolized before it could be collected, 47% of the tissue content of NA were shown to be released during the 5 min stimulation of the normal membrane, and about 55% in the presence of phenoxybenzamine. Prolonged stimulation of a phenoxybenzamine-treated membrane was apt to lead to loss of tissue stores of NA.3. Calculation of the degree of labelling of the NA in the tissue, and of NA released by stimulation, indicated that about 21% of endogenous NA had been replaced by labelled compound both in the tissue and in the overflow.4. Transmitter release per pulse was estimated by applying 720-1330 shocks at frequencies of 4 or 6/sec to membranes exposed to phenoxybenzamine. Mean release of NA per shock and per g tissue was 1.3 ng (corrected for losses). This represents 3.5 x 10(-4) of the tissue content determined at the end of the experiment.

Animals↗
PubMed1971

Release of endogenous noradrenaline from an isolated muscular artery. Release of endogenous noradrenaline from an isolated muscular artery.

1. The release of noradrenaline by field stimulation of vasoconstrictor nerves has been studied in isolated preparations of the main uterine artery of the guinea-pig.2. In preparations from virgin animals stimulation with trains of 3000 square pulses at 5 and 25 pulses/sec resulted in mean overflows of 0.56 ng/g.pulse and 1.53 ng/g.pulse respectively.3. Inhibition of monoamine oxidase and catechol-O-methyltransferase had no consistent effect on overflow at either stimulation frequency.4. Desmethylimipramine (10(-5)M) caused, on the average, a 2.4-fold increase in overflow following stimulation at 5 pulses/sec while phenoxybenzamine (10(-5)M) caused a 3.8-fold increase. Neither of these drugs caused a significant alteration of the overflow during stimulation at 25 pulses/sec.5. Treatment of the tissues with desmethylimipramine plus normetanephrine (4.5 x 10(-4)M) caused no more increase in overflow than treatment with desmethylimipramine alone.6. It is concluded that enzymatic metabolism of noradrenaline at the synapse is of little functional importance in this tissue, and that the most important mechanism of transmitter inactivation is by nervous re-uptake. Although phenoxybenzamine was more effective than desmethylimipramine in increasing transmitter overflow, no evidence was obtained to support the view that this effectiveness was due partly to blockade of ;Uptake 2'.7. There was sometimes very low overflow of noradrenaline from arteries taken from animals in the last week of pregnancy. In these instances overflow following stimulation at 5 pulses/sec was not increased by phenoxybenzamine treatment of the tissue.8. Methylene blue and fluorescence microscopic techniques indicated that the terminal adrenergic axons in each artery possess approximately 8.74 x 10(5) varicosities. The mean tissue content of noradrenaline was found to be 9.6 mug/g or 29 ng/artery. These results have been correlated with known morphological and electrophysiological data to derive a peak post-junctional concentration of noradrenaline during transmission of about 4 x 10(-4)M.9. The fraction of total noradrenaline content of the artery released per pulse (under the influence of phenoxybenzamine) had a mean value of 2.2 x 10(-4).

Animals↗