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K Missala

Publications and source records attributed to K Missala.

At least 19 recordsLinked to original sources
PubMed1992

Alpha-methyltryptophan metabolism in rat pineal gland and brain.

Alpha-methyltryptophan (AMTP), a synthetic amino acid, is metabolized by the rat in vivo to alpha-methylserotonin (AM5HT), which appears in the pineal gland just as it does in the brain. Pineal AM5HT assumes the same diurnal rhythm as serotonin does in control animals. Administration of AMPT results in a decrease of the serotonin content of the pineal gland, but not of its melatonin content. Pharmacological evidence indicates that the uptake of AMTP into the gland is influenced by noradrenergic innervation. No evidence was obtained for formation in vivo of alpha-methyl-N-acetylserotonin or the alpha-methyl analogue of melatonin.

Animals↗
PubMed1990

Alpha-methylserotonin, a substitute transmitter for serotonergic neurons.

1. Administration to rats of alpha-methyltryptophan (AMTP) gives rise to alpha-(AM5HT) in the brain along with a decrease of cerebral 5HT. 2. Analysis of fractions prepared from brains of AMTP-injected rats shows that AM5HT occurs mainly in the synaptosomes. 3. The synaptosomal content of AM5HT in proportion to the total AM5HT in the brain represents the same ratio as for the corresponding fractions of 5HT.

Animals↗
PubMed1990

A new method to measure brain serotonin synthesis in vivo. II. A practical autoradiographic method tested in normal and lithium-treated rats.

We describe here a practical autoradiographic method to estimate the rate of serotonin synthesis in brain. A two-time point method (60 and 150 min after injection of alpha-[14C]methyl-L-tryptophan) was first evaluated in 14 normal rats (7 at each time point). After this the method was tested in lithium-treated rats. In normal rats the rate of serotonin synthesis measured by the two-time point method generally correlated with known concentrations of tryptophan hydroxylase. The rate of synthesis in lithium-treated rats was compared with that in sham-treated rats (NaCl treatment). The results showed a significant increase in the synthesis rate in some cerebral structures. The greatest increases in the serotonin synthesis rate, attributable to the lithium treatment, were observed in the parietal cortex (52%) and caudate nucleus (47%). This is the first investigation to demonstrate, with autoradiographic resolution (approximately 100 microns), the differential changes in the rate of serotonin synthesis in the brain. Lithium had no significant effect on the rate of synthesis in the pineal gland.

Animals↗
PubMed1989

Central regulation of adrenal tyrosine hydroxylase: effect of induction on catecholamine levels in the adrenal medulla and plasma.

The effect of induction of adrenal tyrosine hydroxylase (TH) by various centrally acting drugs on catecholamine levels in adrenal and plasma was investigated in rats. All the drugs tested, namely oxotremorine, Piribedil, B-HT 920, and HA-966, produced significant increases in adrenal dopamine content and plasma epinephrine level. Denervation of the adrenal abolished the increase in adrenal dopamine as it did the induction of tyrosine hydroxylase. The results suggest that the induced increase of adrenal TH activity, as mediated by certain drugs, results in an elevation of the plasma epinephrine level and that the adrenal dopamine content is a better indicator of the catecholamine-synthesizing capacity of the adrenal medulla than are the other catecholamines.

Adrenal Glands↗
PubMed1981

Putrescine metabolism and the study of diamine oxidase activity in vivo.

The catabolism of 14C-putrescine (1,4-tetramethylene-diamine) to labeled CO2 in small laboratory animals has been studied extensively in order to establish the influence of nutritional, endocrine and other factors on this process. Special attention has been paid to treatments that are known to affect the activity of diamine oxidase (DAO, histaminase, EC, 1.4.3.6), a copper-containing enzyme characteristically inhibited by semicarbazide. Thus, copper-deficient rats metabolize putrescine more slowly than their controls. Antimalarial drugs that inhibit histamine N-methyltransferase also inhibit putrescine catabolism in vivo and DAO activity in vitro. Adrenalectomized rats metabolize the diamine at a reduced rate, a result consistent with the previously demonstrated decrease of DAO in the tissues of several species of animal. There is no effect on the rate of catabolism of putrescine when thyroid state is altered. Heparin (up to 15,000 U/kg), which releases DAO from the small (0.1 mg/kg), intestine, and aminoguanidine (0.1 mg/kg), which inhibits the enzyme powerfully, both cause decreased rates of catabolism of the diamine in rats. The putrescine-catabolizing ability returns with a half-time of recovery of 15-18 h, corresponding to the estimates of SHAFF and BEAVEN [36] for recovery of intestinal DAO activity following administration of heparin or cycloheximide. Together with out other results this suggests that what is being measured by putrescine catabolism depends to a significant extent on the activity of DAO in vitro.

Amine Oxidase (Copper-Containing)↗
PubMed1980

Putrescine catabolism in rats given heparin or aminoguanidine.

Rats treated acutely with aminoguanidine, a potent inhibitor of diamine oxidase, or with heparin display reduced ability to metabolize 14C-putrescine to radioactive carbon dioxide. After either drug rats recover 50% of the ability to catabolize putrescine in 15--18 h. This is in close agreement with the half-time for recovery of diamine exidase activity, and indicates that putrecine-catabolizing ability of the rat reflects in a physiologically significant way the function of diamine oxidase in vivo.

Amine Oxidase (Copper-Containing)↗
PubMed1979

Effect of heparin on the metabolism of putrescine in vivo.

Rats and guinea pigs which are given heparin metabolize intraperitoneally injected [14C]-putrescine to 14CO2 at reduced rates. The results have been considered in relation to the heparin-induced liberation of diamine oxidase from tissues into the blood stream.

4-Butyrolactone↗
PubMed1979

Monoamine metabolites in the CSF of epileptic patients.

To assess the possible role of amine neurotransmitters in human epilepsy, we measured metabolites of serotonin (5-hydroxyindoleacetic acid [5-HIAA]), dopamine (homovanillic acid [HVA]), and norepinephrine (3-methoxy-4-hydroxyphenylethylene glycol [MHPG]) in the lumbar cerebrospinal fluid (CSF) of patients with partial complex seizures and in neurologic controls. Untreated epileptic patients had lower concentrations of 5-HIAA and HVA in the lumbar CSF than the controls, but the differences were not statistically significant. Among epileptic patients receiving effective antiepileptic drug treatment, the HVA concentration was within the control range. Mean MHPG concentrations were similar in patients and controls. From the epileptic patients whose CSF was obtained at pneumoencephalography we obtained a second sample of CSF that was originally in the basal cisterns. No significant differences between treated and untreated patients were found for any of the three metabolites. The concentrations of HVA and 5-HIAA were higher in cisternal than in lumbar CSF, but there was no such gradient for MHPG.

Adolescent↗
PubMed1978

Role of pyridoxine in the metabolism of putrescine in the rat.

1. The ability of rats to metabolize radioactive putrescine to 14CO2 in vivo has been studied. 2. Animals made deficient in pyridoxine exhibit a significantly lower rate of catabolism of the diamine. 3. There dose not appear to be an important interaction between the effects of the deficiency and those stemming from treatment of the animals with the diamine oxidase inhibitor aminoguanidine. 4. These results favour the concept of a role of pyridoxal cofactor in the metabolism of diamines, presumably at the diamine oxidase stage.

Amine Oxidase (Copper-Containing)↗
PubMed1977

Action of inhibitors on monoamine and diamine metabolism in the rat.

The effects of a series of inhibitors of monoamine oxidase (EC 1.4.3.4) and diamine oxidase (EC 1.4.3.6) and of two chelating agents were studied in rats, with respect to the catabolism of labeled pentylamine and putrescine to radioactive carbon dioxide. D-Tranylcypromine, clorgyline, and deprenyl inhibited oxidation of the monoamine, with essentially no effect on putrescine, under our test conditions. Aminoguanidine inhibited putrescine but not pentylamine oxidation. Iproniazid, isoniazid, and Lilly 51641 affected the catabolism of both amines. Pargyline inhibited putrescine oxidation, apparently in a reversible manner.

Amine Oxidase (Copper-Containing)↗
PubMed1977

Metabolism of monoamines and diamines in hyperthyroid and hypothyroid rats.

The in vivo rates of catabolism of 14C-labelled pentylamine, ethylamine, putrescine, and cadaverine were studied in thyroidectomized rats and others made hyperthyroid by the daily administration of 0.2 mg of L-thyroxine per kilogram for 20--21 days. Hyperthyroid rats metabolized the monoamines at an accelerated rate; thyroidectomized animals oxidized pentylamine at a reduced rate. There was no effect of hypophysectomy on the rate of pentylamine oxidation. The in vitro monoamine oxidase (MAO) activity of liver was reduced in hyperthyroid rats and unchanged in those thyroidectomized; MAO activity in skeletal muscle was increased in the hyperthyroid rats and decreased in the hypothyroid rats. Because of the large mass of skeletal muscle compared with liver, it is considered that the changes in muscle MAO could play an important role in determining the rate of oxidation of pentylamine in vivo. The oxidation of the two diamines tested was not significantly affected by thyroidectomy; the rates were increased in the hyperthyroid rats, but the increase was significant only for cadaverine.

Amines↗