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PubMedDate not supplied

The permissive role of glucocorticoids in the development of ethanol dependence and tolerance.

In mice chronically treated with ethanol (in a liquid diet containing 6% ethanol ad libitum for 2 weeks), brain tryptophan hydroxylase (TPH) activity was increased (by 30-45% in whole brain), while brain tyrosine hydroxylase activity remained unchanged. Such chronic ethanol treatment also induced susceptibility to audiogenic seizures during withdrawal (60% incidence). When ethanol treatment was given to adrenalectomized (Adx) mice, the increase of brain TPH activity and the development of withdrawal audiogenic seizures were both prevented. In Adx mice receiving daily injections of corticosterone (0.5 mg/mouse), the ethanol-induced increase of brain TPH activity and the occurrence of withdrawal audiogenic seizures were both restored. Similarly, the ethanol-induced increase of liver alcohol dehydrogenase activity (by 60%) was prevented in Adx mice and restored by corticosterone replacement. It was noted that in all three cases replacement with such large doses of the corticoid did not enhance the ethanol effects, but merely restored the effects to the levels observed in intact mice. Apparently, glucocorticoids are required in a permissive role in order for the ethanol effects to occur.

5-Hydroxytryptophan↗
PubMed1977

Does dopamine play a role in schizophrenia?

Inhibition of central dopamine functions appears to be a common basic property of antipsychotic drugs. The mesolimbic and nigrostriatal portions of the dopaminergic system are probably the main targets of these drugs for the mental and the extrapyramidal actions respectively. Dopaminergic hyperfunction, induced by amphetamines or dopa, may lead to a disturbance mimicking paranoid schizophrenia, lending further support for a key role of dopamine in mental functions. While a primary disturbance in dopamine function in schizophrenia cannot be ruled out, the intimate relationship between dopaminergic and other neuronal systems must be emphasized. The possible involvement of other amine, aminoacid or peptide transmitters in schizophrenia cannot be disregarded.

5-Hydroxytryptophan↗
PubMed1978

Antidepressant agents. 9. 3,3-Diphenylcyclobutylamines, a new class of central stimulants.

3,3-Diphenylcyclobutylamine (4), N-methyl-3,3-diphenylcyclobutylamine (6), and N,N-dimethyl-3,3-diphenyl-cyclobutylamine (7) have been prepared and tested as potential antidepressant agents. The secondary (6) and tertiary (7) amines strongly decrease the accumulation of NA and 5-HT in brain slices in vitro and in vivo. The cyclobutylamines also cause motor stimulation. The most potent compound in this respect is the tertiary amine 7. The increase in locomotion is not blocked by pretreatment with phenoxybenzamine, methergoline, or alpha-methyltyrosine. Pretreatment with pimozide or reserpine reduces the hyperactivity induced by 7. This hyperstimulation seems to be caused by a mechanism of action which differs from that of amphetamine. 7 may cause increase in locomotion by release of dopamine from granular stores.

5-Hydroxytryptophan↗
PubMed1977

Effect of hypercapnia and hypocapnia on tryptophan and tyrosine hydroxylation in rat brain.

The effects of induced hypo- and hypercapnia upon the rate of hydroxylation of tryptophan and tyrosine in the rat brain were studied by measuring the accumulation of 5-HTP and DOPA following administration of the aromatic L-aminoacid decarboxylase inhibitor 3-hydroxybenzylhydrazine HCl (NSD 1015). The results suggest that the hydroxylation of tryptophan varies directly with the tissue Po2. On the other hand, the hydroxylation of tyrosine did not show a simple relationship to Po2 but appeared to be influenced by pH changes.

5-Hydroxytryptophan↗
PubMed1977

Biogenic amine synthesis defect in dihydropteridine reductase deficiency.

In the enzymatic hydroxylation of aromatic amino acids, tetrahydrobiopterin is the essential cofactor. Regeneration of tetrahydrobiopterin requires dihydropteridine reductase, without which there should be a deficiency of hydroxylated amino acids and their products, biogenic amines. Assay of biopsied brain cortex of a patient with a deficiency of dihydropteridine reductases showed low concentrations of serotonin and dopamine, and this was reflected in the concentrations of their major metabolites measured in cerebrospinal fluid from lumbar, ventricular, and subarachnoid spaces. The metabolite concentrations were restored to normal, or above normal, by treatment with specific amino acids which bypass the metabolic block at the hydroxylation step. It is postulated that the seizures and neurological deterioration of the patient were related to a deficiency in the synthesis of biogenic amine neurotransmitters.

5-Hydroxytryptophan↗
PubMed1976

Failure to monoaminergic and cholinergic receptor blockers to prevent prostaglandin E2-induced luteinizing hormone release.

Receptor blocking drugs were used to determine whether adrenergic, dopaminergic, serotoninergic, or cholinergic synapses are involved in mediating the LH release induced by intraventricularly injected PGE2. Prostaglandin E2 (5mug) was injected into the 3rd ventricle (3rd V) of ovariectomized rats, and plasma LH concentrations before and after treatment were determined by radioimmunoassay. Phentolamine, 20 or 30 mug, or pronethalol, 20 mug (alpha and beta adrenergic receptor blockers, respectively) injected into the 3rd V failed to alter the elevation of plasma LH evoked by PGE2 injected into the ventricle 10 min later. Likewise, LH release following PGE2 was not changed when a dopaminergic blocker, pimozide (0.63 mg/kg, SC), was injected 2 h prior to PGE2. Two antagonists of serotonin, methysergide maleate (3 mg/kg ip) or cinanserin HC1 (1 mg/kg iv) given 2 h or 45 min before PGE2, respectively, failed to alter the action of PGE2. Atropine (100 or 250 mug) injected into the 3rd V 10 min prior to PGE2 was also ineffective in blocking the increase in plasma LH following PGE2. The results of this study indicate that the effect of PGE2 on LH release is not mediated by adrenergic, dopaminergic, serotoninergic, or cholinergic receptors. They also suggest that PGE2 is not acting trans-synaptically but probably directly on the LHRH neuron to induce the discharge of LHRH into the hypophysial portal vessels which then evokes release of LH from the adenohypophysis.

5-Hydroxytryptophan↗
PubMed1976

Neurotransmitter regulation of growth hormone and ACTH in the rhesus monkey: effects of biogenic amines.

In an attempt to clarify the role of central neurotransmitters in GH and ACTH regulation, chair-adapted unanesthetized adult male rhesus monkeys and chronic indwelling intratrial cannulae were given 30 min infusions of various agonists known to affect central amines, and plasma samples were withdrawn for GH and cortisol determinations. Infusion of acid-saline vehicle alone had no significant effect on plasma GH or cortisol (P less than 0.05). L-Dihydroxyphenylalanine (L-Dopa) (4.5 and 45 mg/kg), but not apomorphine (7 mug/kg), a specific dopaminergic agonist, produced significant elevations of GH. Both noradrenergic (clonidine HCl, 1.5, 15, and 150 mug/kg, and D,L-threodihydroxyphenylserine (D,L-threodops) 90 mg/kg) and serotoninergic (5-hydroxy-L-tryptophan (5-HTP), 45 mg/kg) agonists induced significant GH responses. These findings suggest that GH is regulated in the rhesus monkey by noradrenergic and serotoninergic neurons, whereas participation of dopaminergic neurons has not been established. Significant cortisol responses were only observed following infusion of 5HTP (45 mg/kg). Dopaminergic and noradrenergic agonists not only failed to alter resting cortisol levels but also did not affect the cortisol response to 5-HTP. In the rhesus monkey serotoninergic mechanisms appear to be responsible for the regulation of resting cortisol levels. A catecholamine inhibitory mechanism was not demonstrated in this species.

5-Hydroxytryptophan↗
PubMed1976

Glucocorticoid regulation of the serotonergic system of the brain.

Glucorticoids at concentrations above 10(-7) M stimulate the uptake of tryptophan by brain synaptosomes. Furthermore, in both developmental and drug-induced (reserpine and ethanol) increases of brain tryptophan hydroxylase activity, glucocorticoids are required in order for the increases to occur. If de novo enzyme synthesis is assumed to take place in such increases, we could adopt the working hypothesis that two loci of glucocorticoid action may exist in serotonergic neurons with respect to their specific function: one in the cell body presumably in a sequence of macromolecular events, and the other directly on nerve terminals. Thus, in its immediate action, the hormone may rapidly regulate 5-HT synthesis through an increased uptake of tryptophan by nerve terminals. In the slow action, the hormone may mainly play a permissive role in the induction of tryptophan hydroxylase by factors yet to be identified.

5-Hydroxytryptophan↗
PubMed1976

Review of drug treatment for Down's syndrome persons.

A review of drug treatment for Down's syndrome individuals was presented. Drugs used to modify behavior, as well as drugs used with the goal of affecting cognitive processes, were discussed. Some observations were offered as to the effectiveness of past and current drugs on Down's syndrome and some methodological problems relating to drug studies presented. There have not been any drugs that have demonstrated remarkable improvement in the status of Down's syndrome individuals that have been widely accepted as effective.

5-Hydroxytryptophan↗
PubMed1977

Synthetic melanocyte stimulating hormone release-inhibiting factor (MIF). Part III: effect of L-prolyl-N-methyl-D-leucyl-glycinamide and MIF on biogenic amine turnover.

The effect of the factor that inhibits the release of melanocyte stimulating hormone (MSH), i.e., L-prolyl-L-leucyl-glycinamide (MIF), and L-prolyl-N-methyl-D-leucyl-glycinamide, an analog, on brain norepinephrine (NE), dopamine (DA) and serotonin (5-HT) turnover was examined in rats. The analog (40 mg/kg i.p.), in a fashion similar to MIF (40 and 5 mg/kg i.p.), increased brain DA turnover; only MIF (40 mg/kg i.p.) increased endogenous DA levels. The analog (40 and 5 mg/kg i.p.) decreased brain NE turnover; MIF at the same doses was ineffective. Neither MIF nor the analog affected rat brain 5-HT turnover or the 5-HTP-induced behavioural syndrome in the mouse. These results indicate that the analog, like MIF, exerts effects on central catecholamine turnover. The different biochemical profile of the analog compared to MIF may be importance with regard to potential clinical use in the treatment of Parkinson's disease and depression.

5-Hydroxytryptophan↗
PubMed1976

Analysis for indole compounds in urine by high-performance liquid chromatography with fluorometric detection.

We describe a chromatographic system involving a high-performance chemically-bonded reverse-phase column and fluorescence detection for measurement of indoles in urine. We controlled retention and selectivity by optimizing the methanol content and pH of the mobile phase. Six reference indoles were separated in less than 20 min; three 5-hydroxyindoles were eluted in less than 7 min. About 5-15 ng of aqueous solutions of these compounds can be detected. The combination of selectivity (from use of the chromatographic column) and fluorescence detection permitted analysis for five of the six indoles after a single urine-deproteinization step.

5-Hydroxytryptophan↗
PubMedDate not supplied

The effect of baclofen and aminoxyacetic acid on catalepsy in the rat.

Gabaergic compounds, baclofen and aminoxyacetic acid (AOAA) potentiate the catalepsy induced by neuroleptics. This effect indicates their functional antagonism towards the central dopaminergic system. Both compounds exert a central antiserotonin effect. Baclofen, but not AOAA, also shows weak cholinolytic properties. However, the potentiation of cataleptogenic action of neuroleptics by baclofen and AOAA is not related to their effect on the central serotonergic or cholinergic systems.

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