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At least 73 records · Page 4Linked to original sources
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.

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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cannulae were given 30 min infusions of various agonists known to affect central amines, and plasma samples were withdrawn for GH and cortisol determinations.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.

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PubMed1979

Dopaminergic antagonism of L-5-hydroxytryptophan-induced myoclonic jumping behavior.

We studied the effect of dopamine agonists (levodopa, apomorphine, lergotrile, and M-7 [2(dimethylamino)5,6-dihydroxytetralin] on myoclonic jumping behavior in young male guniea pigs. All these agents had a significant antagonistic effect on the frequency of this serotonin-mediated behavior. The duration of the antagonism corresponded in all cases to the duration of stereotyped chewing behavior induced by these agents alone. The dopamine antagonist haloperidol potentiated jumping behavior. Therefore myoclonic jumping behavior is influenced by dopaminergic mechanisms, and this behavior may be the result of interaction between dopaminergic and serotonergic activity. The role of dopaminergic mechanisms in human myoclonic disorders needs further clarification.

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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.

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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.

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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.

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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↗
PubMed1977

[Metabolic disorders in experimental hepatic insufficiency and parenteral feeding].

Anhepatia is a complete experimental model for the study of metabolic disturbances associated with hepatic insufficiency. The authors report their experience based upon 16 cases of total hepatectomy in the dog. The animals received different types of hepatic assistance : group 1 (2 dogs), carbohydrate assistance (glucose 7 g/kg/24 h) ; group II (2 dogs), carbohydrate and haemostatic assistance : homologous plasma 50 ml/kg body weight per 24 hours previously stored at - 80 degrees C ; group III (2 dogs) same nutrition as in group II, combined with amino acids : leucine 53, 3 mg, isoleucine 46, 6 mg ; valine 53,3 mg alpha-ketonic acid (lg/kg/24 h) ; group IV (10 dogs, same nutrition as in group III, combined with supplements in neuro transmitter precursors : 6 dopa 1,66 mg, 5 hydroxy-tryptophane 2 mg and choline 16, 66 mg/kg/24h. Metabolic disturbances and their course were analysed in detail. Results : (mean survival) - group I : 24 +/- 4 hours; group II : 36 +/- 9 hours; group III : 42 +/- 4 hours; group IV : 90 +/- 9 hours. The average survival differed significantly for groups III and IV (p less than 0,01) in comparison with control groups I and II. The replacement of essential hepatic functions such as blood glucose regulation, coagulation, detoxication and the provision of neurotransmitter precursors made possible 4 days survival after total hepatectomy.

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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.

5-Hydroxytryptophan↗
PubMedDate not supplied

The effect of antihistamine drugs on the neuroleptic-induced catalepsy.

The effect of atropine on the spiperone- or reserpine-induced catalepsy was compared with the effect pure antihistamines (chlorcyclizine, diphenhydramine, mepyramine) and antiserotonin -- antihistamine drugs (cyproheptadine, danitracen). All the drugs were used in equipotent doses in respect of their central cholinolytic action, assassed previously on the basis of the tremorine test. The potency of the antiserotonin action of chlorcyclizine, diphenhydramine and mepyramine was estimated by assessing the ID50 values of these compounds in the test based on antagonism to L-5-hydroxytryptophan action in the mouse. The spiperone-induced catelepsy, was most effectively inhibited by classical histaminolytics and less by drugs of a combined antiserotonin and antihistamine action. For the reserpine-induced catalepsy, differences in action of the two groups of drugs were less distinct. In both cases atropine produced the weakest anticataleptic effect. Amodiaquine, an inhibitor of histamine degradation, enhanced the catalepsy induced by either neuroleptic (the reserpine-induced catalepsy in a statistically significant menner). A possibility that the anticataleptic action of chlorcyclizine, cyproheptadine, diphenhydramine, mepyrymine and danitracen depends on the blockade of the histamine receptors in the brain is discussed.

5-Hydroxytryptophan↗
PubMed1979

DDT-induced myoclonus: serotonin and alpha noradrenergic interaction.

p,p'-DDT (600 mg/kg) produces myoclonic activity in mice which can be reduced by L-5-hydroxytryptophan (L-5HTP) (200 mg/kg), H75/12 (25 mg/kg), serotonin uptake blockers and two alpha-receptor blockers, phenoxybenzamine (5 mg/kg) and trazodone (5 mg/kg). Decreasing endogenous brain serotonin by pretreatment with p-chlorophenylalanine (400 mg/kg i.p.) blocked the antimyoclonic action of all of these drugs except L-5HTP. Seven other alpha-receptor blockers (phentolamine, tolazoline, yohimbine, azapetine, aceperone, nicergoline and prazosin) potentiated the antimyoclonic activity of a small dose of L-5HTP (50 mg/kg) in this animal model. We postulate that an alpha noradrenergic inhibitory synapse may be located in the neural circuit connecting a serotonergic neuron to the final motor response (p,p'-DDT-induced myoclonus).

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PubMedDate not supplied

[Effect of preparations that alter catecholaminergic processes on the serotoninergic syndrome of head twitching in mice].

Specific neuroleptics suppressed head twitching (HT) in mice, provoked by d,1-5-hydroxytryptophane (200 mg/kg i. p.) in doses starting from 0.00025 mg/kg (spiroperidol). L-DOPA and piribedil inhibited HT in doses from 25 and 50 mg/kg respectively, whereas apomorphine and d,1-amphetamine in doses of 1 up to 10 mg/kg exerted ambivalent activity. HT was significantly attenuated by clonidine in doses from 0.25 mg/kg, whereas by noradrenaline, isoprenaline and naphthizine, injected into the brain ventricles, in doses of 1 microgram, and 0.025 microgram per mouse respectively. Destruction of brain catecholaminergic neurons by intraventricular 6-hydroxydopamine (50 micrograms per mouse) caused a strong enhancement of HT. However, partial protection of the adrenergic (but not the dopaminergic) neurons by pretreatment with desipramine or similar drug AW 15,1129 eliminated the protective effect of 6-hydroxydopamine. It is concluded that there is the dopaminergic link in the mechanism of HT and that the stimulation of the central adrenoreceptors inhibits HT.

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