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PubMedDate not supplied

[Effect of vasopressin on changes in the behavioral reactions of rats induced by psychotropic substances].

The effect was studied of arginyl-8-vasopressin (AVP) on changes in rats behavioural reactions, elicited by reserpine, haloperidol, aminazine, amitriptyline or nialamide. It has been shown that AVP administered intraperitoneally in a dose of 0.001 mg/kg, eliminates the deficit of elaboration of conditioned reaction of active avoidance produced by psychotropic drugs, without influencing the motor activity reduction developed after administration of these substances.

Animals↗
PubMedDate not supplied

In vitro inhibition studies of two isozymes of human liver cytochrome P-450. Mephenytoin p-hydroxylase and sparteine monooxygenase.

Human liver preparations were used to screen various drugs for their capability of binding to mephenytoin p-hydroxylase and sparteine monooxygenase, two cytochrome P-450-catalyzed activities that are independently heritable. For this screening, any indication of competitive inhibition by the drug was interpreted as an indication of binding. Among 64 drugs and alkaloids tested, 24 compounds caused inhibition of mephenytoin p-hydroxylation but the inhibition was weak in most cases; by contrast, 40 of the 64 compounds inhibited sparteine oxidation, the inhibition being potent in many cases. The only fairly strong inhibitors of mephenytoin p-hydroxylation were the alkaloid papaverine and the monoamine oxidase inhibitors tranylcypromine and nialamide. The results of these inhibition studies confirm the independence of the two monogenic defects observed in different populations. Metabolism is possibly altered in poor metabolizers of mephenytoin with fewer drugs than in poor metabolizers of sparteine.

Alkaloids↗
PubMed1987

Catecholaminergic properties of cholinergic neurons and synapses in adult rat ciliary ganglion.

Parasympathetic neurons of the ciliary ganglion are innervated by preganglionic cholinergic neurons whose cell bodies lie in the brain stem; the ganglion cells in turn provide cholinergic innervation to the intrinsic muscles of the eye. Noradrenergic innervation of the iris is supplied by sympathetic neurons of the superior cervical ganglion. Using immunocytochemical and histochemical techniques, we have examined the ciliary ganglion of adult rats for the expression of cholinergic and noradrenergic properties. As expected, the postganglionic ciliary neurons possessed detectable levels of choline acetyltransferase immunoreactivity (ChAT-IR). Unexpectedly, many ciliary neurons also exhibited immunoreactivity for tyrosine hydroxylase (TH-IR). Some had dopamine beta-hydroxylase-like (DBH-IR) immunoreactivity, but none contained detectable catecholamines, even after treatment with nialamide and L-DOPA. A sparse plexus of fibers exhibiting faint TH-IR was present in the irises of acutely sympathectomized rats. The terminals of preganglionic axons in the ciliary ganglion exhibited not only immunoreactivity for ChAT, but also for TH and contained stores of endogenous catecholamine. Neither ciliary neurons nor their preganglionic innervation accumulated detectable stores of exogenous catecholamines. Rats sympathectomized as neonates by treatment with 6-hydroxydopamine subsequently had a greater proportion of neurons possessing detectable TH-IR in the ciliary ganglion; both the TH-IR perikarya and their axons in the iris were more intensely immunofluorescent. TH-IR was present in the ciliary neuron cell bodies of mouse, guinea pig, and ferret. These species, however, lacked detectable TH-IR or catecholamine stores in preganglionic terminals. These observations indicate that mature, functionally cholinergic neurons from 2 different embryonic origins, postganglionic ciliary neurons derived from the neural crest and preganglionic neurons derived from the neural tube, display several catecholaminergic properties.

Animals↗
PubMedDate not supplied

[Assessment of the clinical activity of fluoxetin (Prozac) according of the "Stars of Liège" model].

Ten psychiatrists have independently rated the clinical profile of fluoxetin (Prozac) at the daily dose of 20 mg according to a "Stars of Liège" model comprising three parameters of therapeutic activity (antidepressant, psychostimulant and anxiolytic) and three parameters of side-effects (anticholinergic, sedative and hypotensive). Each parameter, graduated from 0 to 5 (no, very weak, weak, moderate, potent, very potent effect) was rated by each investigator according to his personal experience with at least 10 patients. Mean ratings given to fluoxetine show a moderate antidepressant effect, equal to amitriptyline (Rédomex, Tryptizol 75 mg/d, clomipramine (Anafranil 75 mg/d and nialamide (Niamide 100 mg/d, weak psychostimulating and anxiolytic effects, a very weak sedative effect and a lack of anticholinergic and hypotensive effects. Digestive side-effects of moderate intensity were also noted as well as a very weak anorexia. The important variability between investigators in the rating of the clinical profile of fluoxetine suggests that more experience is needed in order to define better its physiognomy.

Anti-Anxiety Agents↗
PubMed1978

Cerebrovascular response to intracarotid infusion of 5-hydroxytryptophan and L-DOPA in cats.

Intracarotid administration of 5-hydroxytryptophan (10 mg/kg) results in a slight vasoconstriction of cerebral vessels. L-DOPA (20 mg/kg) administered by the same route enhances cerebral blood flow. The effect on cerebral blood flow of L-DOPA (20 mg/kg) following intracarotid 5-hydroxytryptophan (10 mg/kg) administration shows a potentiation of cerebral blood flow response in non-pretreated as well as in nialamide- and reserpine-pretreated cats.

5-Hydroxytryptophan↗
PubMed1988

Sites of serotonin uptake in epithelia of the developing mouse palate, oral cavity, and face: possible role in morphogenesis.

With the method of whole mouse embryo culture, together with immunocytochemistry with an antiserum to serotonin (5-HT), sites of 5-HT uptake were found to be transiently expressed in the epithelia of the developing palate, tongue, nasal septum, and maxillary and mandibular prominences during the period of active morphogenesis (embryonic days 12-14; or E12-14). These sites had the ability to take up 5-HT when added to the culture medium in the presence of the MAO inhibitor nialamide and an antioxiant, L-cysteine (NC), and could also be seen after exposure of embryos to the 5-HT precursor L-tryptophan (L-TRP) + NC. These sites were also visible after culturing embryos without any additives, which may have been due to the presence of L-TRP in one component of the culture medium (DMEM) or to 5-HT itself, which is present in relatively high amounts in fetal calf serum. At E12-13, the appearance of 5-HT immunoreactivity (IR) at these sites after treatment with 5-HT + NC was blocked by the 5-HT uptake inhibitor fluoxetine, providing further evidence that these are true sites of 5-HT uptake. However, fluoxetine did not completely block the appearance of these sites in E14 embryos after 5-HT + NC or L-TRP + NC although it was effective with NC alone. This finding could mean that at E14 5-HT uptake into these sites occurs by mechanisms not completely blocked by fluoxetine or that there is some limited capacity for 5-HT synthesis. Taken together with results from previous studies where 1) 5-HT has been reported to stimulate palatal shelf reorientation and palatal mesenchyme cell motility in vitro [Wee et al., J Embryol Exp Morphol 53:75-90, 1979; Zimmerman et al., J Craniofac Genet Dev Biol 3:371-385, 1983] and 2) long-term culturing of mouse embryos in the presence of 5-HT or fluoxetine has been shown to cause malformations of the craniofacial region (Lauder, Thomas, and Sadler, in preparation), the results of the present study suggest that 5-HT could act as a developmental signal in the palate, oral cavity, and face during the period of active morphogenesis.

Animals↗
PubMed1977

[Effect of benzatropine on the O-methylation of striatal dopamine].

After treatment by nialamid, benztropine administered to Rats produced an increase in the level of 3-O-methyldopamine in the corpus striatum. It produced a slight increase in the level of striatal dopamine and no change in the level of norepinephrine. The monoamine oxydase and catechol-O-methyltransferase activities of remaining brain showed no variations by benztropine. The results suggest the possible involvement of striatal dopamine and its extraneuronally catabolism in the antiparkinsonian effect of benztropine.

Animals↗
PubMed1979

[Identification of 4-O-methyldopamine in rat tissues by reverded-phase liquid chromatography (author's transl)].

4-O-Methyldopamine was identified and assayed in tissues from L-dopa treated rats by reversed-phase high-performance liquid chromatography. The initial steps in the separation of catecholamines were performed by alumine, a weak cation-exchange resin, and thin-layer chromatographic techniques. After L-[3 H] dopa administration, the radiochromatogram was superimposed on the fluorochromatogram obtained with authentic marker 4-O-methyldopamine. This metabolite was detected in kidney but not in brain. The 4-O-methyldopamine:3-O-methyldopamine ratio was 0.032 in kidney. The influence of various treatments on this ratio was investigated. A 160% increase was found after L-dopa administration. This effect was potentiated by nialamide pretreatment (550% increase).

Animals↗
PubMed1982

[Interactions between buprenorphine, narcotic analgesic, and centrally acting drugs in prolongation of halothane-induced sleeping and analgesia (author's transl)].

Interactions between buprenorphine, narcotic analgesic, and centrally acting drugs were studied in prolongation of halothane-induced sleeping and analgesia using the D'Amour-Smith method in mice, and the effect of buprenorphine on monoamine metabolism was studied in rat brain. Diazepam and chlorpromazine prolonged the halothane-induced sleeping time dose-dependently. Buprenorphine (0.01, 0.1, and 1 mg/kg s.c.) inhibited the effect of diazepam, but not that of chlorpromazine. Pentazocine and naloxone also inhibited the effect of diazepam, but morphine did not. It is suggested that the inhibitory effect of buprenorphine on prolongation of halothane-induced sleeping time by diazepam is due to its opiate antagonistic property. Since narcotic antagonists inhibited the effect of diazepam, the endogenous opiate system seems to be involved in this effect. Diazepam or droperidol had no effect on the analgesia of buprenorphine, morphine, and pentazocine. Buprenorphine analgesia was inhibited by reserpine and p-chlorophenylalanine, potentiated by 5-hydroxytryptophan, and not affected by alpha-methyl-p-tyrosine or 3,4-dihydroxyphenylalanine. These results suggest that the serotonergic system plays a modulating role in buprenorphine analgesia. Imipramine and nialamide inhibited buprenorphine analgesia in the test at low stimulus intensity, but potentiated at high stimulus intensity. Buprenorphine (0.1, 1 and 10 mg/kg s.c.) increased the dopamine metabolites, 3,4-dihydroxyphenylacetic acid and homovanillic acid, in various brain areas and the serotonin metabolite, 5-hydroxyindoleacetic acid, in midbrain.

Analgesia↗
PubMedDate not supplied

[Pharmacological correction of neurogenic disorders of cerebral circulation].

The paper discusses the data on the effect of adrenergic innervation on the cerebral circulation and possible approaches to the pharmacological action on cerebral blood vessels constriction. Attention is also paid to the effect of alpha-adrenoblockers (dihydroergotoxin, phenoxybenzamine, phentolamine, etc) on adrenoreactive structures and of that of sympatholytics (reserpine, octadin, ornid) on the presynaptic membrane of the adrenoreceptor. Relaxation or elimination of cerebral vessels spasms was observed under the influence of the drugs capable of affecting the central component of cerebral circulation control. Drugs with central adrenergic (nialamide, nitroglycerin) and GABA-ergic (GABA, sodium hydroxybutyrate, depaquin, diazepam, phenazepam, etc) activity exerted the same effect.

Adrenergic Fibers↗
PubMed1982

[On the changes of Holmes positive intracytoplasmic bodies in the mouse locus coeruleus (author's transl)].

The intracytoplasmic inclusion bodies were found to be intensely stained in the normal nerve cells by the modified Holmes method (Katoh and Shimizu, 1982b). In the present study we used ddY mouse under normal and experimental conditions and stained locus coeruleus region, where the inclusion bodies are remarkably rich in number. The inclusion bodies stained by Holmes method were round in shape and 1--3 micrometers in size and were present singly or 2 in one cell. Total number of these bodies amounted to 1569 +/- 166 in the unilateral locus coeruleus in both sexes. Experimental conditions, such as dehydration for 3--6 days, fasting for 3--6 days, dehydration plus fasting for 3--6 days and reserpine (5 mg/Kg) administration markedly decreased the number of the bodies. However castration (10 to 30 days after operation) and vasopressin (2 IU each for 13 days) produced no changes. Nialamide (300 mg/Kg each for 3 days) caused slight increase. In the ontogenetic development the bodies already appeared in the late fetal life.

Animals↗
PubMed1983

[Accumulation of exogenous monoamines in the notochord of lampreys: fluorescence microscopy and radiography study].

Storage of biogenic amines was studied in the notochord of the lamprey (Lampetra planeri) after injection of cold or tritiated amines or their precursors. After injection of dopamine, noradrenaline or 5-hydroxytryptophane, an intense formaldehyde-induced fluorescence was observed in the cytosol of chordal cells and in the perichordal sheat. A similar location occurred after injection of the same tritiated products. No qualitative or significant quantitative differences could be distinguished between the larval and the metamorphosing forms. RO4-4602, a decarboxylase inhibitor, and Nialamide, a monoamine-oxydase inhibitor, did not modify significantly the incorporation of 3H-5-hydroxytryptophan. Using histochemical technique a monoamine oxydase activity could be detected in the nervous system and in the muscle but was not shown in the notochord.

Animals↗
PubMed1983

Differential properties of the microsomal deamination and hydroxylation reactions.

The addition of 1 mM of the metal complexing reagents such as EDTA, alpha, alpha'-dipyridyl, 1,10-phenanthroline and Tiron to the incubation of benzylamine, aminopyrine, p-nitroanisole and aniline, respectively, inhibited selectively the microsomal deamination of benzylamine, whereas the addition of the monoamine oxidase inhibitors tranylcypromine, nialamide and iproniazid specifically decreased the metabolism of aminopyrine, p-nitroanisole and aniline. Pretreatment of rats with 3,4-benzpyrene or phenobarbital increased the liver microsomal concentration of cytochrome P-450 (448) and the rate of aminopyrine and p-nitroanisole demethylation and of aniline hydroxylation whereas pretreatment cytochrome P-450 depressor agents such as cadmium or cobalt lowered the concentration of the hemoprotein and decreased the rate of the demethylation reactions. Phenobarbital and 3,4-benzpyrene pretreatment had either no effect or decreased significantly the rate of the microsomal deamination reaction respectively. The administration of cadmium slightly decreased the rate of benzylamine deamination whilst cobalt produced no significant effect. These results indicate that the microsomal oxidative deamination reaction has different properties than the dealkylation and aromatic hydroxylation reactions, thus suggesting a different enzyme system.

Aminopyrine↗
PubMed1978

Potentiation by substance P of contractions of the isolated vas deferens of the mouse elicited by electric field stimulation and by drugs.

1 Isolated vasa deferentia from the mouse were opened longitudinally and suspended in Krebs solution at 37 degrees C in an organ bath. Contractions of the muscle were elicited by electric field stimulation, noradrenaline (10(-6) M) and acetylcholine (10(-6) M). Continued transmural stimulation evoked a biphasic response comprising a rapid twitch followed about 10 s later by a smaller, sustained rise in muscle tone.2 The amplitudes of nerve-mediated and drug-induced responses were considerably potentiated by substance P (SP) in the dose range 10(-12) to 10(-7) M. Higher concentrations of SP were directly spasmogenic. The sensitizing property of SP was dose-dependent and was usually well maintained, but always disappeared quickly on washing the preparation. In some experiments SP facilitated the twitch, but not the subsequent phase of the electrically-induced contraction or the response to externally applied noradrenaline.3 Phentolamine (10(-6) M) failed to block this effect of SP, but itself potentiated the nerve-mediated twitch, and completely abolished the sustained secondary contraction.4 Desmethylimipramine (10(-6) M) enhanced the delayed contraction but not the immediate contraction.5 The uptake of tritiated noradrenaline (3 x 10(-7) M) by vasa was inhibited by desmethylimipramine (10(-6) M) and increased by nialamide (3 x 10(-5) M), but was not modified by SP (10(-6) M).6 Nerve-mediated release of accumulated radioactivity was accelerated by phentolamine, but not by SP or desmethylimipramine.7 These findings suggest that SP sensitizes the muscle cells to depolarizing stimuli but that it has no facilitatory effect on sympathetic neural elements.

Animals↗
PubMed1980

[Demonstration of generators of the locomotor and respiration rhythms in the cervico-thoracic spinal cord of rabbits].

In curarized Rabbits whose cervico-thoracic cord has been isolated through C2 and Th12 transections, a pharmacological activation (nialamide-DOPA) disclosed distinct rhythmic efferent activities, locomotor-like bursts in forelimb muscle nerves and "respiratory" discharges in the phrenic nerves: they originate respectively from a cervico-thoracic locomotion generator and from a "respiration" generator; these spinal generators appear to be interconnected with each other.

Animals↗
PubMedDate not supplied

Central action of adrenaline.

Adrenaline (A) administered in doses of 10, 50 and 100 micrograms/rat into the right lateral ventricle of the brain (i.v.c.) in rats reduced the spontaneous and exploratory locomotor activity, decreased the body temperature, and increased the effects of narcotics. The reduction of the locomotor activity after A was antagonized by nialamide, alpha-MT, and yohimbine. Total chemical destruction of catecholaminergic neurons and selective destruction of dopaminergic neurons caused increase in A-induced locomotor activity. A had no effect on the locomotor activity in rats subjected to the action of reserpine, reserpine with 6-OHDA, and phenoxybenzamine or propranolol. In rats treated with phenoxybenzamine, propranolol, spiroperidol or subjected to selective destruction of noradrenalinergic neurons adrenaline decreased significantly the locomotor activity. A (10 micrograms) increased and in higher doses inhibited amphetamine-induced hyperactivity. It potentiated amphetamine and apomorphine stereotypy and antagonized catalepsy induced with haloperidol or fluphenazine. In the despair test adrenaline reduced the duration of akinesia. In doses of 0.1, 1.0 and 10 micrograms/kg i.v. A increased slightly the flexor reflex of the hind paw of spinal rats. This action was antagonized by phentolamine as well as by propranolol. In biochemical investigations it was demonstrated that A decreased the level of dopamine in rat brain but had no effect on its utilization. The obtained results indicate that A i.v.c. stimulated catecholaminergic receptors.

Animals↗
PubMed1981

Pharmacology of amezinium, a novel antihypotensive drug. III. Studies on the mechanism of action.

Pharmacological studies on the mechanism of action of 4-amino-6-methoxy-1-phenyl-pyridazinim methyl sulfate (ameziniummetilsulfate, LU 1631, Regulton), in the following briefly called amezinium, are presented. 1. Amezinium increases the arterial blood pressure and heart rate of anaesthetized animals and of pithed rats by stimulating vascular alpha- and cardiac beta 1-adrenoceptors. The action was not modified by ganglionic blockade with hexamethonium. The alpha-adrenergic blocking drug phentolamine antagonized the blood pressure increasing effect and the beta-adrenergic blocking drug propranolol antagonized the heart rate increasing effect. 2. Noradrenaline depletion by pretreatment with reserpine reduced the pressor effect of amezinium to approximately the same extent as it reduced the effect of tyramine. It completely abolished the heart rate increasing effect. Under these conditions, high doses of amezinium reduced the heart rate. 3. Amezinium is taken up by adrenergic neurones. Inhibition of uptake 1 with desipramine reduced the pressor effect of amezinium and of tyramine. 4. Being a substrate of uptake 1, amezinium also inhibited noradrenaline and tyramine uptake. Consequently, it enhanced the pressor effect of exogenous noradrenaline and increased the contractions of the nictitating membrane following preganglionic stimsipramine reduced the pressor effect of amezinium and of tyramine. 4. Being a substrate of uptake 1, amezinium also inhibited noradrenaline and tyramine uptake. Consequently, it enhanced the pressor effect of exogenous noradrenaline and increased the contractions of the nictitating membrane following preganglionic stimsipramine reduced the pressor effect of amezinium and of tyramine. 4. Being a substrate of uptake 1, amezinium also inhibited noradrenaline and tyramine uptake. Consequently, it enhanced the pressor effect of exogenous noradrenaline and increased the contractions of the nictitating membrane following preganglionic stimulation (endogenous noradrenaline). It diminished the effect of indirectly acting sympathomimetic drugs (tyramine). It did not modify the action of the sympathomimetic drugs methoxamine and isoprenaline, which are not subject to uptake 1. 5. Amezinium inhibits monoamine oxidase (MAO). As a result of being concentrated in sympathetic neurones via uptake 1 amezinium causes specific inhibition of intraneuronal MAO; this was demontrated by enhanced restoration of the effects of tyramine and amezinium by noradrenaline infusion in reserpinized animals. The effective doses of amezinium here were lower than the doses necessary to inhibit tyramine and to exert a pressor effect. This is in accordance with the blood pressure increasing effect of amezinium itself by amezinium pretreatment and noradrenaline-infusion. 6. Pretreatment with a MAO inhibitor (nialamide) enhanced the pressor effect of amezinium, probably by also inhibiting extraneuronal MAO...

Animals↗