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At least 73 records · Page 4Linked to original sources

PubMed1979

Experimental aggression and bruxism in rats.

Aggression has been suggested as one of the etiologic factors in bruxism. Experimental bruxism, audible, nonfunctional grinding or clenching of the teeth, was provoked in aggressive animals by drugs affecting central dopaminergic systems. Electric foot-stimulation was used to induce aggression, evident as the threatening or fighting position, in paired male Wistar rats. After initial stimulation, shocks were given only to maintain the characteristic fighting pose. Apomorphine facilitated induction of aggressive behaviour by electric shocks, and the rats receiving both treatments showed bruxism more frequently than controls subjected to shocks alone: up to 95 bruxism periods registered by a tape recorder during 30 min, as opposed to a few sporadic periods in the controls. Without shocks, apomorphine-treated rats displayed stereotypy with locomotion and biting of various objects. Aggression and bruxism were not equally successfully induced after L-dopa given with a peripheral inhibitor of aromatic amino acid decarboxylase (benserazide) or when L-dopa treatment was modified with the inhibitor of dopamine-beta-hydroxylase (diethyldithiocarbamate) or monoamine oxidase inhibitor (iproniazid). However, all the present drug combinations known to enhance central dopaminergic function seemed to increase irritability and disposition to experimental oral dyskinesias. This was observed especially when a sensory stimulus was applied at the same time or the drug had an amine-releasing effect (pheniprazine).

Aggression↗

PubMed1976

Increased survival of experimental skin flaps in rats following treatment with antiadrenergic drugs.

The effect upon the survival of skin flaps of several drugs which affect the adrenergic system was studied in rats. In control animals 41% of the skin flaps had survived seven days after the operation. Reserpine (1 mg/kg) injected intraperitoneally (i.p.) three days and one day before the flap operation increased the surviving flap area by 75% (p less than 0.001) as compared to control rats injected with saline. I.p. injection of guanethidine (5 mg/kg) or bretylium (10 mg/kg) every 12 hours, starting 24 hours before surgery and continued for 5 consecutive days, also increased the surviving flap area (19 and 33% respectively p less than 0.001). The surviving flap area was unchanged when desipramine (5 mg/kg) was injected in the same way and was decreased by 15% (p less than 0.05) following i.p. injection of the MAO inhibitor pheniprazine (5 mg/kg). Treatment with alpha-methyl-p-tyrosine (75 mg/kg), i.p. 30 min before surgery or 6-hydroxydopamine (50 mg/kg) i.v. 24 hours prior to surgery also increased the flap survival (56 and 49% increase in surviving flap area, respectively, p less than 0.001). The results demonstrated that the survival of skin flaps increased when the function of the adrenergic nervous system was inhibited. Enhanced sympathetic nervous activity slightly reduced or did not affect skin flap survival.

Adrenergic Agents↗

PubMed1976

Cellular mechanisms of renal tubular transport of I-dopa and its derivatives in the rat: microperfusion studies.

Proximal tubular transport of L-3,4-dihydroxyphenylalanine (L-dopa) and its derivatives were studied in the rat kidney by microperfusion and capillary perfusion techniques in situ. With the use of microperfusion techniques alone, it was found that L-dopa, L-3-methoxy-4-hydroxyphenylalanine, L-tyrosine and L-phenylalanine rapidly disappeared from the perfusate. The rates of reabsorption were calculated to be 2.05 X 10(-12), 2.13 X 10(-12), 6.35 X 10(-12) and 7.14 X 10(-12) mol/cm/sec, respectively. In contrast, L-alpha-methyldopa and dopamine were only slightly reabsorbed. The permeability coefficients were calculated to be 0.35 X 10(-4) and 0.21 x 10(-4) and 0.21 x 10(-4) cm/sec, respectively. The rate of reabsorption of L-dopa was greatly reduced in the presence of L-phenylalanine in the perfusate, but was not affected by D-dopa. With the stop-flow microperfusion technique with simultaneous capillary perfusion, the zero net flux transtubular concentration difference (deltaC) of labeled dopa was measured. When the initial concentration of 2 mM labeled L-dopa was perfused, the luminal concentration fell to a plateau level of 1.5 mM after a contact time of 20 seconds; i.e., deltaC was 0.5 mM. The net flux was much less than the efflux, suggesting the presence of a secretory or passive back flux of L-dopa. The deltaC of L-dopa was not influenced by the decarboxylase inhibitor, MK-486, and monoamine oxidase inhibitor, pheniprazine, but was significantly reduced by NaCN. Thus the reabsorption of L-dopa in the proximal convoluted tubule is an active process with great structural specificity.

Absorption↗

PubMed1976

Evidence for a physiological role of renal sympathetic nerves in adrenergic stimulation of renin release in the rat.

Previous studies on renin release by an in vitro system of rat kidney slices, which is devoid of hemodynamic influences, have provided evidence that renin release is stimulated by a beta-adrenergic mechanism. We used this system to study effects of tyramine (an indirectly acting amine capable of displacing endogenous catecholmines from sympathetic nerve endings) on renin release. Tyramine (10(-3)M) in the presence of a monoamine oxidase inhibitor (pheniprazine, 10(-5)M) and a phosphodiesterase inhibitor (theophylline, 10(-3)M) significantly (P less than 0.01) stimulated renin release when values were compared to control observations for media containing only the inhibitors. Tyramine-induced stimulation of renin release was blocked by the beta-blocking agent, propranolol (2 X 10(-4) M), and the neural uptake blocking agent, cocaine (10(-5) M), but not by the alpha-antagonist, phentolamine (9 X 10(-4) M). These observations demonstrate a potential role for the sympathetic innervation of the juxtaglomerular apparatus on renin release.

Animals↗

PubMed1976

Drugs and PGO waves in the lateral geniculate body of the curarized cat. III. PGO wave activity and brain catecholamines.

The possible implication of central catecholamines in the phasic phenomenon of ponto-geniculo-occipital (PGO) waves was investigated using PGO waves induced by the benzoquinolizine derivative, Ro 4-1284 (=PGO(1284), and the inhibitor of tryptophan hydroxylase, p-chlorophenylalanine (=PGO(PCPA); they were continuously recorded and counted in the lateral geniculate bodies of unanaesthetized immobilized cats as described in a previous report. The effect on PGO(1284) and PGO(PCPA) of various drugs interacting with the different steps of catecholaminergic transmission was studie. Injections of noradrenaline (NA) and of dopamine (DA) into the lateral brain ventricle tended to decrease the density of PGO(1284). The stimulant of central alpha-adrenoceptors, clonidine, suppressed PGO(1284) and PGO(PCPA) in very small doses. Apomorphine in high doses had inconsistent depressant effects which were probably not related to its stimulant action on DA receptors. Release of brain NA by dexamphetamine and beta-tetrahydronaphthylamine decreased the density of PGO waves, alpha-Methyldopa diminished PGO(PCPA) but not PGO(1284. The MAO-inhibitor, nialamide, depressed PGO(PCPA) more than PCO(1284), whereas pheniprazine was inactive. The inhibitor of catechol-O-methyltransferase, tropolone, reduced the density of bially blocks the uptake of NA, was more potent on PGO(PCPA) than on PGO(1284). The alpha-adrenoceptor blocking agent, phenosybenzamine, markedly increased the density of PGO(PCPA). Similar effects were obtained with thioridazine and clozapine, which aare also known to be blockers of central alpha-adrenoceptors. Inhibition of tyrosine hydroxylase (by alpha-methyltyrosine) and of DA-beta-hydroxylase (by disulfiram or Ro 8-1981), in addition to the inhibition of tryptophan hydroxylase by PCPA, induced PGO waves comparable in density and temporal distribution to those occurring following the application of Ro 4-1284. The acute bilateral lesion of the dorsal and caudal parts of thel ocus coeruleus increased the density of PGO(PCPA). The results strongly suggest that, in addition to the 5-hydroxytryptaminergic system, noradrenergic neurones, probably originating in the locus coeruleus, depress the neurones in the pontine reticular formation involved in the generation of PGO waves.

Animals↗

PubMed1990

Neuropharmacology of pineal secretions.

A connection between pineal function and several psychiatric diseases has been shown recently. The diurnal and seasonal rhythmicity of melatonin production is associated with affective disorders and several types of endogenous depression. The cortisolmelatonin ratio was significantly higher in depressed individuals than in healthy controls. Alterations in melatonin secretion may also occur in non-affective psychiatric disorders, such as chronic schizophrenia. Antidepressants and other psychotropic drugs modify melatonin synthesis. In rodents, monoamine oxidase (MAO) inhibitors (e.g. pheniprazine, harmine or nialamide) increase pineal concentrations of the melatonin precursors, serotonin (5HT) and N-acetyl serotonin (NAS), by enhancing N-acetyl transferase activity. These drugs also increase melatonin, 5HT and NAS in the cerebrospinal fluid. Chronically administered tricyclic antidepressants reduce pineal and serum melatonin content in rodents. In humans, both the MAO-A selective inhibitor clorgyline and the non-selective inhibitor tranylcypromine increase serum melatonin levels. In contrast, serum melatonin remains unaltered by the MAO-B selective inhibitor L-deprenyl. The actions of other drugs on melatonin production, including lithium, propranolol, amphetamine and several monoamine precursors, are in accordance with their psychotropic effects and with their effect on monoamine functions.

Animals↗

PubMed1975

Psychophysical evaluation of toxic effects on sensory systems.

Toxic effects on sensory systems have rarely been evaluated by psychophysical methods. As examples of possible applications four studies are described. Sodium salicylate and kanamycin, both reported to produce hearing deficits in man, have also been demonstrated to affect auditory thresholds in monkeys. With the latter drug the deficits measured were found to be correlated with specific loss of receptor cells in the cochlea. Pheniprazine, known to induce red-green color blindness, was found to disrupt a wavelength discrimination in pigeons. Trans 11-amino-10,11-dihydro-5-(3-dimethylaminopropyl)-5,10-expoxy-5H-dibenzo[a,d]-cycloheptene dihydrochloride, which was found to bleach the tapidum lucidum in dogs when given subacutely, was found to decrease sensitivity to light. The loss in sensitivity measured by behavioral techniques was correlated with the loss of coloration of the tapidum. Monkeys, not having a tapidum, did not show a similar effect.

Acoustic Stimulation↗

PubMed1975

[Antiviral chemotherapeutic agents. XVIII. Adamantane derivatives of amphetamine. Their potential interest as autonomic and antiparkinson agents].

Adamantane isologs of amphetamine, methamphetamine and pheniprazine and several derivatives were synthesized in order to study the influence of their more pronounced lipophilic characteristics on their biological properties. A preliminary examination of their toxicity, antiviral, CNS stimulant and antiparkinson activity is described. The adamantyl amphetamine, which proved active, will be further studied.

Adamantane↗

PubMed1979

Potentiation of the mydriatic effect of norepinephrine in the rabbit after monoamine oxidase inhibition.

Dose-response curves of pupillary dilation after topical administration of norepinephrine or methoxamine have been determined in rabbits after chronic inhibition of ocular monoamine oxidase by treatment with pargyline or pheniprazine. Eyes treated with either monoamine oxidase inhibitor showed an enhanced responsiveness to the mydriatic effect of norepinephrine given either topically or intravenously. Increments in pupil size of the treated and control eyes in response to methoxamine applied topically, on the other hand, were the same. These results suggest that monoamine oxidase may play a role in the iris as one factor influencing the concentration of norepinephrine at the receptors.

Animals↗

PubMed1976

Effects of a hyperbaric environment on respiratory and monoamine oxidase activities.

The effects of a prolonged hyperbaric environment (21 ATA He-O2, 200 +/- 30 mm Hg O2, 32.5 +/- 1 degrees C) were investigated on the respiratory activity of rat liver homogenates and the activity of monoamine oxidase in isolated rat-liver preparations. Exposure to a hyperbaric environment for 84 days caused selective in vitro inhibition of nicotinamide adenine dinucleotide (NAD)-dependent oxidation of pyruvate, D-isocitrate, and alpha-ketoglutarate by rat-liver homogenates. The addition of NAD to the reaction mixture decreased the degree of such an inhibition. No effects on the in vitro activity of liver monoamine oxidase and its inhibition by pheniprazine were observed during exposure of animals to a prolonged high-pressure environment.

Animals↗

PubMedDate not supplied

The influence of antidepressive drugs on the level of acetylcholine and on the acetylcholinesterase activity in the brain of rats.

Rats were treated ip with MAO inhibitos (MAO-I): nialamid (NL), pivalylbenzylhydrazine, tranylcypromine, pheniprazine (Ph) or pargyline, and the leve of total, free and bound acetylcholine (Ach) as well as the acetylcholinesterase (Ach-E) activity were estimated in four parts of rats brain 2 or 16 hr after the treatment. These parameters were estimated also after the treatment with tricyclic antidepressants: desmethylimipramine (DMI), amitriptyline, or protriptiline, and in the conditions of the reversal of reserpine-like syndrom. MAO-I, 2 hr after their application and the reversal of reserpine like-syndrom have not changed the level of measured fractions of Ach in parts of the brain. DMI increased the level of all Ach fractions in the striatum. NL caused the decrease of bound Ach level in all parts of the brain with no changes of free Ach level, 16 hr after the treatment. Ph, 16 hr after the treatment, decrease both fractions of ACh only in the cortex. All studied drugs affected evidently ACh-E activity in various parts of brain. It is concluded that:1) Cholinergic mechanisms in the rat brain are involved in the central action of DMI and of some MAO-I., 3) Cholinergic function of the brain may be modulated by the adrenergic activity, 2) Individual parts of the brain have different susceptibility to the influence of different MAO-I on the ACh-E activity.

Acetylcholine↗

PubMedDate not supplied