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Biomedical subjects

A Mulas

Publications and source records attributed to A Mulas.

At least 19 recordsLinked to original sources
PubMed1998

Dopamine-dependent behavioural stimulation by non-peptide delta opioids BW373U86 and SNC 80: 1. Locomotion, rearing and stereotypies in intact rats.

The unconditioned behavioural effects of two non-peptide delta-opioid receptor agonists, BW 373U86 and SNC 80, were studied in the intact rat. BW 373U86 (0.1-2.5 mg/kg s.c.) and SNC 80 (2.5-10 mg/kg s.c.) dose-dependently elicited locomotion, rearing, stereotyped sniffing, licking and gnawing. These effects were abolished by pretreatment with the delta-opioid receptor antagonist naltrindole (5.0 mg/kg s.c.). In view of the phenomenological similarities between this syndrome and that elicited by dopamine-receptor agonists, the role played by dopamine receptors was investigated. The specific dopamine D1 receptor antagonist SCH 23390 and the specific dopamine D2/D3 receptor antagonist raclopride reduced or even abolished the behavioural stimulation induced by lower doses of BW 373U86 and SNC 80. When higher doses of BW 373U86 were used (2.5 mg/kg), however, raclopride, even at high cataleptic doses (6.0 mg/kg), only partly prevented the behavioural stimulation induced by the delta-opioid receptor agonist. The behavioural stimulation remaining after high doses of raclopride was abolished by the administration of SCH 23390. These results show that delta-opioid receptor stimulation elicits dopamine-dependent behavioural activation in the rat that depends on dopamine receptors, particularly of the D1 subtype.

Animals↗
PubMed1998

Dopamine-dependent behavioural stimulation by non-peptide delta opioids BW373U86 and SNC 80: 2. Place-preference and brain microdialysis studies in rats.

The motivational properties of the non-peptide delta-opioid receptor agonists BW373U86 and SNC 80 were investigated using the place-conditioning paradigm. BW373U86 (0.5-1.0 mg/kg s.c.) and SNC 80 (1.25-5.0 mg/kg s.c.) elicited significant preference for the drug-paired compartment, in a dose-related fashion. Naltrindole (5.0 mg/kg s.c.) pretreatment, while failing to modify preference when given alone, completely prevented place-preference induced by BW373U86 (1.0 mg/kg s.c.) and SNC 80 (1.25 mg/kg s.c.). The dopamine D1 receptor antagonist SCH23390, given at doses that do not affect place-preference (0.012 mg/kg s.c.), completely prevented the place-preference induced by BW373U86 and SNC 80. At the doses effective in eliciting place-preference, BW373U86 and SNC 80 failed to modify extracellular dopamine in the medial nucleus accumbens, while in the dorso-lateral caudate-putamen BW373U86 (1.0 and 2.5 mg/kg s.c.) reduced extracellular dopamine, and this effect was prevented by naltrindole (5.0 mg/kg s.c.). SNC 80, only at the dose of 5 mg/kg s.c., significantly reduced extracellular DA in the dorso-lateral caudate-putamen. The results indicate that stimulation of delta-opioid receptors has incentive properties that might be related to an indirect amplification of post-synaptic dopamine transmission.

Animals↗
PubMed1995

[Intermediate medications in endodontics: a quantitative in-vitro evaluation of 2 phenolic derivatives].

In a series of in vitro experiments with dental elements obtained after an extraction, the persistence in the pulpal chamber of two phenolic compounds largely used as dental medicaments has been evaluated. The substances, p-chlorophenol and eugenol were put in a small piece of cotton inside the dental elements where they were left for 7 days. Spectrophotometric UV determination of p-chlorophenol and eugenol were made after 3 and 7 days. Our results indicate that 25% of the initial amount of p-chlorophenol is found after three days and nearly 1/5 after 7 days. The figures for eugenol are: 1/3 after three days and 1/6 of the initial amount after 7 days. The authors therefore suggest the substances under study be used as dental medicaments with an optimum of three days of interval between two medications, even if a longer interval may be observed due to the good in situ persistence of the two phenols.

Chlorophenols↗
PubMed1991

(D-Ala2)deltorphin II: D1-dependent stereotypies and stimulation of dopamine release in the nucleus accumbens.

In order to investigate the relative role of central delta- and mu-opioid receptors in behavior, the effects of (D-Ala2)deltorphin II, a natural delta-opioid peptide, and PL017, a beta-casomorphin derivative specific for mu receptors, were compared after local intracerebral and intraventricular administration. Intracerebral infusion of the two peptides was done bilaterally in the limbic nucleus accumbens and in the ventral and dorsal caudate putamen of freely moving rats through chronic intracerebral cannulas. After intra-accumbens infusion, the two peptides elicited marked but opposite behavioral effects: while (D-Ala2)deltorphin II evoked dose-dependent motor stimulation characterized by locomotion, sniffing, and oral stereotypies, PL017 elicited motor inhibition with rigidity and catalepsy. These effects were site specific because they could not be evoked from the ventral or from the dorsal caudate. Low doses of naloxone (0.1 mg/kg, s.c.) blocked the effects of PL017 but not those of (D-Ala2)deltorphin II, which instead were reduced by high doses of naloxone (1.0 mg/kg) and by the putative delta-antagonist naltrindole; this drug failed to affect the catalepsy induced by PL017. Therefore, while (D-Ala2)deltorphin II effects were delta-mediated, PL017 effects were mu-mediated. Blockade of dopamine D1 receptors by SCH 23390 abolished (D-Ala2)deltorphin II effects, while blockade of dopamine D2 receptors by raclopride or by haloperidol was without effect. Local application by reverse dialysis of (D-Ala2)deltorphin II (5 microM) to the accumbens resulted in a naloxone-sensitive increase of extracellular dopamine concentrations; these effects could not be evoked from the caudate, nor by PL017 in the accumbens. Intracerebroventricular administration of (D-Ala2)deltorphin II or of PL017 elicited behavioral effects qualitatively similar to those obtained from the accumbens.

Animals↗
PubMed1989

SKF 38393 potentiates yawning induced by LY 171555: further evidence against the autoreceptor hypothesis of yawning.

The effect of concurrent D-1 receptor stimulation by SKF 38393 on the expression of yawning elicited by D-2 receptor stimulation with LY 171555 was studied in the rat. A low dose of SKF 38393 (2.5 mg/kg SC), while failed to elicit yawning, potentiated the effectiveness of LY 171555 in eliciting yawning at all the doses tested (12.5, 25 and 50 micrograms/kg SC) and this effect was abolished by SCH 23390 (0.012 mg/kg SC). The results indicate that in analogy with typical post-synaptic dopaminergic effects (hypermotility-stereotypy), yawning elicited by a D-2 agonist is facilitated by concurrent stimulation of D-1 receptors and therefore is consistent with previous evidence that yawning in response to a D-2 agonist is not mediated by autoreceptors.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1989

[Not Available].

Explore the source record for details and available documents.

Death↗
PubMed1987

The D-1 antagonist SCH 23390 stimulates while the D-1 agonist SKF 38393 fails to affect dopamine release in the dorsal caudate of freely moving rats.

SCH 23390, from doses of 0.012 mg/kg s.c., dose dependently stimulated the release of dopamine (DA) and the output of its metabolites, dihydroxyphenylacetic acid and homovanillic acid, in the dorsal caudate of freely moving rats implanted with transcerebral dialysis fibers. SKF 38393 failed to modify DA release and metabolism at doses of 5, 10 and 25 mg/kg s.c. but at 25 mg/kg s.c. it abolished the effect of 0.025 mg/kg of SCH 23390. Administration of gamma-butyrolactone (700 mg/kg s.c.), which blocks the firing of DA neurons, prevented the effect of 0.050 mg/kg s.c. SCH 23390. The results indicate that D-1 receptors control the release of DA, probably through stimulation of the firing of DA neurons.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1982

In vitro changes in gamma-aminobutyric acid output from the cerebral cortex induced by inhibitors of gamma-aminobutyric acid uptake and metabolism.

The effects of inhibitors of gamma-aminobutyric acid (GABA) metabolism or uptake on GABA output from the cerebral cortex was studied by means of a collecting cup placed on the exposed cortex of rats anaesthetized with urethane. GABA was identified and quantified by a mass-fragmentographic method. Ethanolamine-O-sulphate (10(-2) M) applied directly on the cerebral cortex caused a long-lasting twofold increase in GABA output, whereas DL-2,4-diaminobutyric acid (5 X 10(-3) M) caused a sevenfold increase and beta-alanine was active. The results indicate that glial uptake has little effect on GABA inactivation in the cerebral cortex. The inhibition of neuronal uptake seems a more effective tool to increase GABA concentration in the synaptic cleft, and consequently also in GABA output, than the inhibition of GABA metabolism.

Aminobutyrates↗
PubMed1981

Ipsiversive turning behaviour after discrete unilateral lesions of the dorsal mesencephalic reticular formation by kainic acid.

Discrete axon-sparing lesions were placed unilaterally in the mesencephalon by the local injection of kainic acid. Unilateral lesions of the dorsal reticular formation just beneath the superior colliculus and lateral to the periacqueductal grey resulted in consistent ipsiversive apomorphine-induced circling. Only weak motor asymmetries were observed after unilateral lesions restricted to the superior colliculus or to the periacqueductal grey. The results indicate that the dorsal mesencephalic reticular formation plays an essential role as an output station for striatal postural functions.

Animals↗
PubMed1981

[Our experience with peridural anesthesia in labor].

A clinical study has been carried out on 86 child-bearing mothers, continuous lumbar peridural block being employed, in the light of personal experience, to induce analgesia during labour. The results were positive on the whole as regards duration and the algogenous intensity measured during the dilatation phase and during expulsion.

Adult↗
PubMed1976

Changes in regional brain acetylcholine levels during drug-induced convulsions.

Acetylcholine (ACh) levels were determined in the brain of rats killed by decapitation or focussed microwave radiation during drug-induced convulsions. During metrazol or strychnine-induced convulsions a diffuse decrease in ACh levels was found in rats killed by decapitation. When the rats were killed by radiation and the brain was only divided into three large regions, strychnine caused no changes in ACh levels; metrazol caused a decrease in the cerebral cortex and lower brainstem. When discrete brain regions were investigated in rats killed by radiation, metrazol-induced convulsions were associated with a decrease in ACh level in all regions dissected and strychnine-induced convulsions with a decrease in the hippocampus and caudate nucleus only. Picrotoxin-induced convulsions were associated with a decrease in ACh level in the cerebral cortex, hippocampus, midbrain and medulla-pons, those induced by bicuculline with an increase in ACh level in the frontal cortex, hippocampus, midbrain and medulla-pons, by dimefline with an increase in the frontal cortex, midbrain and medulla-pons and a decrease in the caudate nucleus. The experiments show that each type of convulsant affects ACh levels in discrete brain regions in a different way.

Acetylcholine↗