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Biomedical subjects

J Borrell

Publications and source records attributed to J Borrell.

At least 73 records · Page 4Linked to original sources
PubMed1980

The effects of acute and chronic administration of morphine on the turnover of brain and adrenal catecholamines in rats.

Brain and adrenal catecholamine turnover in adult female rats treated with morphine was investigated. A different time course response of brain and adrenal catecholamines to alpha-methyl-p-tyrosine methyl-ester (AMT) administration in normal rats was observed; the catecholamine turnover rate in adrenal glands appeared to be much slower than in the brain. Acute morphine increased the turnover of brain dopamine and noradrenaline as well as of adrenal catecholamines, whereas chronic morphine treatment induced a decrease in the turnover of brain noradrenaline. Withdrawal induced by nalorphine produced an increase in the utilization of brain noradrenaline and adrenal catecholamines; this effect could be related to the withdrawl stress situation induced by the opiate antagonist. Although the mechanism of morphine action may implicate other neurotransmitters besides catecholamines, our results contribute to evidence that brain and adrenal catecholamines could be involved in the mechanism of morphine tolerance and/or dependence.

Adrenal Glands↗
PubMed1980

Sound stimulation and its effects on the pituitary-adrenocortical function and brain catecholamines in rats.

The purpose of the present study was to investigate in rats, the effects of sound stimulation upon both the pituitary-adrenal activity (evaluated by the levels of serum corticosterone (B)) and brain dopamine (DA) and noradrenaline (NA). Serum B in rats placed inside the experimental chamber without any sound stimulation was increased and brain DA decreased. For this reason, prior to any sound application, animals were kept in the experimental chamber for 115--120 min, when values had returned to basal levels. The results obtained on the effects of sound frequencies between 500 and 4,000 cps indicated a greater response in the rat pituitary-adrenal system to the lowest frequency (500 cps) we studied. Adrenal cortex hyperactivity occurred in the initial stage of daily repeated 500 cps sound stimulation. During extended periods of daily exposure, the activity of the pituitary-adrenal axis gradually diminished. Changes in the pituitary-adrenal activity, induced by sound stimulation, are closely related to changes in brain NA. The results obtained suggest that at least some of the effects of sound stimulation might be mediated by brain noradrenergic pathways and agree with the hypothesis concerning the existence of a central noradrenergic nervous component which could participate in the control of ACTH secretion.

Acoustic Stimulation↗
PubMed1980

Cholinergic inputs to the amygdala and the control of gonadotrophin release.

Adult female rats castrated 4 weeks before were implanted bilaterially into the basomedial area of the amygdala with drugs known to mimic or to counteract the actions of acetylcholine. The animals were sacrificed at different time intervals after the implantation of the different compounds, and serum levels of LH and FSH were measured by radioimmunoassay. The data obtained indicate that the intra-amygdalar implantation of the muscarinic blocker atropine induces a significant increase of the release of LH without altering FSH secretion. The implantation of two cholinomimetic drugs, pilocarpine, an almost pure muscarinic agonist, and carbachol, which possesses both muscarinic and nicotinic properties, exerted an inhibitory effect only on LH release. On the contrary, the intra-amygdala placement of the nicotinic blocker mecamylamine was followed by an increase of FSH with no changes in LH. These observations may suggest that cholinergic signals reaching the amydgala may be of some relevance in the mechanisms controlling gonadotrophine secretion. Muscarinic receptors seem to play an inhibitory role in the regulation of LH secretion, while nicotinic receptors seem to modulate in an inhibitory way FSH release.

Amygdala↗
PubMed1979

Effects of morphine upon the pituitary-adrenal system and adrenal catecholamines: a comparative study in cats and rats.

The aim of the present study was to investigate the effects of acute and chronic administration of morphine upon the pituitary-adrenal activity and adrenal catecholamines in rats and cats, two animal species with very different behavioural patterns of response to the opiate. Acute administration of the drug induced in both animal species an activation of the pituitary-adrenal system. Chronic administration of morphine to cats and rats induced a depression in the pituitary-adrenal function. No significant changes in the adrenal levels of catecholamines were observed in rats treated chronically with the drug. However, in the cat, the effects of morphine on adrenomedullary function seemed to depend on the stage of morphine treatment. The behavioural patterns of response in both animal species during chronic administration of the opiate, as well as the effects of induced withdrawal with nalorphine (an antagonist of morphine), indicated that dependence on morphine had developed, not only in the rats, but also in the cats. Acute morphine administration had a sedative effect, while in the cats the opiate produced a species-specific manic response characterized by hyperexcitement and aggressive behavior.

Adrenal Glands↗
PubMed1979

Adrenergic inputs to the amygdala and the control of gonadotrophin release.

Drugs able to mimic or to antagonize the action of catecholamines have been implanted bilaterally into the basomedial region of the amygdala of adult castrated female rats. The animals were killed at different intervals after the implantation of the different drugs, and serum levels of LH and FSH were measured by radioimmunoassay. The results have shown that the intra-amygdalar implantation of the alpha-adrenergic blocker phenoxybenzamine induces a significant increase of the release both of LH and FSH. The implantation of the beta-adrenergic blocker propranolol brings about a rise of LH only. The dopamine receptor blocker pimozide stimulates the release of LH and exerts a biphasic effect (stimulation followed by inhibition) of FSH secretion. The alpha-receptor stimulant clonidine and the dopaminergic drug 2-Br-alpha-ergocryptine were without significant effects. From these observations it is suggested that the adrenergic signals reaching the basomedial area of the amygdala (possibly from the brain stem) may be involved in the modulation of gonadotrophin secretion.

Adrenergic Fibers↗
PubMed1978

Effect of pentobarbital on serum levels of LH, FSH and prolactin in long-term ovariectomized rats.

The intraperitoneal (i.p.) administration of sodium pentobarbital (30 mg/kg) to long-term ovariectomized adult rats results in a prolonged depression of serum LH levels and in a biphasic decrease of serum prolactin (Prl) titers, but does not modify serum levels of FSH. Consequently, caution should be used when interpretating neuroendocrine results obtained in animals submitted to pentobarbital anesthesia.

Animals↗
PubMed1975

Adrenal, plasma and urinary corticosteroids during single or repeated administration of morphine in cats.

Corticosteroids and ascorbic acid in the adrenal glands of adult cats have been investigated after single or repeated administration of morphine. Also plasma levels and urinary excretion of corticosteroids were determined. A significant increase in the content of corticosteroids in the glands and plasma was found after initial injection of morphine. After 7 days of consecutive morphine treatment a fall of corticosteroids in the glands was observed; after 2 weeks of daily injections the content of adrenal corticosteroids was significantly lower than in the control animals but no change was found in the plasma. Administration of the drug during 1 month led to a highly significant decrease of corticosteroids in the glands as well as in plasma. No significant change in adrenal ascorbic acids was found whether the adrenal corticosteroids were higher or lower than in the control cats. Urinary corticosteroids were high during the first week of morphine treatment but thereafter the excretion declined progressively and was lower than the control level after 13 days of treatment. The significant decrease of corticosteroids observed after repeated administration of morphine and the rise in adrenal corticosteroids found after the injection of nalorphine to the morphinized animals suggest that some kind of morphine dependence had been developed in the cats after repeated administration of the drug.

Adrenal Cortex Hormones↗
PubMedDate not supplied

Chronic administration of morphine in cats: effects on adrenal and urinary catecholamines.

Adrenaline and noradrenaline levels in the adrenal glands and the excretion of both bioamines in urine of adult cats were investigated after chronic administration of morphine and nalorphine-induced withdrawal. After 7 days of daily consecutive morphine treatment, a significant increase in the adrenal noradrenaline content and a drop in adrenaline content were observed. After 2 weeks of daily injection of morphine, no significant changes were observed in the adrenal catecholamine level. One month of treatment with the opioid caused a significant increase in the adrenal content of both adrenaline and noradrenaline. Urinary excretion of catecholamines was significantly increased during the 4 weeks of treatment. In animals subjected to spontaneous or induced withdrawal with nalorphine, the adrenal content of catecholamines was altered and the ratio adrenaline/noradrenaline in the adrenal gland was shifted towards noradrenaline. A first injection of morphine produced an excitant manic response characterized by hyperexcitement and aggressive behaviour; animals chronically treated with the drug showed a progressively diminished response to this effect of the drug. It is concluded that physical dependence on morphine is reached by cats chronically treated with morphine and that this effect of the drug influences adrenomedulllary function in a different fashion depending on the stage of morphine treatment.

Adrenal Glands↗
PubMedDate not supplied

The Met-enkephalin analog D-Ala2-Met-enkephalinamide decreases the adrenocortical response to ACTH in dispersed rat adrenal cells.

The effects of the Met-enkephalin analog D-Ala2-Met-enkephalinamide (DALA) on basal and ACTH-stimulated corticosterone secretion from dispersed adrenal cells were investigated. Low doses (10(-10) and 10(-12) M) of DALA resulted in no apparent alteration in the response to ACTH (8 X 10(-9), 3.2 X 10(-8) or 1.6 X 10(-7) M). High doses of DALA (10(-8) and 10(-6) M) produced a decline in the steroidogenic response to ACTH. The opiate receptor antagonist naloxone (10(-4)-10(-10) M) did not influence the basal production of corticosterone or the stimulating action exerted by ACTH. However, the presence of naloxone reversed the blocking action on corticosterone production that was exerted by DALA. These findings indicate that enkephalins may decrease adrenocortical responsiveness to ACTH.

Adrenal Cortex↗
PubMedDate not supplied

Corticosteroidogenesis modulation by beta-endorphin and dynorphin1-17 in isolated rat adrenocortical cells.

Two opioid peptides, beta-endorphin and dynorphin1-17 were bioassayed with isolated rat adrenocortical cells. beta-Endorphin increases basal production of corticosterone as well as the adrenal responsiveness to low doses of ACTH, these effects being partially reversed by naloxone. Dynorphin1-17, without affecting basal corticosterone synthesis, increases adrenocortical responsiveness to ACTH; naloxone does not influence this effect. It is suggested that peripheral opioid peptides may participate in the maintenance of the homeostatic balance by modulating adrenal corticosteroidogenesis.

Adrenal Cortex↗