Adrenal and brain catecholamine responses to acute and chronic morphine administration to rats, after inhibition of tyrosine hydroxylase and monoamine oxidase.
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Adrenal Glands↗
Biomedical subjects
C Guaza
Publications and source records attributed to C Guaza.
Evidence for a modulatory role of catecholamines on hypothalamic somatostatin in the rat.
The influence of catecholamines (CA) on hypothalamic somatostatin (HPT-SRIF) was investigated in rats by using several drugs which interfere with brain CA metabolism. Depletion of brain CA stores by alpha-methyl-rho-tyrosine (AMT) increased HPT-SRIF, while augmented brain CA levels following L-dopa administration decreased HPT-SRIF content. Blockade of dopamine beta-hydroxylase activity by disulfiram depleted brain noradrenaline (NA) and decreased HPT-SRIF. The selective increase in brain NA stores caused by threo-dihydroxyphenylserine (DOPS) also produced an increase in HPT-SRIF. Increased dopamine (DA) and decreased NA levels after disulfiram + L-dopa (1 h) treatment did not modify HPT-SRIF, whereas unaltered NA and greatly increased DA levels following disulfiram + L-dopa (2 h) treatment produced a drastic reduction of HPT-SRIF. The results suggest that DA and NA exert an influence on HPT-SRIF, supporting previous observations.
Animals↗
Adrenal hormones and brain catecholamines responses to morning and afternoon immobilization stress in rats.
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Adrenal Cortex Hormones↗
Pituitary-adrenal responses to sub-chronic treatment with phenobarbital and/or phenytoin (diphenylhydantoin) in rats.
The response of the pituitary-adrenal axis of the male rat to sub-chronic dose treatment with phenobarbital and/or phenytoin under basal and stress conditions was investigated. Plasma corticosterone levels were measured in rats sacrificed either in the morning or in the afternoon, subjected or not to 2 hours of immobilization stress. Phenobarbital did not seem to significantly affect the pituitary-adrenal activity under basal conditions or in the response to stress. Phenytoin induced a disruption of the corticosterone diurnal variation present in the rat under basal conditions and seemed to partially inhibit the pituitary-adrenal response to stress when applied in the morning. The combined treatment with phenobarbital and phenytoin affected the afternoon rise in corticosterone levels present under basal conditions, as well as stress response at the same time of the day. The reported results agree with the hypothesis about the existence of mechanisms controlling ACTH release under basal conditions, dissociable from those controlling ACTH release in response to stress situations, and that phenytoin could influence some or others differently, depending on the animal's endocrine situation.
Animals↗
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↗
Effects of acute and prolonged administration of chlordiazepoxide upon the pituitary-adrenal activity and brain catecholamines in sound stressed and unstressed rats.
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Acoustic Stimulation↗
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↗
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↗
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↗
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↗
Enkephalins interfere with early phases of voluntary ethanol drinking.
The relationship between the opiate peptides Leu-enkephalin and [D-Ala2-Met5]enkephalinamide (DAME) and the initial expression and maintenance of ethanol preference was studied in male Wistar rats. Subcutaneous administration of both peptides prior to the first choice test between water and ethanol induced reductions on ethanol intake and subsequently on total fluid intake. Leu-enkephalin treatment also diminished ethanol preference in the day of treatment and in consecutive days. Neither Leu-enkephalin nor DAME treatments modified rats sucrose preference or intake. The results suggest that the enkephalins studied, when administered in the early phases of ethanol preference, interfere with the mechanisms involved in the propensity to drink ethanol.
Alcohol Drinking↗
[Theiler's virus encephalomyelitis infection as a model for multiple sclerosis: cytokines and pathogenic mechanisms].
Theiler's murine encephalomyelitis virus (TMEV) disease is induced following intracerebral inoculation of TMEV, a member of picornavirus family, in susceptible animals. The pathogenesis of paralytic syndrome is associated with a chronic progressive demyelinating disease characterized by perivascular of immune inflammatory cells. Although TMEV induced demyelinating disease (TMEV IDD) is initiated by virus specific CD4+ T cells targeting CNS persistent virus, CD4+ T cell responses against self myelin epitopes activated via epitope spreading contribute to chronic disease pathogenesis. In the present report we delineated possible pathogenic mechanisms related with inflammatory process, leading to demyelination and axonal loss. The importance of proinflammatory cytokines in sustaining the inflammatory process and cause direct oligodendrotoxicity is emphasized. Different approaches in therapeutic strategies affecting cytokines are also presented.
Animals↗
[Cannabinoid system and neuroinflammation:therapeutic perspectives in multiple sclerosis].
INTRODUCTION: The endocannabinoid system consists of cannabinoid receptors, endogenous ligands and the enzymatic elements involved in their synthesis and breakdown. AIM: To report on currently held knowledge about the functioning of the system as a modulator of the neuroinflammatory processes associated with chronic diseases such as multiple sclerosis. DEVELOPMENT: Cannabinoids are synthesised and released on demand and their production increases in times of neuroinflammation and neural damage. In this context then, their actions in the microglial cells and in the astrocytes are characterised by a lowered expression of inflammatory mediators and pro-inflammatory cytokines. Furthermore, cannabinoids can play a role as neuroprotectors by means of different types of mechanisms and, in experimental models of multiple sclerosis, they slow down the symptoms, reduce inflammation and can favour remyelination. CONCLUSIONS: The clinical use of cannabinoids or pharmacological agents that affect the endogenous cannabinoid system during inflammation of the central nervous system and in multiple sclerosis is currently under consideration and subject to debate. Detailed analysis of the results obtained over the past decade has made it possible to establish the existence of several mechanisms of action of cannabinoids in pathologies affecting the central nervous system that are accompanied by chronic inflammation. Likewise, they also clearly show that the cannabinoid system is an interesting proposal as a new therapeutic tool.
Animals↗
[Interactions between the immune system and the neuroendocrine system. Implications of the hypothalamo-hypophyseal-adrenal axis].
The immune and neuroendocrine systems are now recognized to be linked and involved in bidirectional communication. That interrelationship involves shared usage of common signal molecules and their receptors. The Immune System and its products can modulate neuroendocrine functions and neuroendocrine peptides and hormones can affect important immunological parameters. Specifically, this article review the evidence for immune-neuroendocrine interactions in relation to the Hypothalamic-Pituitary-Adrenocortical axis. Neuroendocrine-immune interactions appears to play an important role in psychosocial influences on immunologically resisted and mediated diseases.
Corticotropin-Releasing Hormone↗