Biomedical subjects

C Guaza

Publications and source records attributed to C Guaza.

At least 55 records · Page 3Linked to original sources

PubMed1992

Interleukin-2 induces corticotropin-releasing hormone release from superfused rat hypothalami: influence of glucocorticoids.

The present work shows that interleukin-2 (IL-2) is able to increase in a dose-dependent manner (25-100 U/ml) CRF release from continuous perifused hypothalami. The effects of IL-2 and IL-1 on CRF secretion are potentiated by the simultaneous action of the two cytokines at the hypothalamus. The stimulatory effect of IL-2 on CRF secretion is significantly inhibited by the presence of dexamethasone in the perifusion medium. However, the CRF response to IL-2 was similar in adrenalectomized animals and sham-operated rats. It is suggested that the action of IL-2 on hypothalamic CRF secretion is integrated in the communication between the immune system and the hypothalamic-pituitary-adrenocortical axis, and that such action is subjected to glucocorticoid negative feedback modulation. The mechanism underlying the effect of IL-2 on CRF release is unknown, but arachidonic acid metabolites do not seem to be involved, since neither a lipooxygenase (nordihidrogueretic acid) nor a cyclooxigenase (indomethacin) inhibitor affected the hypothalamic secretory response to IL-2.

Adrenalectomy↗

PubMed1990

Administration of leu-enkephalin impairs the acquisition of preference for ethanol.

The effects of subcutaneous administration of leu-enkephalin (LEU-E) (10, 100 and 300 micrograms/kg) and LEU-E (100 micrograms/kg) plus naloxone (2.5 mg/kg) on ethanol preference and fluid intake have been investigated in rats. Under our procedural conditions, rats develop ethanol preference through forced ethanol drinking (conditioning session). Preconditioning administration of LEU-E induced a reduction of later ethanol preference. Post-conditioning administration of LEU-E (10 and 100 micrograms/kg) also attenuated the development of ethanol preference. NX antagonized the effects of LEU-E on ethanol preference and fluid consumption in the two experimental procedures used, indicating an involvement of opioid receptors in the LEU-E-induced impairment of the acquisition of ethanol preference.

Alcohol Drinking↗

PubMed1990

Effects of the kappa opioid receptor antagonist MR-2266-BS on the acquisition of ethanol preference.

Using a paradigm by which rats forced to drink a weak ethanol solution (2.5% w/v) (conditioning session) develop ethanol preference in consecutive retention testing days, the effects of the administration of the kappa opioid antagonist MR-2266-BS, prior to or after the forced ethanol session, were studied. Pre-conditioning subcutaneous (s.c.) administration of 1 mg/kg of MR-2266-BS induced a decrease in subsequent ethanol consumption without significantly modifying the acquisition of ethanol preference. Post-conditioning administration of MR-2266-BS (0.1, 1, 5 or 10 mg/kg) induced both a dose-dependent reduction in ethanol consumption and in preference throughout the three following days. The results of the present study provide further support of the involvement of kappa-type opioids on drinking behavior, and suggest that kappa receptors may be involved in the consumption and development of preference to ethanol.

Alcohol Drinking↗

PubMed1990

D-Ala2-Met5-enkephalinamide impairs the acquisition of ethanol preference without influencing sucrose preference.

The effects of subcutaneous (SC) administration of D-Ala2-Met5-enkephalinamide (DAME) (1, 10 and 100 micrograms/kg), synthetic analog of Met-enkephalin, on the acquisition of ethanol preference were studied in male Wistar rats. Under our procedural conditions, rats develop ethanol preference by a forced ethanol drinking session (conditioning session). Preconditioning administration of DAME (100 micrograms/kg) induced a reduction in ethanol consumption on the day of treatment and on subsequent testing days, but did not reliably modify later ethanol preference. Postconditioning administration of DAME (1, 10 and 100 micrograms/kg) markedly impaired the acquisition of ethanol preference. However, under the same schedule of treatment, DAME failed to affect subsequent rats' sucrose preference. These results suggest that, when administered after rats' first exposure to ethanol, DAME could interfere either with the reinforcement mechanisms of ethanol consumption induced by its intake, or with the storage of the information related to the ethanol incentive value.

Alcohol Drinking↗

PubMed1989

Glucocorticoids modulate rat hypothalamic corticotrophin-releasing factor release induced by interleukin-1.

Continuous in vitro perifusion of rat hypothalami with interleukin-1 beta (IL-1) increased corticotropin-releasing factor (CRF) secretion in a dose-dependent manner, in the range of 1 to 5 U/ml. The stimulatory action of IL-1 was significantly attenuated by dexamethasone, both by addition to the perifusion medium and by in vivo dexamethasone pretreatment. The data suggest that an immunoneuroendocrine interaction circuit, subjected to glucocorticoid negative feedback, has an essential role in maintaining organism homeostasis.

Adrenocorticotropic Hormone↗

PubMed1989

Beta-endorphin administration interferes with the acquisition and initial maintenance of ethanol preference in the rat.

Attention has been focused on the possibility of an interaction between the endorphinergic system and ethanol intake. In the present study, the effects of subcutaneous (SC) administration of beta-endorphin (beta-E) (0.25, 1 and 5 micrograms/kg) and/or naloxone (NX) (1 or 2.5 mg/kg) on ethanol preference (EP) have been investigated in rats. Under our procedural conditions, rats developed ethanol preference (EP) by a forced ethanol drinking session (conditioning session). Preconditioning administration of beta-E (1 microgram/kg) reduced later EP. When beta-E was administered postconditioning, the opioid affects ethanol preference depending on the dose: both 0.25 micrograms/kg and 5 microgram/kg reduced EP, but the dose of 1 microgram/kg did not alter it. Administration of beta-E (1 and 5 micrograms/kg) before the first testing session attenuated EP. NX antagonized the effects of beta-E on EP in the three experimental procedures used, indicating that mu-opioid receptors might be involved in the beta-E-induced reductions on EP. Our results provide further evidences for a beta-endorphinergic system involvement on the mechanism leading to consumption of ethanol.

Alcohol Drinking↗

PubMed1988

Involvement of kappa type opioids on ethanol drinking.

The effects of the administration of the kappa agonist dynorphin1-17 and/or the kappa antagonist MR-2266-BS on ethanol preference was investigated using a paradigm by which rats develop alcohol preference. Administration of dynorphin shortly before or after the conditioning session (forced ethanol exposure) failed to affect later ethanol preference. However, dynorphin treatment prior to the first choice session reduced ethanol preference during the three consecutive testing days. This effect was reversed by the simultaneous administration of the kappa antagonist MR-2266-BS. The results of the present study provide further support for evidence of the involvement of dynorphinergic systems on drinking behavior and suggest that kappa-type opioid mechanisms may be involved in the consumption and development of preference to ethanol in rats.

Alcohol Drinking↗

PubMed1988

Naloxone decreases ethanol consumption within a free choice paradigm in rats.

The effect of subcutaneous naloxone administration on the consumption of a weak ethanol solution in rats on the three consecutive days (testing days) was investigated using a behavioral paradigm which includes a first forced ethanol exposure (conditioning day) followed by a two-bottle ethanol/water choice procedure. Besides reducing fluid intake, naloxone treatment prior to forced ethanol exposure interferes with the acquisition of ethanol preference. Post-conditioning naloxone administration fails to affect ethanol preference. Administration of naloxone prior to the first testing session induces a reduction on total fluid intake, at the day of treatment; a decrease on ethanol preference throughout the three consecutive testing days is also observed with the higher dose of the antagonist (5 mg/kg). An involvement of endogenous opioids in ethanol consumption is suggested through the modulation of alcohol reinforcement or the affective quality of the gustatory cue.

Alcohol Drinking↗

PubMed1988

Immune activation and psychoneurogenic stress modulate corticosterone-releasing effects of lymphokines and ACTH.

Possible modulatory effects of psychoneurogenic stress and endotoxin-induced immune activation on the in vitro corticosterone-releasing effects of lymphokine-containing supernatants (LCS) and adrenocorticotropic hormone (ACTH) were studied in rats. We have found that activation of the immune system by endotoxin increases the in vitro sensitivity of the adrenocortical cells to LCS and ACTH. In addition, we found that psychoneurogenic stress not only produced an increase of in vitro adrenal sensitivity to ACTH, but it also enhanced the release of corticosterone after perfusion of LCS. A synergistic interaction between ACTH and LCS was observed in all experimental groups of animals studied. An increased adrenal sensitivity to LCS and ACTH after stress or immune activation might have a functional significance, since the adrenal cortex is a major site in the response of the organism to alterations in the homeostatic balance. On the other hand, the temporal pattern of in vitro corticosterone release after LCS was different in all groups under study compared with that observed after ACTH challenge. LCS elicited a more rapid corticosterone response that lasted for a shorter time than after giving ACTH. These latter results suggest that different mechanisms may underlie the effects of LCS and ACTH on adrenal corticosteroidogenesis. In conclusion, the present findings further reinforce the existence of possible physiologically relevant interactions between the immune system and the pituitary-adrenal axis.

Adrenal Glands↗

PubMed1987

Corticosterone-releasing activity of immune mediators.

Products derived from the activated immune system have been reported to modulate neuroendocrine function. In addition, a direct connection between neuroendocrine and immune responses to stress has recently been proposed. We now provide evidence that heterogeneous lymphokine-containing supernatants from mitogen-stimulated rat spleen cells can stimulate both basal and corticotropin-induced corticosterone secretion from rat adrenal cells in an in vitro perifusion system. Moreover, thymosin alpha 1, a 28-amino acid residue peptide found both in thymus and lymphocyte-derived supernatants was also able to synergistically stimulate corticotropin-stimulated corticosterone release, without affecting basal corticosterone output in this same in vitro adrenal cell perifusion system. These results reinforce the suggestion about the existence of bidirectional interactions between the immune and neuroendocrine systems. They also indicate that this communication may occur directly at the adrenal gland level, a major effector site of the body's response to stress.

Adrenal Glands↗

PubMed1986

Effects of adrenaline on the acquisition and maintenance of ethanol preference in a taste conditioning paradigm.

The effects of subcutaneous adrenaline administration on preference for ethanol (2.5% solution) have been investigated, using a two-bottle choice situation. Administration of the amine (50 micrograms/kg) immediately after the conditioning session significantly attenuated ethanol preference. Adrenaline treatment (10, 50 or 100 micrograms/kg) prior to the first retention test induced a significant reduction in ethanol preference. When the amine was injected prior to conditioning only the dose of 100 micrograms/kg reduced later ethanol preference. Our results indicate that systemically administered adrenaline impairs the acquisition of preference to a weak ethanol solution. It is suggested that this effect of the amine may be linked to interference with consolidation of memory and retrieval processes.

Animals↗

PubMed1985

Brain catecholamines during ethanol administration, effect of naloxone on brain dopamine and norepinephrine responses to withdrawal from ethanol.

The variations in brain dopamine (DA) and norepinephrine (NE) levels after ethanol administration have been studied in rats. Acute ethanol administration significantly decreased brain DA and NE levels. After chronic ethanol intake no changes were observed in brain catecholamines. Ethanol withdrawal induced significant decreases in DA and NE concentrations in the brain. The administration of naloxone, antagonist of opiate receptors, blocked the effects of ethanol deprivation on brain catecholamines. These data suggest that endogenous opioids may be involved in the ethanol-withdrawal syndrome.

Animals↗

PubMed1985

Prolonged ethanol consumption influences shuttle box and passive avoidance performance in rats.

Rats were chronically maintained on an ethanol liquid diet for 16 days. Three weeks after cessation of ethanol intake, animals were tested for the acquisition of shuttle box avoidance and the retention of passive avoidance behaviour. Alcohol consuming rats showed a significant impairment of acquisition in the shuttle box task, and a slight impairment in the retention of the passive avoidance response. It is concluded that ethanol or its metabolites can induce long-term effects on learning and memory processes, even after cessation of drug consumption.

Alcohol Drinking↗

PubMed1985

Modifications in adrenal hormones response to ethanol by prior ethanol dependence.

Ethanol was administered to rats by means of a liquid diet for 16 days; after an ethanol-free interval of four weeks, animals received a test (IP) dose of ethanol (2 g/kg), and the adrenocortical and adrenomedullary responses were evaluated. Chronically ethanol-exposed animals showed tolerance to the stimulatory effect of ethanol in the pituitary-adrenal axis. Likewise, previously dependent rats showed tolerance to the increase in the activity of the adrenomedullary function induced by acute administration of the drug. Our results indicate that chronic ethanol ingestion can induce persistent changes after complete alcohol abstinence.

Adrenal Cortex↗

PubMed1984

Effect of ethanol on corticosterone production by dispersed adrenal cells of the rat.

The action of ethanol on adrenal steroidogenesis "in vitro" has been studied. It has been found that ethanol did not change the basal production of corticosterone by dispersed adrenal cells, but significantly reduced its response to ACTH stimulation. It is suggested that the inhibitory action of ethanol on steroidogenesis "in vitro" could have a physiological meaning, because the response to ACTH stimulation of adrenal cells from rats treated "in vivo" with ethanol showed a clear dose-related inhibition.

Adrenal Cortex↗

PubMed1984

Effect of naloxone administration upon responses of adrenal hormones to withdrawal from ethanol.

Rats maintained on an ethanol-liquid diet developed physical dependence after 16 days. Activation of adrenocortical function and overactivity of the sympathoadrenal system were observed during withdrawal from ethanol. The opiate antagonist naloxone prevented the adrenomedullary response, and attenuated, though not significantly, the increases in serum corticosterone induced by ethanol deprivation. These findings suggest that endogenous opioid pathways may be involved in the ethanol-withdrawal syndrome.

Adrenal Cortex↗

PubMed1983

Adrenomedullary responses to acute and chronic ethanol administration to rats.

The variations in levels of adrenal dopamine (DA), noradrenaline (NA) and adrenaline (A) after acute and chronic ethanol administration have been studied in rats. A relatively moderate dose of ethanol (2 g/kg) induced significant increases in DA levels, while NA and A concentrations did not change, or decreased depending on the interval of time elapsed after ethanol injection. These findings, together with those obtained in rats pretreated with alpha-methyl-p-tyrosine methyl ester (AMT), indicate an increased turnover of adrenal catecholamines (CA) after acute ethanol treatment. Chronic ethanol intake leads to significant increases in DA levels in the adrenal glands of rats subjected to ethanol feeding for 12 and 16 days; no changes were observed in NA or A concentrations in these groups of animals. After 30 days of ethanol ingestion, the levels of the three CA are within the control range, a fact that could suggest some adaptation of the sympatho-adrenal system to ethanol. After 16 days of treatment, tolerance to acute effects of ethanol on adrenomedullary system was not clear.

Adrenal Medulla↗

PubMed1983

Adrenocortical response to acute and chronic ethanol administration in rats.

Acute ethanol administration (2 g/kg IP) induced a significant rise in serum corticosterone levels which seemed to be related to blood ethanol concentration. Chronic ethanol administration, in the form of a liquid diet for 16 or 30 days, did not alter the levels of serum corticosterone. Chronic treatment of rats with a liquid diet containing ethanol resulted in the development of tolerance.

Adrenal Cortex↗