Is the adrenal cortex a putative site for the action of interleukin-1?
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Adrenal Cortex↗
Biomedical subjects
J Borrell
Publications and source records attributed to J Borrell.
Interleukin-1-beta induces pituitary adrenocorticotropin secretion: evidence for glucocorticoid modulation.
Using an in vitro continuous perifusion system, the effects of interleukin-1 (IL-1) on adrenocorticotropin (ACTH) secretion at the pituitary level were investigated. On one hand, we observed that IL-1 beta increases ACTH secretion from perifused anterior pituitary cells in a dose-dependent manner, between 1.5 and 6 pM. This stimulatory action of IL-1 on ACTH was significantly attenuated by a short in vitro dexamethasone pretreatment. This fact suggests a regulatory glucocorticoid negative feedback analogous to that observed upon the pituitary action of corticotropin-releasing factor (CRF). We also examined the effect of simultaneous treatment with IL-1 and CRF. The results indicated that the effect of IL-1 resulted additive to the CRF-induced ACTH secretion. It is concluded that the anterior pituitary could be an important site of IL-1 action to activate the hypothalamic-pituitary-adrenocortical axis function, and that this action is under an inhibitory glucocorticoid regulation.
Adrenocorticotropic Hormone↗
Mutually antagonistic effects of corticosterone and prolactin on rat lymphocyte proliferation.
The present study was designed to evaluate the immunological outcome resulting from experimental conditions involving different corticosterone and prolactin ratios in rats. One set of experiments was conducted to assess the effects of prolactin and corticosterone on the in vitro mitogen-induced proliferation of spleen lymphocytes from animals previously submitted to the manipulation of their glucocorticoid status throughout adrenalectomy (ADX) and/or exposure to acute stress. The results indicated that prolactin (5 x 10(-9) M) induced a significant increase in concanavalin A- (ConA) induced proliferation of splenocytes only from ADX-control, unstressed, rats. However, a lower dose of prolactin (10(-9) M) failed to influence lymphoproliferation. Corticosterone (2 x 10(-8) and 10(-7) M) induced a dose-dependent reduction in lymphocyte proliferation in all experimental groups. Further experiments were conducted to study the relative potency of prolactin to antagonize the in vitro corticosterone-induced suppression of ConA-stimulated lymphocytes. The results showed, on the one hand, that higher doses of prolactin (10(-8) and 5 x 10(-8) M) were effective in stimulating ConA-induced lymphocyte proliferation in control, undisturbed, rats. They also showed that when prolactin and corticosterone are simultaneously added to the cultures, the immunostimulatory effect induced by a dose of 10(-8) M of prolactin can either predominate over a weak suppressive action of corticosterone (2 x 10(-8) M) or totally antagonize to normal values a marked immunosuppression induced by a higher dose of corticosterone (10(-7) M). These data support the view that different ratios between prolactin and corticosterone concentrations can result in differential immunological outcome.(ABSTRACT TRUNCATED AT 250 WORDS)
Acute Disease↗
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↗
In vitro adrenocortical responsiveness to ACTH in rats subjected to different emotional situations.
Corticosterone production in isolated adrenocortical cells from adult male Wistar rats subjected to different emotional situations and the possible relationship between adrenocortical and behavioral responses were studied. On the basis of an inhibitory avoidance paradigm (IAP), in which the innate preference of rats for a dark environment is suppressed by application of an aversive electric footshock (acquisition trial, AT), the following set of conditions was studied: Rats trained in the IAP (a) without application of electric footshock; (b) with application of electric footshock; (c) rats trained as in (b) but subjected to forced extinction (by staying for 5 min in the dark compartment 24 h after the AT, the animals overcome their fear for the dark box). Rats trained in conditions (a) and (c) displayed significantly shorter retention latencies, and concomitantly showed a significantly lower adrenocortical responsiveness than rats trained under condition (b). However, no significant differences in circulating ACTH or corticosterone levels among the various experimental groups were found. Furthermore, animals tested for retention 24, 48, 72 or 168 h after the AT showed an increased loss of the behavioural response so that the greater the time lapse, the more the retention behavior diminished concomitantly with the adrenocortical responsiveness to ACTH. Our results suggest that a good retention of the newly acquired behavior is related to an increased adrenocortical responsiveness to ACTH. Forced or innate extinction of the same behavior is accompanied by a diminished adrenocortical responsiveness. Taken together, these results also emphasize that altered adrenal responsiveness to ACTH is a better and more accurate index of the degree of emotionality associated with different behavioral performances than 'punctual' ACTH or corticosterone plasma levels.
Adrenal Cortex↗
Interleukin-1 affects the behavioral despair response in rats by an indirect mechanism which requires endogenous CRF.
Interleukin-1 (IL-1) administered intracerebroventricularly (i.c.v.) to rats significantly reduces the level of immobility in animals forced to swim in a confined space. Immunoneutralization of endogenous CRF (corticotropin-releasing factor) by i.c.v. administration of CRF-antiserum prevents the IL-1-induced sinking in rats. This shows that the release of cerebral CRF, probably from the hypothalamus, may mediate the behavioral effect promoted by IL-1. Taken together our results suggest the existence of a complex interface between immune, neuroendocrine and behavioral regulation.
Animals↗
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↗
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↗
Dynorphin1-17 can enhance or impair retention of an inhibitory avoidance response in rats.
The possible effects of subcutaneous administration of dynorphin1-17 on retention of an inhibitory avoidance behavior have been studied in rats. Post-training or pre-test administration of dynorphin1-17 in doses of 25 or 50 micrograms/kg facilitated retention performance in rats subjected to a footshock of 0.2 mA n the acquisition trial. However, the same doses of the opioid peptide exerted a deleterious effect on retention performance when a footshock of 0.4 mA was used after either post-training or pre-test administration. Post-training injection of the kappa-receptor antagonist MR-2266 in doses of 0.5, 1 or 2.5 mg/kg failed to affect retention behavior. However, the previous administration of 2.5 mg/kg of MR-2266 prevented the facilitatory effect exerted by dynorphin1-17 after post-training, as well as after pre-test administration. Our results suggest that dynorphin1-17 may be involved in modulating the consolidation, as well as the retrieval, of recently acquired information.
Animals↗
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↗
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↗
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↗
Naloxone prevents the facilitatory effect upon retention induced by adrenaline administration in rats.
The possible involvement of endogenous opioid peptides in the development of the facilitatory effect of adrenaline on memory has been investigated. For this purpose post-training administration of adrenaline and/or naloxone was carried out in rats tested in an inhibitory avoidance paradigm and subjected or not to pre-training (extensive familiarization with the training situation prior to the acquisition trial). Adrenaline injected subcutaneously in a dose of 500 micrograms/kg facilitated retention performance in rats both subjected or not to pre-training. Naloxone administered SC (400 micrograms/rat) did not influence retention behaviour in rats subjected or not to pre-training, nor did ICV (0.80 ng/rat) administration. Interestingly, the opiate antagonist when injected SC (400 micrograms/rat) prevented the facilitatory effect exerted by adrenaline in pretrained as well as in not pre-trained rats. However, ICV administration of naloxone (0.80 microgram/rat) dit not influence the behavioral effects exerted by the bioamine. These data suggested a role of endogenous opioid peptides on the facilitatory effect of adrenaline on memory, possibly independent of novelty factors and thus of the brain beta-endorphin system. In addition, our results point to the periphery as the most likely site for such interaction.
Animals↗
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↗
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↗
Psychoneurogenic stress influences upon retention of an inhibitory avoidance response in the rat.
Hormones and peptides involved in the response of an organism to stress play a modulating role in learning and memory processes. We studied whether psychoneurogenic stressors such as sound stimulation or novelty influence retention of an inhibitory avoidance response. An impairing effect on retention was observed when these stressors were applied shortly after the acquisition trial, but not after a 3-h delay. However, sound stimulation and novelty applied shortly before the retention test may facilitate retention behavior. It is suggested that the effect of psychoneurogenic stressors on retention behavior may be linked to influences on consolidation and retrieval processes mediated through the neurohumoral response of the organism to stress.
Acoustic Stimulation↗
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↗
Beta-endorphin impairs forced extinction of an inhibitory avoidance response in rats.
The effect of subcutaneous administration of beta-endorphin on forced extinction (FE) of an inhibitory avoidance behavior has been studied in rats. Animals subjected to FE displayed significantly shorter retention latencies than those of the corresponding control group, not subjected to FE. Subcutaneous administration of 0.1, 1 and 10 micrograms/kg of beta-endorphin 10 min before or immediately after FE session, delayed extinction of the inhibitory avoidance behavior in an inverted U-shaped dependent manner. The opiate antagonist naloxone (NX) administered subcutaneously (0.4 mg/kg) did not influence extinction behavior. However, the same dose of NX, when injected previously to the administration of beta-endorphin (1 microgram/kg), prevented the effect on extinction induced by the opioid. Our results suggest that beta-endorphin may be involved in modulating forced extinction of a recently acquired information, likely influencing relearning phenomena associated with this particular way of forgetting.
Animals↗