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J Borrell

Publications and source records attributed to J Borrell.

At least 55 records · Page 3Linked to original sources
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

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↗
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↗
PubMed1987

Neonatal administration of vasopressin antiserum induces long-term deficits on active and passive avoidance behaviour in rats.

Two-day-old male rats received a subcutaneous injection of arginine-vasopressin (AVP) antiserum and avoidance behaviour was studied 3 months later. Rats treated with the antiserum showed a clear retention deficit in a one-trial learning, step-through passive avoidance situation. Anti-AVP treatment also induced an impairment on the acquisition of a two-way active avoidance task. Systolic blood pressure was lower than normal in these animals. The results obtained appear to be indicative of the high vulnerability of the developing nervous system, and are discussed in the context of the different hypothesis on the role of central or peripheral mechanisms in the behavioural effects of AVP. Although no definite conclusions may be drawn in this regard, the present data strongly suggest that neonatal administration of AVP antiserum exerts long-lasting effects upon the functionality of several physiological mechanisms related to the behavioural adaptation of the organism.

Animals↗
PubMed1986

Evidence for a central but not adrenal, opioid mediation in hypertension induced by brief isolation in the rat.

Naloxone was found to provoke a hypotensive effect related to the dose on high blood pressure (BP) induced by short-term isolation in young rats. Another opiate antagonist, nalorphine, also reduced the arterial pressure of socially deprived rats. In contrast, naltrexone methylbromide that selectively blocked peripheral opiate receptors did not alter the elevated BP. To investigate whether adrenomedullary opioids were somehow implicated in the development of isolation-induced hypertension, bilaterally adrenalectomized rats were kept under social deprivation for 7 consecutive days. The data obtained indicated that high systolic BP developed in the same manner as in intact rats run in parallel. In conclusion, central opioids appear to be involved in BP elevation due to the stress generated by brief social deprivation in young rats.

Adrenalectomy↗
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

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

Naloxone influences retention behaviour depending on the degree of novelty inherent to the training situation.

The effects of immediate posttraining subcutaneous administration of naloxone (0.25, 1 or 5 mg/kg) on retention behaviour of rats trained in an inhibitory avoidance task, subjected or not to familiarization with the training situation prior to the training trial (pretraining) have been investigated. Naloxone did not influence performance of pretrained rats not subjected to footshock at training. The drug did not significantly modify retention latencies of pretrained rats subjected to a weak footshock. However, administration of naloxone facilitated retention behaviour of non-pretrained rats subjected to a weak footshock. Likewise, naloxone significantly increases retention latencies of pretrained rats subjected to a high footshock at the training trial. These data indicate that naloxone influences retention behaviour depending on the degree of novelty linked to the training situation: a facilitatory effect of the drug is observed when the training trial becomes associated with a clear novel situation for the animals (high footshock in pretrained rats or a weak footshock in non-pretrained animals).

Animals↗
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

Corticosterone decreases the efficacy of adrenaline to affect passive avoidance retention of adrenalectomized rats.

Short-term (48h) adrenalectomy (ADX) resulted in a deficit in the retention of a passive avoidance response. An inverted U-shaped dose-response relationship was found following immediate post-learning administration of adrenaline (A). A in a dose range of 0.005 - 5 micrograms/kg s.c. facilitated later retention. While corticosterone (CS) replacement alone had no effect, pretreatment with CS (300 micrograms/kg) was followed by a shift in the dose-response curve of A in ADX rats. Ten thousand times higher doses of A were required to improve retention behavior. Administration of the potent synthetic glucocorticoid dexamethasone failed to affect the responsiveness to A. It is concluded that corticosterone decreases the efficacy by which adrenaline affects later retention behavior of ADX rats. The specificity of corticosterone in this interaction suggests the involvement of the corticosterone receptor system which has its predominant localization in hippocampal neurons.

Adrenal Glands↗
PubMed1983

Inhibitory avoidance deficit following short-term adrenalectomy in the rat: the role of adrenal catecholamines.

Impaired retention of an inhibitory avoidance response was observed in rats subjected to adrenalectomy (ADX) up to 120 hr before the single learning trial. Corticosterone substitution failed to normalize this behavioral deficit. Rats ADX 240 hr prior to the learning trial showed a normalized behavior. Adrenomedullectomy (ADXM) 48 or 240 hr before learning caused a similar impairment as in short-term ADX rats. The 240-hr ADX rats subjected to corticosterone substitution showed the same behavioral deficit as short-term ADX rats or ADXM ones. Immediate postlearning subcutaneous injection of adrenaline in a dose range of 0.005-5.0 micrograms/kg or of noradrenaline (0.005-0.5 microgram/kg) to 48-hr ADX rats resulted in a dose-related improvement of later retention behavior. Higher doses of catecholamines were less or ineffective. Postlearning treatment of 48-hr ADXM rats with adrenaline (0.5-500 micrograms/kg) caused a similar pattern of behavioral changes. It is concluded that adrenal catecholamines play an important role in the modulation of consolidation of memory. In addition, the high circulating ACTH levels that follow long-term ADX may correct for the behaviorial deficit induced by the absence of adrenomedullary catecholamines.

Adrenal Glands↗
PubMed1982

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↗
PubMed1981

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↗