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Biomedical subjects

C Sandi

Publications and source records attributed to C Sandi.

At least 55 records · Page 3Linked to original sources
PubMed1992

Unilateral hippocampal lesions prevent recall of a passive avoidance task in day-old chicks.

The role of the hippocampal system in learning and memory processes in the chick was investigated. A series of experiments examined the effects of lesions in the hippocampal system on the acquisition and retention of a passive avoidance task. Chicks given pretraining bilateral hippocampal lesions showed a decrease of retention of the avoidance response evaluated 3 h posttraining. When given unilaterally, left, but not right lesions, resulted in reduced avoidance. However, bilateral posttraining lesions, made 1 h after training, did not interfere with retention of the task. These results suggest an involvement of the hippocampal system in learning processes in the chick.

Animals↗
PubMed1992

Behavioral factors in stress-induced immunomodulation.

Individual differences in the exploratory response to novelty were found to be related with the vulnerability to develop stress-induced immunological alterations. We studied the effect of exposure to inescapable shock on antibody formation against sheep red blood cells (SRBC) in rats selected according to their locomotor activity in a novel situation. Interestingly, antibody titers were only enhanced in shocked animals with the highest locomotor activity. These results emphasize the importance of taking into account individual differences for the study of the mechanisms involved in stress-induced immunomodulation, suggesting a behavioral procedure (novelty reactions) to deal with individual variability in the effects of stress on the immune system.

Animals↗
PubMed1992

Prolonged increase of corticosterone secretion by chronic social stress does not necessarily impair immune functions.

The influence of a chronic social stress upon immunity was investigated in Wistar rats, submitted for four weeks to two different behavioral situations, balanced in a factorial design: housing with three females and membership rotation. The combination of these two factor led to adrenal enlargement (43.3%), thymus involution (39.5%) and increased basal corticosterone levels, all indices of activation of the hypothalamic-hypophysis-adrenal axis. However, neither natural killer cell activity, splenocyte reactivity to mitogen nor the rate of spontaneous development of antibodies against Mycoplasma pulmonis, a common pathogen of the respiratory tract, were changed in the endocrine activated animals. Analysis of the data on kinetics of stress at 1, 7 and 28 days after the initial mixing of the animals gave the same results. These data question the immunosuppressant activity usually conferred to corticosteroids, at least when adrenal hyperactivity is induced by chronic environmental stressors.

Adrenal Glands↗
PubMed1992

Behavioral, neuroendocrine, and immunological outcomes of escapable or inescapable shocks.

The present study was designed to evaluate the effects of repeated exposure to escapable or inescapable shocks on subsequent behavior in an activity cage, and on the reactivity of the hypothalamic-pituitary-adrenocortical (HPA) axis and the immune system. We also studied the possible influence of behavioral factors on the behavioral and physiological impact of stress. Although exposure to different stressful situations pointed out marked differential effects in subsequent behavior, it failed to elicit differences in the neuroendocrine and immunological parameters studied. However, interesting results were found in analyzing the influence of behavioral factors. The degree of control exerted over the shock was inversely related to ACTH and corticosterone levels. In addition, individual differences in the exploratory activity to novelty were correlated with poststress lymphoproliferation and antibody formation. These data indicate that the behavioral and physiological outcomes of stress depend on the interrelations between environmental and individual factors (including both preexisting individual differences and the coping responses during stress).

Adrenocorticotropic Hormone↗
PubMed1992

Effects of HPA hormones on adapted lymphocyte responsiveness to repeated stress.

Acute stress-induced immune alterations can result in adapted function with prolonged exposure to the same stressor. The present study was designed to evaluate the possible role of the hypothalamic-pituitary-adrenocortical (HPA) axis on the adaptation of spleen lymphocyte responsiveness to repeated stress. For this purpose, we selected a stressful protocol (aversive auditory stimulation) that induced an initial suppression (1 day), followed by a return to control values with repeated application (4 days), of mitogen-induced lymphocyte proliferation. Because rats exposed to 4 days of noise sessions show enhanced adrenocorticotropin (ACTH) and corticosterone levels, we tested the possibility that adaptation of lymphoproliferation by repeated stress was due to a desensitization of splenic lymphocytes to stress-released HPA hormones. The results showed that corticotropin-releasing factor (10(-9) M) and corticosterone (5 x 10(-8) and 10(-7) M), as well as dexamethasone (10(-8), 5 x 10(-8), and 10(-7) M), significantly suppressed lymphoproliferation from both control and stressed rats in a similar way. ACTH (10(-9) and 5 x 10(-9) M) did not significantly influence Concanavalin-A-stimulated spleen lymphocytes. These data indicate that adaptation of lymphocyte proliferation by repeated noise stress occurs without accompanying alterations in lymphocyte responsiveness to HPA hormones.

Acoustic Stimulation↗
PubMed1992

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↗
PubMed1991

Different responsiveness of spleen lymphocytes from two lines of psychogenetically selected rats (Roman high and low avoidance).

Roman high- (RHA) and low-avoidance (RLA) rats have been genetically selected on the basis of their active avoidance behavior, and have been shown to differ on numerous behavioral, neurochemical and neuroendocrine parameters, especially in response to stress. We investigated the activity of splenic lymphocytes in vitro. Natural killer cell activity against YAC-1 tumoral cells and the mitotic response to plant lectins concanavalin A and phytohemagglutinin were much lower for lymphocytes isolated from RHA rats, in males as well as in females. The difference between the two strains was even larger when measured in a stressed state, immediately after active avoidance learning. On the other hand, the mitotic response to bacterial lipopolysaccharide, a B-cell-specific mitogen, was not different between the two lines, indicating that the difference in lymphocyte reactivity is limited to the T-lineage. The lower activity of T-cells in the RHA line had no consequence upon the ability of these animals to build up an antibody response against sheep red blood cells. These results indicate that Roman lines are an interesting animal model for the study of the relationships between the brain and the immune system, as well as for the analysis of the genes involved in the control of behavior.

Animals↗
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

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↗
PubMedDate not supplied

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↗
PubMedDate not supplied

The role and mechanisms of action of glucocorticoid involvement in memory storage.

Adrenal steroid hormones modulate learning and memory processes by interacting with specific glucocorticoid receptors at different brain areas. In this article, certain components of the physiological response to stress elicited by learning situations are proposed to form an integral aspect of the neurobiological mechanism underlying memory formation. By reviewing the work carried out in different learning models in chicks (passive avoidance learning) and rats (spatial orientation in the Morris water maze and contextual fear conditioning), a role for brain corticosterone action through the glucocorticoid receptor type on the mechanisms of memory consolidation is hypothesized. Evidence is also presented to relate post-training corticosterone levels to the strength of memory storage. Finally, the possible molecular mechanisms that might mediate the influences of glucocorticoids in synaptic plasticity subserving long-term memory formation are considered, mainly by focusing on studies implicating a steroid action through (i) glutamatergic transmission and (ii) cell adhesion molecules.

Animals↗
PubMedDate not supplied

[Glucocorticoid involvement in memory consolidation].

Glucocorticoids, hormones secreted by the adrenal cortex, can get access to the brain, where they induce a variety of cellular, molecular, and functional actions. Recent evidence showed that glucocorticoids are potent modulators of cognitive processes, such as learning, memory, and retrieval. In particular, the stress response induced by learning a new task, together with the consequent release of glucocorticoids, have been critically involved in memory consolidation processes. In general, these hormones induce facilitating effects on the strength at which newly acquired information is stored into a long term memory, mainly by activating intracellular glucocorticoid receptors. Such receptors belong to the family of nuclear hormone receptors and exert their actions by modulating the transcription of a variety of genes and, therefore, by critically regulating the synthesis of a wide number of proteins. Since protein synthesis appears to be a requirement of almost all forms of long term memory, glucocorticoids might induce their cognitive effects by affecting gene expression. This review focus on the involvement of glucocorticoids and their receptors in a variety of animal models for learning and memory.

Animals↗
PubMedDate not supplied

[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↗