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Biomedical subjects

A E Panerai

Publications and source records attributed to A E Panerai.

At least 19 recordsLinked to original sources
PubMed1995

Effects of an anti-beta-endorphin serum on tonic immobility in rabbits.

The involvement of endogenous beta-endorphin (beta-EP) in tonic immobility (TI) was evaluated in rabbits following the intracerebroventricular (ICV) administration of a specific antibody. Rabbits were tested twice with a 1-week intersession interval. For each animal, results of Session 1 were used as the baseline. Six hours before the beginning of Session 2, a bilateral ICV injection of specific anti-beta-EP serum or aspecific gamma-globulin (vehicle) was performed. Results showed that pretreatment with anti-beta-EP serum increased TI duration, whereas no change occurred in the vehicle group. In a parallel experiment we evaluated TI duration in the presence of formalin pain: TI increased in animals pretreated with aspecific gamma-globulins and decreased in the animals pretreated with anti-beta-EP serum. Results suggest that the beta-EP system acts to limit TI duration, but that this effect is reversed by persistent pain.

Animals↗
PubMed1995

The beta-endorphin inhibition of mitogen-induced splenocytes proliferation is mediated by central and peripheral paracrine/autocrine effects of the opioid.

In this study we show that the opioid peptide beta-endorphin exerts a tonic inhibitory effect on the proliferative response of splenocytes to the polyclonal mitogen phytohemoagglutinin throughout two separate sites of action: one central and one peripheral. The intracerebroventricular administration of beta-endorphin, in fact, induces a significant inhibition of splenocyte proliferation. In contrast, both the intracerebroventricular and the peripheral administration of anti-beta-endorphin gamma globulins induce a significant increase in proliferation. Moreover, an increase of splenocyte proliferation was observed also after the intravenous administration of gamma globulins and intraperitoneal naloxone, and this effect was still present in hypophysectomized rats. The data reported suggest that beta-endorphin exerts a tonic inhibitory effect on proliferation, acting centrally, and peripherally throughout a paracrine/autocrine mechanism. FACS experiments show that the effect observed is not the consequence of an alteration of lymphocyte trafficking induced by the opioid.

Analysis of Variance↗
PubMed1995

Age-related changes in mitogen-induced beta-endorphin release from human peripheral blood mononuclear cells.

beta-Endorphin is an opioid peptide synthesized in the pituitary, hypothalamus, and immunocytes, known to affect immune responses both when added in vitro and when its synthesis is increased in vivo (e.g., during stress). We show here that, similar to its concentrations in peripheral blood mononuclear cells, the release of the opioid peptide from these cells after stimulation with polyclonal mitogens such as PHA or Con-A is also age dependent. Moreover, the effect of both mitogens on Ca2+ homeostasis changes with age. Finally, the ionophore ionomycin and the Ca2+ ATPase blocker thapsigargin induce the same age related effect on beta-endorphin release. For these reasons, we suggest that calcium homeostasis might be important for the differences observed in the release of the opioid from cells obtained from younger (< or = 30 years) or older (> or = 45 years) volunteers.

Adult↗
PubMed1995

CRH and the noradrenergic system mediate the antinociceptive effect of central interleukin-1 alpha in the rat.

After intracerebroventricular administration, both interleukin-1 alpha and corticotropin-releasing hormone increase nociceptive thresholds evaluated by the hot-plate test in the rat. Pretreatment with 6-hydroxydopamine or prazosin fully prevents the action of both substances. Moreover, the effect of interleukin-1 alpha is completely blocked by the intracerebroventricular administration of the corticotropin-releasing hormone antagonist alpha-helical CRH 9-41. Our results suggest an involvement of CRH and the noradrenergic system in the antinociceptive effect of central interleukin-1 alpha.

Animals↗
PubMed1995

Immunoendocrine reshaping with age.

The interaction of the endocrine, immune, and nervous systems in modulating each other's activity opens the track for a new way of looking to the effects ongoing on each of the three systems. This new approach finds it bases in old times, since evolution shows how we missed for many years a relation between the three systems that was clearly manifested in lower species. In this chapter, the effects of aging on the immune, endocrine and nervous systems are proposed as the consequence of the influences of each system on the others.

Aging↗
PubMed1994

Fluoxetine reduces inflammatory edema in the rat: involvement of the pituitary-adrenal axis.

The acute effect of the non-tricyclic, pro-serotoninergic, antidepressant drug fluoxetine on inflammatory edema was evaluated in the rat. Fluoxetine significantly and dose dependently reduced the swelling induced by the injection of 10% brewer's yeast suspension in the hindpaw. Both adrenalectomy and hypophysectomy prevented the effect of fluoxetine. In contrast pretreatment with the corticotropin-releasing hormone antagonist alpha-helical CRH-(9-41) did not interfere with the anti-inflammatory action of fluoxetine. Moreover, the drug induced a significant increase of corticosterone plasma concentrations in vivo, whereas, in vitro, it did not stimulate beta-endorphin release from anterior pituitary cells. Our data suggest that fluoxetine exerts a potent anti-inflammatory action by inducing pituitary-adrenocortical activation via serotonin.

Adrenalectomy↗
PubMed1994

Intermittent but not continuous inescapable footshock stress affects immune responses and immunocyte beta-endorphin concentrations in the rat.

It is well known that a variety of stressors influence immune responses. The opioid peptide-beta-endorphin (BE) is deeply involved in stress responses, is synthesized in cells of the immune system, and participates in the modulation of immune function. We analyzed the ability of two different stress paradigms to modulate the beta-endorphin concentrations in the immune cells and the immune response in the rat. Two and 24 h after the exposure to inescapable intermittent footshock (1.6 mA, 60 Hz, 1 s, every 5 s for 20 min) the concentrations of beta-endorphin in splenocytes, peripheral blood mononuclear cells and lymph node cells were significantly increased. In contrast, the exposure to a continuous footshock for 3 min did not affect the concentrations of the opioid peptide. Similarly, phytohemoagglutinin-induced proliferation of splenocytes and natural killer activity were significantly impaired only after the exposure to intermittent footshock stress. On the contrary, plasma corticosterone levels were similarly elevated after both paradigms of stress. The pretreatment with the corticotropin-releasing hormone (CRH) receptor antagonist prevented both the stress-induced increase of immunocyte BE and immunosuppression. In conclusion, our data suggest that intermittent and continuous footshock stressors activate different neuroendocrine responses and that CRH plays a central role in mediating the immune effects of the intermittent footshock stress. The possible relationship between the beta-endorphin changes and immunosuppression is discussed.

Acute Disease↗
PubMed1994

Decreased beta-endorphin content in peripheral blood mononuclear leukocytes from patients with Crohn's disease.

Increased activation of lymphocytes in inflammatory bowel disease is reflected by alterations of various immunological functions including enhanced spontaneous secretion of rheumatoid factor by mononuclear cells. since in rheumatic diseases increased secretion of rheumatoid factor is associated with decreased levels of beta-endorphin in circulating blood mononuclear leukocytes, we investigated levels of leukocyte beta-endorphin in inflammatory bowel disease and compared them with those in hepatobiliary disorders and in healthy subjects. Levels of beta-endorphin were measured in extracts from peripheral blood mononuclear leukocytes by radioimmunoassay. beta-Endorphin levels ranged from 0 to 67 pg/10(6) cells. Mononuclear leukocytes from ulcerative colitis patients contained as much beta-endorphin as those from healthy control subjects. In patients with Crohn's disease, levels of beta-endorphin were reduced by as much as roughly 50%. An inverse relationship was found between leukocyte beta-endorphin on the one hand and erythrocyte sedimentation rate, blood granulocyte or thrombocyte counts, and C-reactive protein levels in plasma on the other. In patients with various hepatobiliary disorders including fatty liver disease, viral hepatitis, primary biliary cirrhosis, and cryptogenic or alcoholic cirrhosis, beta-endorphin levels were not significantly different from the normal range values. Data indicate that leukocyte beta-endorphin may be involved in regulation of the systemic inflammatory activity of Crohn's disease.

Adult↗
PubMed1994

Chlomipramine differently affects inflammatory edema and pain in the rat.

In the rat, the acute administration of the antidepressant drug chlomipramine significantly reduces the edema and the hyperalgesia induced by yeast injection in the paw. However, the intensity and time course of the two effects differ. Moreover, adrenalectomy enhances the antinociceptive effect, whereas it does not affect the antiedema action of chlomipramine. Our data suggest a dissociation between the antiinflammatory and the analgesic effect of acute chlomipramine.

Adrenalectomy↗
PubMed1994

Beta-endorphin concentrations in brain areas and peritoneal macrophages in rats susceptible and resistant to experimental allergic encephalomyelitis: a possible relationship between tumor necrosis factor alpha and opioids in the disease.

Since the central nervous system and neuropeptides modulate immune functions, we investigated whether the different susceptibility of Lewis and Brown Norway rats to experimental allergic encephalomyelitis could also reflect differences in beta-endorphin and substance P concentrations in brain areas and macrophages during the development of the disease. We show that beta-endorphin concentrations increase much more in the hypothalamus and macrophages of Lewis rats during the development of the disease, while the increase is much lower or absent in Brown Norway rats. Tumor necrosis factor-alpha seems to play an important role in this difference. The administration of the opiate receptor antagonist naltrexone worsens the development of the disease, suggesting that the increase of the opioid beta-endorphin might represent a mechanism to downregulate the immune response. In both strains, the concentrations of substance P do not change.

Animals↗
PubMed1994

Beta-endorphin content in HIV-infected HuT78 cell line and in peripheral lymphocytes from HIV-positive subjects.

We investigated beta-endorphin (BE) content in an HIV-infected cell line and in peripheral blood mononuclear cells (PBM) from HIV-positive subjects. HIV infection increased BE content in HuT78 cell line compared to uninfected cells. Accordingly, BE content was greater in HIV-positive subjects than in healthy controls, both in fresh PBM and in mitogen-stimulated or unstimulated cultured cells. Further, in PHA-stimulated cultures, BE increase was correlated with disease progression. Opioids are known to decrease immune responsiveness in vivo, and it may be that the increased BE concentrations contribute to HIV-associated immune deficiency. In HIV-positive subjects, but not in healthy controls, intracellular BE concentration was positively correlated with PHA-induced PBM proliferation. The latter data suggest an alternative explanation: that the increased BE content represents a paradoxical response of the host in an attempt to balance virus-induced immunodepression. Thus, BE may be important in fine-tuning of the immune response with its up- and downregulation dependent upon differences in immune status.

Adult↗
PubMed1994

Chlorimipramine and nortriptyline but not fluoxetine and fluvoxamine inhibit human polymorphonuclear cell chemotaxis in vitro.

We examined the ability of antidepressant drugs belonging to different classes to interfere with human polymorphonuclear cell migration in vitro. 1. The tricyclic antidepressant drugs chlorimipramine and nortriptyline were able to block, in a dose related fashion both spontaneous and formyl-methionyl-leucyl-phenylalanine stimulated migration. This effect was already evident at very low concentrations (10(-7)M). 2. The atypical non-tricyclic antidepressant drugs fluoxetine and fluvoxamine did not affect polymorphonuclear cell mobility. 3. The ability of antidepressant drugs to interfere with polymorphonuclear cell physiology seems to depend on their chemical structures.

Antidepressive Agents↗
PubMed1994

Intracerebroventricular interleukin-1 alpha increases immunocyte beta-endorphin concentrations in the rat: involvement of corticotropin-releasing hormone, catecholamines, and serotonin.

The opioid peptide beta-endorphin (BE) is synthesized and secreted by the cells of the immune system and has been shown to participate in the modulation of immune responses, e.g. during stress. Interleukin-1 (IL-1) is a potent activator of the corticotropin-releasing hormone (CRH) system in the hypothalamus, and it has been shown to be involved in many stress responses, including immunosuppression. We studied the effect of centrally injected IL-1 alpha on immunocyte BE concentrations in the rat. IL-1 alpha (1 ng/rat, intracerebroventricularly) significantly (P < 0.01) increased the concentrations of the peptide in splenocytes, lymph node cells, and peripheral blood mononuclear cells 2 and 24 h after treatment. Intracerebroventricular, but not iv, administration of 2 micrograms IL-1 receptor antagonist blocked the IL-1 alpha-induced increase. These effects were also prevented by the intracerebroventricular administration of the CRH receptor antagonist alpha-helical CRH-(9-41). Treatment with 6-hydroxydopamine and 5,7-dihydroxytryptamine, which deplete the catecholaminergic or the serotoninergic systems, respectively, blocked the increase in BE induced by the cytokine. In contrast, hypophysectomy and treatment with indomethacin did not modify the effect of IL. The increase in immunocyte BE, therefore, seems to depend on the activation of CRH, catecholamines, and serotonin, but to be independent of activation of the hypothalamus-pituitary-adrenal-axis and prostaglandins. The immunocyte BE increase could be involved in the immunosuppression induced by central IL-1 alpha.

Adrenalectomy↗
PubMed1994

Veralipride for hot flushes induced by a gonadotropin-releasing hormone agonist: a controlled study.

OBJECTIVES: To evaluate the efficacy of veralipride, a benzamide derivative, in the treatment of hot flushes induced by GnRH agonists (GnRH-a) and to study peripheral blood mononuclear cell beta-endorphin concentrations during drug administration. DESIGN: Randomized, placebo-controlled, double-blind trial. SETTING: Academic department of obstetrics and gynecology. PATIENTS: Forty women of mean age 43 +/- 5 years who experienced disturbing hot flushes during a 4-month course of tryptorelin depot for myoma-associated menorrhagia. INTERVENTIONS: Treatment with oral veralipride 100 mg/d (20 subjects) or matching placebo (20 subjects) during the third month of GnRH-a administration. MAIN OUTCOME MEASURES: Modifications of frequency and severity of hot flushes as shown by a 0 to 6-point vasomotor scoring system and variations of beta-endorphin levels in peripheral blood mononuclear cells. RESULTS: Two subjects in each group dropped out of the study. The median (range) vasomotor score at the end of the second month of treatment was 4 (3 to 6) in both the veralipride and placebo group. At the end of the third and fourth months the median (range) scores were, respectively, 2 (0 to 6) versus 4 (1 to 6) and 2 (0 to 5) versus 4 (1 to 6). No significant variations in mononuclear cell beta-endorphin concentrations were recorded. Serum PRL levels rose from 11.7 +/- 5.7 to 132.3 +/- 65.0 ng/mL (conversion factor to SI unit, 1.0) during veralipride administration and returned to 10.6 +/- 3.7 ng/mL after drug withdrawal. CONCLUSION: Veralipride reduced vasomotor symptoms induced by a GnRH-a. Transient hyperprolactinemia was the main side effect observed. The mode of action of the drug in GnRH-a-treated patients and possible interactions with endogenous opioid peptides need further elucidation.

Adult↗
PubMed1993

Cloned microglial cells but not macrophages synthesize beta-endorphin in response to CRH activation.

The properties of microglial cell clones, obtained from embryonic mouse brain primary cultures immortalized with recombinant retroviruses, have been investigated and compared with the properties of macrophage clones similarly obtained. Macrophage clones differed from microglial clones in some functions but shared most of the immunological properties. Interestingly, microglial cells were able to produce beta-endorphin, and this production was regulated differently in microglial cell clones when compared with macrophages clones. Although lipopolysaccharide (LPS) treatment induces an increase in beta-endorphin concentration in both cell types, only microglial clones and primary microglial cell cultures respond to the neuroendocrine stimulus corticotropin releasing hormone (CRH). In addition, in these cells, beta-endorphin release is regulated by a classical neurotransmitter, such as noradrenaline, adding some evidence of communication between neurons and microglial cells.

Animals↗
PubMed1993

Benzodiazepine induced chemotaxis of human monocytes: a tool for the study of benzodiazepine receptors.

Different ligands of both the "peripheral" and the "central" benzodiazepine receptors were tested for their ability to induce human monocyte chemotaxis. Only the ligands interacting with the "peripheral receptor" (diazepam and Ro 5-4864) were active, and their action was blocked by the specific antagonist PK 11-195, but not by the calcium channel blocker nimodipine. As expected, GABA did not stimulate chemotaxis and it did not modulate the chemotaxis induced by other benzodiazepine receptor ligands. The benzodiazepine inverse agonists FG 7142 and Ro 15-3505 were inactive on chemotaxis when given alone, but they enhanced the "peripheral" ligand induced chemotaxis. This effect was blocked by an agonist and an antagonist of the "central" receptor. These results suggest an interaction between the two different classes of benzodiazepine receptors on human monocytes.

Benzodiazepines↗
PubMed1993

Naloxone-induced analgesia: involvement of kappa-opiate receptors.

Rats treated with an acute high dose (30 mg/kg) or 4 days with a lower dose (5 mg/kg) of naloxone or naltrexone show an analgesic response at the hot-plate test. This paradoxical analgesic effect of the two mu-opiate receptor antagonists is blocked by the kappa opiate receptor antagonist MR 1452, and is modulated by the kappa opiate receptor agonist U 50-488. Our results suggest that kappa opiate receptors are involved in naloxone-induced analgesia and are consistent with a high degree of plasticity of the opiatergic system.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗