S. Pieretti

Dexamethasone induces biphasic effect on morphine hypermotility in mice : a dose-related phenomenon

The present study examined interaction between dexamethasone (DEX) and morphine on the locomotor activity in groups of mice by using the activity cage test. Morphine administration (30-75-150 mg/kg, ip) induced a dose-related increase of the locomotor activity of mice, whereas DEX per se (0.1-1.0-10 mg/kg, ip) did not modify the activity of control mice. Pretreatment of mice with DEX 0.1 mg did not alter the hyperactivity produced by the three doses of morphine. In contrast, DEX administered at 1.0 mg reduced the morphine effects on locomotor activity, whereas DEX at 10 mg potentiated the morphine hypermotility. Our results suggest that DEX may play an important regulatory role on the central effects of morphine through a differential modulation of brain excitability systems.

Des-tyrosine-γ-endorphin effects on morphine analgesia in mice

Abstract 1. 1. The effects that were induced by a β-lipotropin fragment des-tyrosine-γ-endorphin (DTγE) devoid of opiate activity that was administered intraperitoneally or intracerebroventricularly to mice under morphine analgesia were investigated. The interaction of this peptide with the analgesic effects of morphine was examined using the hot plate and the tail flick test. 2. 2. Intraperitoneal acute treatment with DTγE did not change the analgesic effects of morphine. 3. 3. Intraperitoneal semi-chronic treatment performed for 4 days with DTγE enhanced morphine analgesic effects. 4. 4. The intracerebroventricular acute treatment with DTγE reduced morphine analgesia in a dose-dependent way. 5. 5. These results indicate that DTγE, although devoid of opioid activity per se , may interact with the opioid system, probably through an indirect mechanism.

Pain and Child: A Translational Hypothesis on the Pathophysiology of a Mild Type-2 Diabetes Model

Pediatric pain management underwent many changes since the undertreatment of pain in children was reported in the literature in 1980. Increasing data also suggest that long-term behavioural effects can be observed in children, following pain episodes as early as in the neonatal period. Therefore, the knowledge about safe and effective management of pain in children should be applied with greater effectiveness into clinical practice. Other advances in the field include the findings of long-term residual behavioural and metabolic effects induced by pain experienced during the critical periods of development in laboratory animals. Recent data in laboratory animals and clinical data in children suggest that early repeated and/or severe pain and other stressful procedures applied in the perinatal periods may produce not only behavioral, but also important hormonal, immune and metabolic long-term effects. In this paper we shall report data on some metabolic conditions described in adult humans following disruption of hormonal-metabolic programming produced in the peri-natal period. Quite similar signs can be found between animal models and human conditions, most of them being connected with hypothalamus-pituitary-adrenal hormones (HPA) dysfunction. In addition, some signs in animal models, such as overweight and abdominal overweight are prevented by treatment with the μ- and δ-opioid receptor antagonist naloxone during the lactating period. This indicates that some long-term consequences following stress received during the early phases of life in mammals may be bound to the HPA system dysregulation, whereas others are bound to different (e,g., opioid) endogenous brain receptors and/or neuromediators alteration.