Effects of Propofol on the Liver Oxidative-Antioxidant Balance in a Rat Model of Parkinson's Disease.

Background: Parkinson's disease is caused by the destruction of dopaminergic neurons in the substantia nigra of the midbrain. One of the possible factors involved in the pathogenesis of Parkinson's disease is impaired oxidativeantioxidative balance.

Objectives: The present study aimed to evaluate selected parameters of the liver oxidative-antioxidative system in a Wistar rat model with Parkinson's disease treated with propofol.

Evaluation of the analgesic effect of morphine on models of acute nociceptive pain in rats with a central noradrenergic system lesion.

Objectives: Stimulation of some noradrenergic system receptors demonstrates a synergistic anti-nociceptive effect with the opioid system at the level of peripheral tissues, spinal cord, and supraspinal structures. Furthermore, opioids stimulate the noradrenergic descending pathways originating from the substantia nigra by presynaptic inhibition of the GABA neuron ends. It is thus important to determine whether a disruption to the adrenergic transmission obtained via DPS-4 administration to neonatal rats impacts the perception of noxious stimuli mediated by 5-HT3-serotonin receptors at the level of spinal cords or higher tiers of the central nervous system.

Impairment in Pain Perception in Adult Rats Lesioned as Neonates with 5.7-Dihydroxytryptamine.

Background: Whereas some studies have demonstrated the essential role of 5-hydroxytryptamine (5-HT) in tramadol and acetaminophen analgesia, other research has presented conflicting results. To dispel doubts, some aspects of the involvement of 5-HT in the antinociceptive properties of these drugs remain to be clarified.

Objectives: The aim of this study was to determine whether the serotoninergic system dysfunction produced by neonatal 5-HT lesion in rats may affect the antinociceptive effects of tramadol and acetaminophen administered in adulthood.