Memory impairment and hippocampus specific protein oxidation induced by ethanol intake and 3, 4-methylenedioxymethamphetamine (MDMA) in mice.

Ethanol and 3, 4-Methylenedioxymethamphetamine (MDMA) are popular recreational drugs widely abused by adolescents that may induce neurotoxic processes associated with behavioural alterations. Adolescent CD1 mice were subjected to ethanol intake using the drinking in the dark (DID) procedure, acute MDMA or a combination. Considering that both drugs of abuse cause oxidative stress in the brain, protein oxidative damage in different brain areas was analysed 72 h after treatment using a proteomic approach.

Influence of chronic caffeine on MDMA-induced behavioral and neuroinflammatory response in mice.

Rationale: Previous research suggests that chronic daily caffeine administration protects against brain injury in different animal models of neurodegenerative diseases, such as Parkinson's and Alzheimer's diseases, ischemic and traumatic brain injury, and allergic encephalitis. However, little is known about the effects of chronic caffeine administration on 3,4-methylenedioxymethamphetamine (MDMA)-induced neuroinflammation.

Objective: The present study examines whether chronic caffeine (10, 20, or 30 mg/kg, i.

Paclitaxel-induced neuropathic pain is age dependent and devolves on glial response.

Background: Paclitaxel is an antimitotic antitumour drug highly effective against a broad range of cancers considered refractory to conventional chemotherapy. One of the main serious side effects of paclitaxel treatment is the induction of peripheral neuropathic pain that often diminishes the patient's quality of life. In this study, we evaluated the severity of the neuropathy induced by paclitaxel and the inflammatory reaction in the dorsal horn of the spinal cord in young, adult and aged male CD1 mice.

Transgenic over expression of nicotinic receptor alpha 5, alpha 3, and beta 4 subunit genes reduces ethanol intake in mice.

Abuse of alcohol and smoking are extensively co-morbid. Some studies suggest partial commonality of action of alcohol and nicotine mediated through nicotinic acetylcholine receptors (nAChRs). We tested mice with transgenic over expression of the alpha 5, alpha 3, beta 4 receptor subunit genes, which lie in a cluster on human chromosome 15, that were previously shown to have increased nicotine self-administration, for several responses to ethanol.

Alteration of neuropathic and visceral pain in female C57BL/6J mice lacking the PPAR-α gene.

Rationale: Peroxisome proliferator-activated receptors (PPARs) participate in the control of chronic neuropathic and inflammatory pain, and these receptors could play a role on acute pain.

Objectives: We used null (PPAR-α -/-) and wild-type female mice and the PPAR-α blocker GW6471 to evaluate (1) the role of PPAR-α on neuropathic pain, (2) the involvement of PPAR-α on visceral and acute thermal nociception, and (3) tissue levels of pro-inflammatory factors.

Methods: Neuropathic pain was induced by sciatic nerve ligature.

Behavioural and neuroinflammatory effects of the combination of binge ethanol and MDMA in mice.

Rationale: Binge drinking is a common pattern of alcohol consumption among young people. Binge drinkers are especially susceptible to brain damage when other substances are co-administered, in particular, 3,4-methylendioxymethamphetamine (MDMA).

Objective: To evaluate the behavioural consequences of voluntary binge ethanol consumption, alone and in combination to MDMA.

GPR3 orphan receptor is involved in neuropathic pain after peripheral nerve injury and regulates morphine-induced antinociception.

GPR3 is an orphan G-protein coupled receptor broadly expressed in brain structures controlling emotional-like behaviors and pain. GPR3 receptor up-regulates cAMP and promotes neurite outgrowth in mammalian neurons, being a good candidate to participate in the pathophysiology of neurodegenerative diseases as well as brain and spinal cord injuries. In this study, we evaluated the role of GPR3 receptor in the development and expression of neuropathic pain after sciatic nerve ligature, and the inflammatory reaction in the dorsal horn of the spinal cord in both Gpr3-/- and Gpr3+/+ mice.

CRF₂ mediates the increased noradrenergic activity in the hypothalamic paraventricular nucleus and the negative state of morphine withdrawal in rats.

Background And Purpose: Recent evidence suggests that corticotropin-releasing factor (CRF) receptor signalling is involved in modulating the negative symptoms of opiate withdrawal. In this study, a series of experiments were performed to further characterize the role of CRF-type 2 receptor (CRF₂) signalling in opiate withdrawal-induced physical signs of dependence, hypothalamus-pituitary-adrenal (HPA) axis activation, enhanced noradrenaline (NA) turnover in the hypothalamic paraventricular nucleus (PVN) and tyrosine hydroxylase (TH) phosphorylation (activation), as well as CRF₂ expression in the nucleus of the solitary tract-A₂ noradrenergic cell group (NTS-A₂).

Experimental Approach: The contribution of CRF₂ signalling in opiate withdrawal was assessed by i.

Intracranial self-stimulation facilitates a spatial learning and memory task in the Morris water maze.

Learning and memory improvement by post-training intracranial self-stimulation has been observed mostly in implicit tasks, such as active avoidance, which are acquired with multiple trials and originate rigid behavioral responses, in rats. Here we wanted to know whether post-training self-stimulation is also able to facilitate a spatial task which requires a flexible behavioral response in the Morris water maze. Three experiments were run with Wistar rats.

Intracranial self-stimulation improves memory consolidation in rats with little training.

Post-training intracranial electrical self-stimulation can improve learning and memory consolidation in rats. However, the molecular mechanisms involved are not known yet. Since previous paradigms of this kind of facilitation are relatively unsuitable to try a molecular approach, here we develop a single and short model of learning and memory facilitation by post-training self-stimulation that could make easier the research of its neural and molecular basis.

[Gestational herpes. Presentation of a case and review of the literature].

Herpes gestationis (HG) is a rare autoimmune blistering complication of pregnancy. It is of unknown etiology and it occurs once in every 3,000 to 50,000 pregnancies. The diagnosis can strongly be suggested by the clinical picture, but it must be confirmed using immunopathological methods.