[The cannabis pandemic: why use this expression? Epidemiology].

Using the term of pandemic to characterize the current use of cannabis is fully warranted considering the results of recent surveys [Halte au cannabis. Paris: Odile Jacob; 2006]. A pandemic is defined as an epidemic affecting populations in a very wide geographical zone which may involve one or several continents.

[Illicit drugs, medications and traffic accidents].

The European Union (EU) has 25 member-states and 455 million inhabitants. Statistics on traffic accidents in the EU show that more than 45,000 people are killed annually, including 5200 in France. At the same time, nearly two million persons in the EU require medical treatment for traffic-accident-related injuries, including 109,000 in France.

[Pharmacology, an innovative factor in therapeutic research].

As members of the pharmacology training group set up by the committee of pharmacological science of the French Academy of Pharmacy, we examine the situation of pharmacology in drug discovery. Today, it is obvious that by integrating genome sequencing, cellular and molecular biology, and bioinformatics, pharmacology has become a cross-disciplinary science. Pharmacologists must become knowledgeable in a wide range of domains, using the major points in each to direct them towards the discovery and development of new therapeutic agents.

Deleterious poly(ADP-ribose)polymerase-1 pathway activation in traumatic brain injury in rat.

Traumatic brain injury produces nitric oxide and reactive oxygen species. Peroxynitrite, resulting from the combination of nitric oxide and superoxide anions, triggers DNA strand breaks, leading to the activation of poly(ADP-ribose)polymerase-1. As excessive activation of this enzyme induces cell death, we examined the production of nitrosative stress, the activation of poly(ADP-ribose)polymerase-1, and the role of this enzyme in the outcomes of traumatic brain injury produced by fluid percussion in rats.

[Report of the "Health and Environment" commission of the National Academy of pharmacy. Carbon monoxide and environmental health: are carbon monoxide levels in urban areas a health hazard?].

In an urban environment, carbon monoxide is produced by incomplete combustion, particularly in motor vehicles. Air pollution caused by CO produced by motor vehicles is controlled by legislation. Legal regulations have considerably lowered emission levels authorized for new vehicles and total CO emission levels.

[New provisions for prevention and fight against doping].

Doping which is largely a sport-related phenomenon, led the French government of enact a series of laws in 1965, 1984, and 1989. Due to the apparent extension of doping, a new law was enacted on March 23, 1999. This law concerns medical surveillance of athletes and prevention and fight against doping.

[Neuronal death: potential role of the nuclear enzyme, poly (ADP-ribose) polymerase].

Poly(ADP-ribose) polymerase (PARP, EC 2.4.2.

[Inefficacy of N-methyl-D-aspartate receptor complex antagonists on behavioral and histologic consequences of global cerebral ischemia in rats].

Glutamic acid, an excitatory amino acid, has been proposed to play a major deleterious influence in cerebral ischemia. However, the neuroprotective activity of various glutamate receptor antagonists is often low or absent, according to the animal model used. In the present study, we examined the effect of several antagonists acting on glutamate receptors of the N-methyl-D-aspartate (NMDA) type in rats submitted to a brief (5 minutes) global cerebral ischemia.

A microdialysis study investigating the mechanisms of hydroxyl radical formation in rat striatum exposed to glutamate.

Considerable evidence has linked hydroxyl radicals (.OH) to excitotoxicity. Glutamate infused through a microdialysis probe into rat striatum induced a massive .

iNOS contribution to the NMDA-induced excitotoxic lesion in the rat striatum.

1. The aim of this study was to assess whether an excitotoxic insult induced by NMDA may induce an iNOS activity which contributes to the lesion in the rat striatum. 2.

[Behavioral and neurochemical methods in research on new psychotropics].

Since the discovery of the antipsychotic effects of chlorpromazine by the French psychiatrists DELAY and DENIKER in 1952, preclinical pharmacologists have proposed several laboratory tests, that have been used to demonstrate the potential activity of drugs in the treatment of mental disorders including schizophrenia, depressive illness and anxiety. Tests are divided into behavioural tests and neurochemical tests. Electrophysiology tests are not considered in this paper.

Reduction of tyrosine nitration after N(omega)-nitro-L-arginine-methylester treatment of mice with traumatic brain injury.

Oxygen free radicals and nitric oxide (NO) have been proposed to be involved in the cascade of injury elicited by traumatic brain injury. However, the mechanism(s) of injury remain to be explored. Since superoxide generation is triggered by traumatic brain injury, the cytotoxic peroxynitrite could be formed, but it is not known if this actually occurs.

Protective effect of melatonin in a model of traumatic brain injury in mice.

The pineal hormone melatonin has recently been shown to exert neuroprotective activity in a variety of experimental neuropathologies in which free radicals are involved. This neuroprotective effect has been attributed to the antioxidant properties of melatonin. Considering that free radicals also play a deleterious role in traumatic brain injury (TBI), the purpose of the present study was to determine whether melatonin would have a beneficial effect in this pathology.

Glutamate induces hydroxyl radical formation in vivo via activation of nitric oxide synthase in Sprague-Dawley rats.

It was recently reported that neuronal nitric oxide synthase (NOS) generates oxygen-derived free radicals in vitro at low concentrations of L-arginine. Using the microdialysis technique, we monitored both hydroxyl radical (.OH) and nitric oxide (.

Deleterious Ca-independent NOS activity after oxidative stress in rat striatum.

The aim of this study was to assess whether oxidative stress induces deleterious NOS activity in the central nervous system (CNS). For this purpose, the mitochondrial toxin malonate, which promotes free radical production, was infused into the left striatum of rats. Forty-eight hours after injection, an increase in Ca-independent NOS activity was observed in the injected striatum.

Calcium-independent NO-synthase activity and nitrites/nitrates production in transient focal cerebral ischaemia in mice.

1. The temporal changes in constitutive NO-synthase (cNOS) and in calcium-independent NO-synthase activities were studied in mice subjected to 2 h of transient focal cerebral ischaemia. The changes in brain nitrites/nitrates (NOx) content were also studied.

[Behavioral and neurochemical methods in research on new psychotropic drugs].

Since the discovery of the antipsychotic effects of chlorpromazine by the french psychiatrists Delay and Deniker in 1952, preclinical pharmacologists have proposed several laboratory tests, that have been used to demonstrate the potential activity of drugs in the treatment of mental disorders including schizophrenia, depressive illness and anxiety. Tests are divided into behavioural tests and neurochemical tests. Electrophysiology tests are not considered in this paper.

alpha-Phenyl-N-tert-butylnitrone attenuates excitotoxicity in rat striatum by preventing hydroxyl radical accumulation.

Various in vitro experiments have indicated that oxygen-derived free radicals may contribute to excitotoxic neuronal death. In the present study we induced excitotoxicity in rat striatum by perfusing glutamate at a high concentration through a microdialysis probe. We observed an increased formation of hydroxyl radicals (.

Dose- and time-dependence of L-NAME neuroprotection in transient focal cerebral ischaemia in rats.

1. In this study the effect of the dose and administration time of NG-nitro-L-arginine methyl ester (L-NAME), an NO-synthase inhibitor, in a model of transient focal cerebral ischaemia in rats was investigated. 2.

Reduction of the neurological deficit in mice with traumatic brain injury by nitric oxide synthase inhibitors.

This study investigates the effect of the NO synthase inhibitors, NG-nitro-L-arginine methyl ester (L-NAME) and 7-nitroindazole (7-NI), on the neurological deficit 24 h after a moderate closed head injury in mice. Low doses of L-NAME or 7-NI given soon after the injury significantly reduced the neurological deficit compared to the vehicle-treated group. L-Arginine (300 mg/kg) did not alter the neurological deficit, but reversed the protective effects of both L-NAME and 7-NI when given at the same time.

Reduction of the neurological deficit in mice with traumatic brain injury by nitric oxide synthase inhibitors.

This study investigates the effect of the NO synthase inhibitors, NG-nitro L-arginine methyl ester (L-NAME) and 7-nitro indazole (7-NI), on the neurological deficit 24 h after a moderate closed head injury in mice. Low doses of L-NAME or 7-NI given soon after the injury significantly reduced the neurological deficit compared to the vehicle-treated group. L-Arginine (300 mg/kg) did not alter the neurological deficit, but reversed the protective effects of both L-NAME and 7-NI when given at the same time.

Short therapeutic window for MK-801 in transient focal cerebral ischemia in normotensive rats.

The present study investigates the role of N-methyl-D-aspartate (NMDA) receptors in a model of transient focal cerebral ischemia in normotensive rats. The left middle cerebral artery and both common carotid arteries were occluded for 60 min. Preliminary studies indicated that this gave reproducible infarctions of the cortex and striatum.