SVTR

26 July 2007; | doi:10.1038/news070723-9 / http://www.nature.com/news/2007/070723/full/070723-9.html

Sex change wipes out invasive species

'Trojan chromosomes' enlisted in battle against alien invaders.

Louis Buckley

Altering their chromosomes could help deal with fishy pests. NOAA

Gender-bending chemicals could provide a new way to combat invasive species, say researchers. Originally conceived as a cure for the enormous populations of Asian carp and tilapia plaguing the Mississippi River, scientists now think the approach could be used to battle unwelcome crustaceans, molluscs, fish, amphibians and reptiles around the world.

Invasions of exotic species are thought to be second only to habitat destruction as a threat to global biodiversity. The traditional approach to dealing with these interlopers has been to introduce a known predator and let nature take its course. But this has led to numerous disasters - for example, cane toads swamped Australia after being introduced to control the cane beetles blighting the country's sugar crop.

In Florida, tilapia were deliberately introduced to control an aquatic weed, Hydrilla, that has been choking US rivers since the 1960s. Two species of snail were also introduced at a later date by the authorities, says Gutierrez, but neither they nor the tilapia chose to feed on Hydrilla, both preferring native species to the invader.

Hormone-determined gender

In 2004, alerted to Florida's problems with invasive species, Juan Gutierrez, a bio-mathematician at Florida State University, constructed a mathematical model of a population in which males carry two different sex chromosomes (XY) and females are XX. In many species of fish, amphibians, and other animals, gender is determined not only by sex chromosomes, as it is in humans, but also by environmental conditions such as the presence of hormones, explains Gutierrez.

By exposing genetic males to female hormones, or vice versa, it is therefore possible to create a male that is genetically XX, or a female that is XY or even YY. Such individuals, with the genetics of one sex but the physical characteristics of the other, are referred to as carriers of 'Trojan sex chromosomes'.

In Gutierrez's model, repeated introduction of YY females resulted in an extremely male-dominated population, as all offspring produced from meetings between males (XY) and YY females are male, and many more males are born in subsequent generations. With fewer and fewer females around, the birth rate declined and finally ground to a halt, and the population was extinct within just a few decades. His calculations have been published in the Journal of Theoretical Biology.

But Gutierrez is cautious about trying out his ideas in the real world just yet. "More research is needed to better understand how sex reversal can be efficiently achieved in various potential target species," he says. "The approach is not a quick fix for invasive species, but rather a long-term solution that will require a committed effort over many years."

Non-GM

The idea of controlling an invasive population by manipulating its sex ratio is nothing new, says Gutierrez. However, previous plans required using transgenic organisms, which is undesirable as it carries the risk that the genes will 'escape' into the wild. Using hormones gets round this problem. "With our technique the animals are not genetically modified," explains Gutierrez. "We're not introducing new genes - it's very different."

The approach has numerous advantages, says Samuel Cotton of the University of Lausanne, Switzerland, who has reviewed Gutierrez's theory. "The method only affects the target species, so there is no probability of collateral ecological damage," he notes. "Also, it is reversible - if there are any unwelcome side-effects you can just stop adding YY females."

Gutierrez has joined forces with John Teem of the Florida Department of Agriculture to examine how the strategy might stop the spread of another invasive species - the apple snail - throughout the state's waterways. They are aiming to publish an advanced version of the model later this year, which will allow scientists and policy-makers to assess the suitability of the technique for specific cases.

But whether the issue will receive adequate support is far from certain. "The problem is big, expensive, and the government agencies in charge of it are under-funded," Gutierrez says. "The Program of Research on the Economics of Invasive Species Management had only US$4.9 million to spend between 2003 and 2006. One can only wonder why the agency in charge spends only $4.9 million in four years for a problem that according to conservative estimates costs the United States $200 billion per year."

References

1. Gutierrez, J. B. & Teem, J. L. J. Theor. Biol. 241, 333-341 (2006).
2. Cotton, S. & Wedekind, C. Trends Ecol. Evol. doi:10.1016/j.tree.2007.06.010 (2007).

26 July 2007; | doi:10.1038/news070723-10 / http://www.nature.com/news/2007/070723/full/070723-10.html

Single gene deletion boosts lifespan

Mutant mice live longer, age slower and eat more.

Heidi Ledford

Reducing the influence of adrenaline helps mice live longer. Getty

Researchers have created a mutant mouse that lives longer despite eating more and weighing less - all thanks to the loss of a single protein.

Without this protein, the body is less susceptible to the heart-pounding effects of the hormone adrenaline, and may become more resistant to some forms of stress.

Scientists are already developing drugs to inhibit this protein, called type 5 adenylyl cyclase (AC5). "Clearly we would be very interested in such a compound," says cardiologist Stephen Vatner, who is part of the team that discovered this effect.

Currently, the main focus of ageing research is on using calorie restriction as a way of activating a metabolic 'fountain of youth'. The new discovery, that knocking out a single cardiac gene could lengthen lifespan, was an unexpected byproduct of heart research.

Vatner, together with Junichi Sadoshima and other colleagues at the New Jersey Medical School at the University of Medicine and Dentistry of New Jersey in Newark, had initially set out to determine whether getting rid of AC5 leads to a healthier heart.

Drugs that block adrenaline signalling, called beta-blockers, are known to help patients who have had heart attacks or suffer from an irregular heartbeat. As the researchers revealed in 2003, mutant mice lacking AC5 were more resistant to heart failure caused by pressure within the heart.

But in the process, the research team also realised that the mutant mice lived longer than their normal counterparts. Now, in a paper published in Cell this week, they report that the treated mice lived 30% longer and did not develop the heart stress and bone deterioration that often accompanies ageing.

Anti-cancer properties

AC5 could boost longevity by reducing the trauma caused when chemically reactive forms of oxygen accumulate. The accrued damage from these molecules is thought to contribute to ageing. AC5 mutants make more of a protein called ERK2, which regulates oxidative-stress responses. When Vatner and his colleagues increased ERK2 levels in budding yeast, these yeast lived longer.

There are several mysteries about the mice lacking AC5. Young mutants weigh the same as their normal counterparts, but elderly AC5 mutants weigh less - even though they eat more. That suggests a metabolic change, says Vatner, which could be mimicking calorie restriction.

It is also possible that mice without AC5 are more resistant to cancer, Vatner adds. "The major reason that old mice die is not because of heart failure," says Vatner. "The majority of normal mice die from some sort of tumour." It is possible, he says, that the mutants are longer lived because they are able to stave off tumour formation.

The wonder drug

All of that makes an AC5 inhibitor sound like a miracle drug, but the solution may not be that simple.

In the absence of AC5, mutant mice still respond to adrenaline, but the hormone's effect on the heart is less pronounced. But adrenaline responses come in handy during stressful 'fight-or-flight' situations, cautions Michael Bristow, a cardiologist at the University of Colorado Health Sciences Center in Denver. AC5 is part of a complicated pathway, he adds, and the full ramifications of knocking it out are not yet known.

There could also be mental side-effects, notes H. Kirk Hammond, a cardiologist at the University of California, San Diego in La Jolla. Mice that lack AC5 do not respond as well to morphine or antipsychotic drugs such as haloperidol.

Both Bristow and Hammond agree that the results are exciting and that they open up a new avenue of ageing research. But Hammond adds that although an AC5 inhibitor may make a fine drug for protecting the heart, there are more straightforward options for boosting longevity. "I think first what I would do is get people to slow down on the highway, stop eating Big Macs and stop smoking," says Hammond.

References

1. Okumura, S. et al. Proc. Natl Acad. Sci. USA 100, 9986-9990 (2003).
2. Yan, L. et al. Cell 130, 247-258 (2007).

27 July 2007; | doi:10.1038/news070723-11

Medical opinion comes full circle on cannabis dangers

Frequent use more than doubles psychosis risk, says new large-scale analysis.

Daniel Cressey

Cannabis may be responsible for 14% of UK psychotic illnesses. Getty

Frequent cannabis use more than doubles the risk of developing psychotic illnesses such as schizophrenia, according to the most rigorous analysis of the evidence to date.

The finding, which comes from a new study that combines results from 35 previous surveys, represents a significant U-turn from previous suggestions that cannabis is harmless to mental health. The analysis is published in medical journal The Lancet, which in 1995 began one of its issues with the sentence: "The smoking of cannabis, even long term, is not harmful to health."¹

In fact, having used the drug even once increases your risk of developing psychotic problems by 41%, according to the new research². This suggests that 14% of all psychotic illness in Britain is caused by cannabis use.

'Serious risks'

"The message that has to be made clear is there are potentially quite serious risks from using cannabis," says study author Stanley Zammit of Cardiff University, UK. "For psychotic outcomes there certainly is enough evidence to warn people of the risk."

Zammit adds that the new analysis is the "most thorough" to date. "This adds a certain robustness to the evidence," he says.

Previously there have been questions over whether cannabis actually causes psychotic illness, or whether people with psychiatric problems self-medicate with the drug. Although the new study cannot conclusively settle the argument, it offers the best evidence short of conducting a full randomized trial, in which participants are given either cannabis or a placebo.

Zammit and his colleagues combined data from 35 longitudinal trials, in which populations are observed over time. They found that, even after allowing for other factors, such as other substance use and intelligence, people who have taken cannabis are 41% more likely to develop schizophrenia or other psychotic problems than those who have never used it. Those who used cannabis most frequently were more than twice as likely to suffer problems.

It was less clear whether cannabis use was also linked to depression, suicidal thoughts or anxiety.

Drug law rethink

The increased risk of psychosis, particularly in long-term cannabis users, is worrying, despite the actual risk of developing schizophrenia only being 1% of the population overall³. "Those figures are frankly quite staggering," says Neil McKeganey, director of the University of Glasgow's Centre for Drug Misuse Research. "Because cannabis is our most widely used illegal drug, I think any increased risk we have to be greatly concerned with. One can't take any comfort in the fact they may be relatively small numbers."

The discovery will exacerbate the current controversy over Britain's cannabis laws. Several high-ranking politicians have recently admitted using the drug in the past. A review has also been announced of the 2004 change that saw cannabis downgraded from Class B to Class C, the least serious class of illegal drugs.

In an editorial⁴ accompanying the new study, Merete Nordentoft and Carsten Hjorthøj of Copenhagen University Hospital, Denmark, say: "In the public debate, cannabis has been considered a more or less harmless drug compared with alcohol, central stimulants [such as amphetamines], and opioids. However, the potential long-term hazardous effects of cannabis with regard to psychosis seem to have been overlooked."

References

1. Anon. The Lancet 346, 1241 (1995).
2. Zammit, S. et al. The Lancet 370, 319-328 (2007).
3. Schultz, S. et al. Am. Fam. Physician 76, 1821-1829 (2007).
4. Nordentoft, M. et al. The Lancet 370, 293-294 (2007).

Extrait du BE Etats-Unis N°36 - Ambassade de France aux Etats-Unis

Considérée comme la " molécule du plaisir ", la dopamine est libérée par le striatum en récompense d'une " action de plaisir ".

http://www.futura-sciences.com/fr/sinformer/actualites/news/t/vie-1/d/dopamine-molecule-du-plaisir-et-sensibilite-aux-dependances_9030/

Source : INSERM

La maladie de Parkinson est liée à un déficit en dopamine, un neurotransmetteur¹ qui agit sur le contrôle des mouvements. A partir de modèles animaux, de cultures de cellules souches et d'observations chez l'homme postmortem, l'équipe d'Etienne Hirsch² a mis en évidence un rôle insoupçonné et pourtant essentiel de la dopamine dans la génération de nouveaux neurones. Les chercheurs démontrent que la dopamine agit sur des cellules souches situées dans l'hippocampe et dans la zone sous-ventriculaire du cerveau, pour les faire proliférer et générer de nouveaux neurones. Le déficit en dopamine de la maladie de Parkinson diminuerait le renouvellement des neurones. Ces travaux, publiés dans la revue Nature Neuroscience du mois de juillet, montrent également que l'utilisation d'outils pharmacologiques comme les agonistes de la dopamine³ peuvent agir sur la plasticité du cerveau.

 http://www.futura-sciences.com/fr/sinformer/actualites/news/t/vie-1/d/la-dopamine-facteur-de-plasticite-du-cerveau_3891/

• B4 / FONCTIONNEMENT DU SYSTEME NERVEUX (fin) | 09-06-2008
• B4/ FONCTIONNEMENT DU SYSTEME NERVEUX (suite) | 09-06-2008
• B4 : LE FONCTIONNEMENT DU SYSTÈME NERVEUX (suite) | 06-06-2008
• B4 : LE FONCTIONNEMENT DU SYSTÈME NERVEUX (suite) | 02-06-2008
• Azhdarchid volait-il ? | 01-06-2008
• L'allaitement maternel corrélé à l'intelligence (publication) | 01-06-2008
• Le poisson fossile qui allait accoucher | 01-06-2008
• La « Terre boule de neige » brusquement déglacée par le méthane ? | 01-06-2008
• B4 : LE FONCTIONNEMENT DU SYSTÈME NERVEUX (suite) | 30-05-2008
• B4 : LE FONCTIONNEMENT DU SYSTÈME NERVEUX (suite) | 30-05-2008
• B4 : LE FONCTIONNEMENT DU SYSTÈME NERVEUX (suite) | 29-05-2008
• 3/ L’ORGANISME EN FONCTIONNEMENT(fin) | 29-05-2008
• 3/ L’ORGANISME EN FONCTIONNEMENT(suite) | 29-05-2008
• un papillon hermaphrodite | 27-05-2008
• De nouveaux organismes vivants à plus de 1 600 m sous terre ! | 27-05-2008