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Please quote Nature Neuroscience as the source of these items.

The May 2010 issue of Nature Neuroscience is available online.

May 2010

Addicted to junk food

Nature Neuroscience pp 635 - 641

High-calorie food can be just as addictive as smoking or the abuse of drugs suggests work published online this week in Nature Neuroscience. Although the findings cannot be directly transferred to human obesity, the study shows that overconsumption of high-calorie food can trigger addiction-like responses in the brain, and that junk food can turn rats into compulsive eaters in a laboratory setting.

Addicts are known to show blunted activation of brain circuits responsible for reward in response to normally positive experiences. Paul Kenny and colleagues measured rats' sensitivity to rewarding experiences. When the researchers regularly offered rats a choice of high-calorie foods such as bacon, sausage, cake, and chocolate, in addition to their regular, healthier but less appetizing chow, the animals over-consumed calories and gained weight rapidly. Their reward sensitivity also plummeted, as has been shown before for addictive drugs. This blunting of reward response persisted for at least two weeks after the high-calorie food was no longer available.

A true addict, whether rat or human, will also compulsively consume their drug even when it is clearly detrimental to their own health. To test this, the team trained their rats to expect painful foot shocks when seeing a light signal. Although normal rats stop eating even the most delicious junk food when the light comes on, the obese rats used to a high-calorie diet just kept feeding.

The scientists also found decreased levels of a specific dopamine receptor in the overweight rats, as has been reported in humans addicted to drugs. Artificially decreasing levels of this dopamine receptor in another group of rats accelerated their loss of reward sensitivity when given access to the high-calorie food diet.

Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats pp 635 - 641

Paul M Johnson & Paul J Kenny

Published online: 28 March 2010 | doi: 10.1038/nn.2519


Failure of cannibalization in Huntington disease

Nature Neuroscience pp 567 - 576

The inability to get rid of mutant protein accumulation in Huntington's disease (HD) is because the neuronal protein degradation machinery fails to recognize and package proteins for destruction. The work published online this week in Nature Neuroscience suggests potential therapeutic targets that may be beneficial for HD.

One of the cellular hallmarks of HD is the accumulation of the mutant protein Huntingtin which eventually leads to cell death in the brain. Normally, excess protein accumulation can be removed by a cellular process called autophagy in which cells digest their own components along with any proteins that are tagged for degradation. Abnormal autophagy is also seen in other neurodegenerative disorders.

Using cells collected from HD patients and mouse models of HD, Ana Maria Cuervo and colleagues show that the cellular 'vehicles' which deliver proteins to the degradation machinery, fail to recognize their cargoes. Because mutant Huntingtin is not cleared away properly, the scientists attribute this cellular defect to an increase of protein aggregates that is characteristic of HD cells.

Cargo recognition failure is responsible for inefficient autophagy in Huntington's disease pp 567 - 576

Marta Martinez-Vicente, Zsolt Talloczy, Esther Wong, Guomei Tang, Hiroshi Koga, Susmita Kaushik, Rosa de Vries, Esperanza Arias, Spike Harris, David Sulzer & Ana Maria Cuervo

Published online: 11 April 2010 | doi: 10.1038/nn.2528


Anxious interactions

Nature Neuroscience pp 622 - 629

Cross-talk between two compounds — serotonin and corticotrophin-releasing factor- — is important to control anxiety-like behavior in mice reports a study published online this week in Nature Neuroscience.

Both corticotrophin-releasing factor (CRF) and serotonin signaling have been implicated in anxious behavior, but it was previously unknown how these two pathways may interact at a cellular level to regulate anxiety.

Stephen Ferguson and colleagues used molecular and biochemical techniques to show that the corticotrophin-releasing factor type 1 receptor (CRFR1) forms a complex with the type 2 serotonin receptor (5-HT2) in mouse neurons. The CRFR1 receptor "helps" the 5-HT2 receptors that have been recycled inside the neuron get back to the neuron's surface. To demonstrate the behavioral relevance of this interaction, the authors injected CRF into the prefrontal cortex of mice, and followed this with an injection of a 5-HT2 receptor agonist. These mice showed an increase in anxiety-like behaviors. However, these compounds had no effect on the mice's behavior when each compound was administered alone, suggesting that the specific interaction between the CRFR1 and 5-HT2 receptor led to the increase in anxiety-like behavior.

CRF receptor 1 regulates anxiety behavior via sensitization of 5-HT2 receptor signaling pp 622 - 629

Ana C Magalhaes, Kevin D Holmes, Lianne B Dale, Laetitia Comps-Agrar, Dennis Lee, Prem N Yadav, Linsay Drysdale, Michael O Poulter, Bryan L Roth, Jean-Philippe Pin, Hymie Anisman & Stephen S G Ferguson

Published online: 11 April 2010 | doi: 10.1038/nn.2529

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