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Oxytocin could help treat alcohol use disorder
The neuropeptide oxytocin blocks enhanced drinking in alcohol-dependent rats, according to a US study published in PLOS Biology. Targeting the oxytocin system, the authors noted, may provide novel pharmaceutical interventions for the treatment of alcohol use disorder. Administering oxytocin can decrease consumption, withdrawal symptoms and drug-seeking behaviour associated with several drugs of misuse, and showed promise as a pharmacological approach to treating drug addiction. But first, we need to understand how oxytocin mediates these effects in animal models. To address this question, the researchers tested the hypothesis that oxytocin administration could normalise the maladaptive brain changes that occur in alcohol dependence and thereby reduce alcohol drinking in an established rat model of alcohol dependence. The authors investigated oxytocin’s effects on dependence-induced alcohol consumption and altered signaling of the inhibitory neurotransmitter g-aminobutyric acid (GABA) in the central nucleus of the amygdala (CeA) – a key brain region in the network affected by alcohol dependence. The experiments demonstrated that oxytocin administered systemically, intranasally or into the brain blocked excess drinking in alcohol-dependent but not in non-alcohol-dependent rats. Moreover, oxytocin blocked GABA signaling in the CeA. Taken together, these results provide evidence that oxytocin likely blocks enhanced drinking by altering CeA GABA transmission. These results provided evidence that aberrations in the oxytocin system may underlie alcohol use disorder and that targeting this system, possibly by intranasal administration, could prove a promising therapy in people who misuse alcohol.
Restoring cellular functions in the pig brain after death
A system that can restore brain circulation and some cellular functions in a pig brain hours after death is reported in Nature. This approach may offer a platform for studying the intact brain, but requires further testing before broader applications can be explored. Mammalian brains are very sensitive to decreased oxygen levels; short periods of interrupted blood flow lead to rapid depletion of oxygen and energy stores, which is thought to cause neuronal death and irreparable brain damage. Some studies have questioned whether this cascade of damaging events is inevitable within a short period after blood flow disruption. Researchers from Yale University in the United States postulated that certain cellular brain activities may have the capacity to be partially restored, even a few hours after death. They tested this theory by developing BrainEx, a system designed to mimic pulsating blood flow (perfusion) at normal body temperature (37°C). In this study, 32 pig brains, obtained from food-processing facilities, were placed in this system 4 hours after death. During a 6-hour perfusion period, the authors observed a reduction in cell death and evidence for the restoration of some cellular functions, including synaptic activity. However, there was no evidence of global network activity or full brain function during the experiments. The findings indicated that the brain possesses a greater capacity for cellular restoration than was previously appreciated, and that deterioration after cessation of blood flow may be a protracted rather than rapid process. Two related comment pieces in Nature (here and here) consider the implications of research in this area.
Using genetic profiles to predict obesity risk at birth
US researchers have come up with a scoring system based on genetic markers that predicts an individual’s inborn risk for obesity. Using data from the largest existing genome-wide study of obesity, they applied new algorithms to integrate information from more than 2 million genetic variants affecting body mass index (BMI). The resulting score accurately predicted BMI and obesity in more than 300 000 individuals spanning birth to middle age. The study, published in Cell, also revealed that some people are much more susceptible to obesity than others: those scoring in the top 10% were 13.15 kg heavier on average than those in the lowest 10% and were 25 times as likely to develop severe obesity. The impact of the score started to become discernable at around age 3 years. While the score is not a perfect predictor – some people with a genetic predisposition never become obese – the researchers contend that genetic profiles can help identify high risk individuals and help doctors recommend ways to avoid health risks associated with a high BMI before they materialise. Using a $50 genetic test called a microarray that detects variations and mutations among millions of genetic markers, researchers said their scoring approach will one day predict genetic risk for a range of health conditions, such as heart disease, breast cancer and atrial fibrillation. Interventions might include prescribing preventive cholesterol-lowering medication, lifestyle counseling or using wearable technology, such as an Apple Watch, to detect irregular heartbeats.
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