Molecules wired for obesity discovered

Researchers from across the globe have pinpointed a set of molecules that wire the body weight centre of the brain.

Research teams  tried to uncover key genes that guide the process of brain development.

"We know that the brain, in particular an area called the hypothalamus, has a very important role in the regulation of food intake and blood sugar," explains one of the researchers.

Researchers have focused on the hypothalamus for years in an effort to study the epidemic of obesity, which affects nearly 14 million children and adolescents in the United States. "What we don't yet understand," he says, "is how these circuits in the hypothalamus are being organised. We want to know how the brain puts itself together and what exactly governs that process." Understanding this is key because circuits must be established properly in order for the brain to ultimately perform complex functions like maintaining proper weight.

Why do certain brain cells connect to one area while specifically avoiding other, nearby cells? 

Researchers investigate how this precise wiring is achieved. Understanding how brain cells in the hypothalamus form these specific, complex connections and how this process can be adversely affected could provide insight into the development of childhood obesity. 

The researcher studied a group of molecules called semaphorins, which are found in abundance in the developing hypothalamus. Brain cells release semaphorins to communicate with other brain cells. These messages act as a sort of road map, guiding cells towards or away from other cells. But what happens to the brain when that road map is no longer functioning properly?

The Dr. who led the study, blocked semaphorin signaling in cells of the hypothalamus. She discovered that brain cells no longer grew the way they were supposed to, showing that semaphorin provide an essential map for them to follow. In addition to connections failing to establish, loss of semaphorin action in a preclinical model also caused elevated body weight. "What we are seeing is that semaphorins are guiding and shaping development of hypothalamic circuits that ultimately regulate calorie intake," explains the Dr.

A Prof. was also analysing genetic information from individuals with obesity. His team tested 1,000 DNA samples and found that individuals with early-onset obesity had more rare mutations in genes involved in semaphorin signaling than healthy individuals. The finding that people with obesity have rare mutations in semaphorin signaling shows that semaphorins are important in maintaining healthy body weight.

"We have now discovered the genes that establish the precise neural connections that form these circuits," says the Dr. who led the study and is co-first author on the paper. "This work provides new insights into the development of hypothalamic circuits that regulate appetite and metabolism."

This study gives a much clearer picture of what occurs in the developing brain. Semaphorin signaling appears to shape the physical architecture of the brain and influence circuitry governing body weight.

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researchers identify pathway that may protect against cocaine addiction

A study by researchers  gives insight into changes in the reward circuitry of the brain that may provide resistance against cocaine addiction. Scientists found that strengthening signalling along a neural pathway that runs through the nucleus accumbens — a region of the brain involved in motivation, pleasure, and addiction — can reduce cocaine-seeking behaviour in mice.

Research suggests that about 1 in 5 people who use cocaine will become addicted, but it remains unclear why certain people are more vulnerable to drug addiction than others.

A key step in understanding addiction and advancing treatment is to identify the differences in brain connectivity between subjects that compulsively take cocaine and those who do not. 

Until now, most efforts have focused on finding traits associated with vulnerability to develop compulsive cocaine use. However, identifying mechanisms that promote resilience may prove to have more therapeutic value.

In the study, mice were conditioned to receive an intravenous dose of cocaine each time they poked their nose into a hole in their enclosure. Cocaine was then made unavailable for periods of time during the day. Some of the mice would stop seeking the drug once it was removed while others would obsessively continue to poke the hole in an effort to obtain the drug.

Mice that quickly stopped seeking the drug were found to have stronger connections along the indirect pathway — a neural tract that forms indirect projections into the mid-brain and contains cells called medium spiny neurons expressing dopamine D2 receptors (D2-MSNs). A parallel pathway — known as the direct pathway -- forms direct projections into the mid-brain neurons and contains medium spiny neurons expressing D1 receptors (D1-MSNs). These two pathways are thought to work together in complementary but sometimes opposing ways to affect behaviour.

Researchers were very surprised by the results of the study because we were originally looking for vulnerability factors for developing compulsive drug use. Instead,they found changes that only happened in subjects that show a resilience to becoming compulsive drug users. Resilient mice had a strong inhibitory circuit that allowed them to exert better control over their drug intake.

To test this observation, researchers used lasers to activate individual neurons, and found that stimulating D2-MSNs in the nucleus accumbens decreased cocaine seeking in the mice. Blocking D2-MSN signalling with a chemical process increased motivation to obtain cocaine.

This research advances the understanding of how the recruitment, activation and the interaction among brain circuits can either restrain or increase motivation to take drugs.

Previous studies have shown that people with lower levels of dopamine D2 receptors in the striatum, a brain region associated with reward and working memory, are more likely to develop compulsive behaviours toward stimulant drugs.

Dopamine is a key neurotransmitter involved in reward-based learning and addiction. Cocaine disrupts communication between neurons at the synapse, the small junction between nerve cells, by blocking the re-absorption of dopamine into the transmitting neuron. As a result, dopamine continues to stimulate the receiving neuron, causing feelings of alertness and euphoria.

Brain Circuitry Yields Clue to Autism

A problem with a certain brain circuit may be one reason why 7-month-old infants who later develop autism are slower to shift their gaze and attention from one object to another, compared with infants who do not develop autism.

That's the finding of a study that included 97 children who underwent an eye-tracking test and brain scan at age 7 months and a full clinical assessment at age 25 months.

The results showed that infants later diagnosed with autism were about 50 milliseconds slower in shifting their gaze from one object to another, compared with those who did not develop autism.

The study, also found that gaze shifting in infants who did not develop autism was linked with a specific circuit in the brain. This association was not found in infants who later developed autism.

These findings suggest that 7-month-old who go on to develop autism show subtle yet overt behavioural differences prior to the emergence of the disorder. They also implicate a specific neural circuit ... which may not be functioning as it does in typically developing infants, who show more rapid orienting to visual stimuli.

Autism is a developmental disability that can cause significant social, communication and behavioural challenges.