http://www.nytimes.com/2009/08/18/science/18angier.html:

To rattle the rats to the point where their stress response remained demonstrably hyperactive, the researchers exposed the animals to four weeks of varying stressors: moderate electric shocks, being encaged with dominant rats, prolonged dunks in water. Those chronically stressed animals were then compared with nonstressed peers. The stressed rats had no trouble learning a task like pressing a bar to get a food pellet or a squirt of sugar water, but they had difficulty deciding when to stop pressing the bar, as normal rats easily did.

…Happily, the stress-induced changes in behavior and brain appear to be reversible….

But with only four weeks’ vacation in a supportive setting free of bullies and Tasers, the formerly stressed rats looked just like the controls, able to innovate, discriminate and lay off the bar. Atrophied synaptic connections in the decisive regions of the prefrontal cortex resprouted, while the overgrown dendritic vines of the habit-prone sensorimotor striatum retreated.

and from the article abstract:

Using two different operant tasks, we revealed that, in making choices, rats subjected to chronic stress became insensitive to changes in outcome value and resistant to changes in action-outcome contingency. Furthermore, chronic stress caused opposing structural changes in the associative and sensorimotor corticostriatal circuits underlying these different behavioral strategies, with atrophy of medial prefrontal cortex and the associative striatum and hypertrophy of the sensorimotor striatum. These data suggest that the relative advantage of circuits coursing through sensorimotor striatum observed after chronic stress leads to a bias in behavioral strategies toward habit.

and from the ScienceNOW summary article http://sciencenow.sciencemag.org/cgi/content/full/sciencenow;2009/730/3:

In the first test, they taught the rats to hit a lever to score one of two possible treats: a sip of a sugary solution or a food pellet. The scientists then changed the game, providing the rats with all of the snacks they wanted before giving them the option to press the lever. Satiated, the unstressed rats hit the lever significantly less. But the stressed rats continued pressing at the same rate.

For the second test, the scientists trained the rodents to use two levers, one for each treat. After the rats learned the rules, the researchers picked one treat to dispense randomly, whether or not the rat hit the lever. The relaxed animals hit that treat’s lever less often, while the stressed rats continued to hit both levers with equal frequency.
….
When the scientists studied a region of the rats’ brains called the dorsal striatum, they also found striking differences between the two groups. In stressed rats, neurons in the dorsomedial striatum, an area associated with goal-directed behavior (for example, pressing a lever to get a specific treat), had shrunk, making fewer connections to other cells. Meanwhile neurons in the dorsolateral striatum, an area that controls habits (such as pressing the same lever regardless of outcome), had grown and formed more branches.

For decades, psychiatrists have known that users of PCP, a street drug sometimes called angel dust, have symptoms nearly identical to those of people with schizophrenia. By the 1980s, scientists had discovered that PCP blocked brain receptors that are triggered by an amino acid called glutamate. This led some companies and scientists to study ways to stimulate glutamate receptors as a treatment for schizophrenia.

But the brain has many different kinds of glutamate receptors, and figuring out how to stimulate or block them in medically beneficial ways has proved complicated. Instead of focusing on the receptors blocked by PCP, Dr. Schoepp concentrated on modulating the action of glutamate receptors in the brain’s prefrontal cortex, an area responsible for personality and learning.

The drug, “LY2140023″, is an mGlu2/3 agonist. It showed statistically significant results in a (mid-sized?) clinical trial. Here’s the paper:

Sandeep T Patil, Lu Zhang, Ferenc Martenyi, Stephen L Lowe, Kimberley A Jackson, Boris V Andreev, Alla S Avedisova, Leonid M Bardenstein, Issak Y Gurovich, Margarita A Morozova, Sergey N Mosolov, Nikolai G Neznanov, Alexander M Reznik, Anatoly B Smulevich, Vladimir A Tochilov, Bryan G Johnson, James A Monn & Darryle D Schoepp. Activation of mGlu2/3 receptors as a new approach to treat schizophrenia: a randomized Phase 2 clinical trial. Nature Medicine 13, 1102 – 1107 (2007).

Neurocritic also has a blog post about this.

Reviews the use of photosensitive proteins in neuroscience and even gives a shout-out to Ed Boyden, of Stanford and MIT fame…

– Davie (who had the same advisor as Ed for about a day and is therefore 0.01% more famous by association)

People with Williams syndrome, a genetic disorder, have “trouble with space and numbers” but “a love of company and conversation combined, often awkwardly, with a poor understanding of social dynamics and a lack of social inhibition”. Elsewhere, I believe that Williams syndrome patients have been described as feeling as though everyone is their friend.

The genetic cause of Williams syndrome is known.

The article also goes into the theory that human intelligence and language evolved to deal with large social groups, especially such complexities as deception, and posits that Williams syndrome allows us to dissociate some aspects of social intelligence from others, and from other aspects of intelligence.