It is now possible to map the activity of nearly all the neurons in a vertebrate brain at cellular resolution. What does this mean for neuroscience research and projects like the Brain Activity Map proposal? Read more
Again, we’re behind on blogging – you guys are keeping us busy with great neuroscience – but here is the story of a pair of papers that appeared back to back in last week’s issue and a continuation of the discussion started here by Noah about the process of joint publication. The two papers by Tobias Boeckers and colleagues and by Eunjoon Kim and colleagues were independently submitted and both describe autism-like phenotypes of mice with mutations in the gene Shank2. In human studies, SHANK2 has been associated with rare cases of autism and these two mice add to the ever-growing list of rodents (according to SFARI.org, 17 rodent models debuted in 2011 alone) that are being created to investigate the functional consequences of genetic mutations linked to autism, in the hopes of understanding mechanisms underlying core symptoms. Shank2 is a scaffolding protein that regulates excitatory synapse function by holding together various molecules such as neurotransmitter receptors and signaling proteins. Mutations in another member of the same gene family, SHANK3, are also associated with human autism, and mutant mice display behaviors reminiscent of ASD symptoms, such as social deficits and obsessive behavior. So this protein family, and more generally, glutamatergic transmission, is potentially one promising line of investigation. Read more
It really is an embarrassment of riches here at Nature these days, what with so many excellent neuroscience-related studies emerging. Just in the last couple of weeks, we’ve had the following studies: … Read more
Sometimes an experiment will just reach off the page and slap you in the face, demanding attention. This happens to me every so often and I must admit, our latest paper from the lab of Florien Engert induced such an experience. There have been several cool, technical tours-de-force (is that proper grammar??) over the last few years involving different creatures navigating in a virtual environment while neuronal activity was monitored. These include a mouse running on a spherical treadmill, as well as a fly marching along a similar treadmill-style ball. But in these examples, having the subject head-fixed (for the stability of recordings in the brain, either with electrodes or through imaging) was moderately non-intrusive since walking motions were independent of the head. The same can’t be said for the subject in this latest example of a virtual reality navigator: a wriggling, swimming fish. Therefore, a more creative solution had to be sought and in a paper published online yesterday, Ahrens, Engert and colleagues decided that paralysis was the way to go in order to follow the neural activity of this navigating fish. Read more
It is commonly believed that distinct mini-networks of neurons, firing together, may be the means by which memories and other conceptual encoding requirements are handled in the brain. However, it is only recently that we have had the tools available to directly test the sufficiency of such a mechanism. Today, a new study in Nature from the lab of Susumu Tonegawa documents the ability to use light as a means to activate distinct subsets of neurons responsible for the encoding of fear memories. Read more
You warily walk into a dark compartment, wondering if there is food inside. Suddenly there is a loud tone and you feel an uncomfortable surge of electricity through your feet. This goes without saying, but it won’t take long before you will learn to be afraid of that tone. However, over time, you hear the tone without the shock, and slowly (foolishly??) accept that the previous connection may no longer hold. Read more
Alzheimer’s disease (AD) is a devastating neurodegenerative disease that could become an even more massive public health problem than it already is, if current projections hold. Some predict that by 2050, 1 in 85 individuals will be affected by the disease. Currently, there is no cure, but there are neurotransmitter-enhancement-based strategies to slow down the cognitive deficits [the loss of cholinergic neurons is implicated in some of the memory problems associated with AD so therefore, pharmacological enhancement of brain acetylcholine concentration can partially alleviate some memory-based symptoms.] However, as with many neurodegenerative diseases, these stop-gap treatments only work for so long, until the cells responding to neurotransmitter supplementation treatments die off completely. Therefore, diverse strategies designed to cure or at least slow down AD are imperative. Read more
