The neocortex is an evolutionarily new part of the brain unique to mammals and is responsible for high level sensation, movement and cognition. It wouldn't be fair to summarize in a sentence or two what cortex "does," but it is clear that it is an important part of the brain. Korbinian Brodmann famously divided the human cortex into about 50 areas based on histology of the six cortical layers in different parts of the brain; Brodmann's areas are still used today because their functions follow their histological structure. While cortical areas have largely stereotyped wiring patterns, some connectivity “motifs” are thought to be area-specific, varying based on the type of input the area receives. It is unknown whether the type of input (i.e. statistics of incoming activity that vary with types of sensory stimuli) to a given cortical area determines the types of connectivity motifs present in that region. And while classical cortical “rewiring”experiments from Mriganka Sur’s lab have shown that primary sensory cortices are somewhat tolerant to process foreign inputs, it is not clear to what extent those circuits constitute basic computational units or if foreign inputs cause reorganization of connections within the circuit.
Preparing for SfN 2011, I have to give a shout-out to one of the coolest emerging technologies in neuroscience, optogenetics. Optogenetics, as everyone no doubt knows by now, is a method that allows researchers to control the electrical activity of neurons using light. Scientists infect certain types of neurons with an algae transmembrane channel protein that allows the flow of ions into a cell when light of preferred wavelength shines upon it. The method has been described well elsewhere (Steve Ramirez waxes poetic about it on the Mind the Gap Junction blog). Optogenetics is an amazing method for many reasons, but mainly because by allowing us to directly activate or silence neurons, it makes it possible to establish causal relationships in neural circuits: if neuron A is hyperactive, the mouse runs around in circles; if A is silenced, perhaps the mouse is unable to run in circles; therefore, activity in neuron A causes the mouse to run in circles. This is important because traditional electrophysiological methods allow us to only record activity without manipulating it directly (stimulating electrodes are rather crude spatially), and the methods that did allow us to manipulate activity (i.e. pharmacology or stimulating electrodes) have a myriad of effects that make precise causes of behavior unclear (i.e. does TTX act only on sodium channels? Which types? etc).
As optogenetics becomes more and more refined and widespread, I can't help to wonder what it will do for the most prevalent of neurological diseases. Will this method cure Alzheimer's? How about Parkinson's? Optogenetics promises to show us circuit-level interactions among neurons and perhaps even to nail down the network effects of particular diseases. But if we're looking to find cures for diseases instead of just fixes, we ought to not forget our molecular biologists and maybe even geneticists. That's not to say that treatments for neurological diseases are worthless! There are, after all, no cures for any brain diseases so far - so anything will be useful. With all this enthusiasm over optogenetics, we have to be honest about its capabilities and limitations.