Watch it online at the TED website.

I’m a fan of it because it is an open-access journal featuring a “tiered system” and more.  From their website:

The Frontiers Journal Series is not just another journal. It is a new approach to scientific publishing. As service to scientists, it is driven by researchers for researchers but it also serves the interests of the general public. Frontiers disseminates research in a tiered system that begins with original articles submitted to Specialty Journals. It evaluates research truly democratically and objectively based on the reading activity of the scientific communities and the public. And it drives the most outstanding and relevant research up to the next tier journals, the Field Journals.

I’m a big fan of the variety of specialty journals they have:

• Aging Neuroscience
• Behavioral Neuroscience
• Cellular Neuroscience
• Computational Neuroscience
• Enteric Neuroscience
• Evolutionary Neuroscience
• Human Neuroscience
• Integrative Neuroscience
• Molecular Neuroscience
• Neural Circuits
• Neuroanatomy
• Neuroenergetics
• Neuroengineering
• Neurogenesis
• Neurogenomics
• Neuroinformatics
• Neuromethods
• Neuropharamacology
• Neuroprosthetics
• Neurorobotics
• Synaptic Neuroscience
• Systems Neuroscience

Interviews Boyden and Deisseroth. Follow the link a video of an optogenetically controlled mouse.

Some shortcomings of step ChR2 and future research directions:

Deisseroth expects ongoing efforts to improve key features of these channels. “One disadvantage is that some of the mutants have reduced current compared to wild type, so multiple mutations may help to bring those current levels back up to wild-type levels,” he says. Projects designed to improve membrane targeting and to apply a composite of opsins, including the red light–responsive channelrhodopsin from Volvox carteri, are also in the works in his laboratory.

The subcellular organization of neocortical excitatory connections : Article : Nature.

They used ChR2 (with TTX and 4-AP to block action potentials) to find where on the dendritic tree particular inputs synapsed onto L3 and L5 cells and to measure the strength of those inputs. ChR2 depolarizes the input axon locally (60um spot diameter) at points of (potential) axodendritic contact. If you’ve heard the term “potential synapse” before, then think of this technique as a way of checking potential synapses and seeing if there really is an actual synapse there.

The technique allowed them to map on a L3 barrel cortex pyramidal cell where different thalamic inputs (VPm, POm) and cortical inputs (M1, barrel L2/3, barrel L4):

sCRACM stands for subcellular ChR2-assisted circuit mapping.

Another channelrhodopsin breakthrough from Deisseroth’s lab. This time light is not required to keep the channel open. Light merely triggers opening and closing behavior. Blue-shifted light opens channels and red-shifted light closes them. This looks like another potentially powerful neurotechnology for interrogating circuits and systems.

Relevant fig:

An amazing paper from Neuron demonstrating adaptive (circadian clock-governed) binning in the retina, based on dopamine modulation of gap junction (electrical) synapses between retinal photodetectors. During the day, abundant dopamine release weakens gap junctions coupling rods and cones together so that visual acuity is high. When light is scarce (at night), there is less dopamine and the electrical coupling between rods and cones is increased. This is analogous to on-chip binning in CCD (digital) cameras. Binning increases signal (in light-limited systems, eg. seeing at night) by increasing optical input area and by reducing single element noise (ie. noise at different photoreceptors should be independent) at the cost of resolution. So, the retina activates photoreceptor binning at night to boost low-light signals and deactivates it during the day to increase resolution. The dopamine comes from cells in the interplexiform layer, whose dopamine release is itself governed by melatonin projections.

Also, I never knew that gap junction strengths were directly modifiable. It looks like the D2 receptors are G-protein coupled to PKA, which acts on the gap junctions.

Right now, it appears that there’s a bit of controversy in the field. Earlier this year, in Science, a group from Rockefeller found that DEET masked sensitivity to human odors by interfering with a particular odorant receptor. This impressive result was recently question by entomologists from UC-Davis in a PNAS paper claiming that DEET acts directly on a particular olfactory receptor neuron and does not attenuate the response to the same human-emitted odorant, as found in the earlier paper. Although the results appear to be conflicting, the studies use different techniques and thus it is likely that DEET’s action might be more complex than either paper claims. Still, the idea of identifying a target for chemical intervention by looking at electrophysiological responses to DEET is smart.

In related work, earlier this year a group from Colorado State University, as described in this PNAS overview, “conducted a rigorous search of a library of N-acylpiperidines, using an artificial neural network to identify strong candidates, and then tested them in the laboratory on human volunteers.” They found a candidate molecule that has a ~4X longer repellency effect than DEET. Here’s a photo from the experiments (DEET vs. untreated hand)… ouch!