Maybe junk DNA is not junk?

Short blocks from the noncoding parts of the human genome have instances within nearly all known genes and relate to biological processes — Rigoutsos et al. 103 (17): 6605 — Proceedings of the National Academy of Sciences

Not directly neuroscience-related but this is a pretty cool paper nonetheless. Basically, the authors use automated pattern recognition to pick out small strings in the “non-coding” regions of the human genome. They show that these pyknons are found at regular distances within coding regions and UTRs. Even more intriguing is that

approx. 40% of the known microRNAs are similar to 689 pyknons and that the pyknons subsume 56 of the 72 recently reported 3′ UTR motifs, lending further support to the possibility of a connection between the pyknons and RNAi/PTGS.

Both RNAi (RNA interference) and PTGS (post-transcriptional gene silencing) have recently been found to be major regulatory mechanisms for endogenous gene silencing and regulation. Here’s a link to a primer on PTGS and RNAi.

NMDA receptor might not be coincidence detector for LTD side of STDP

Two Coincidence Detectors for Spike Timing-Dependent Plasticity in Somatosensory Cortex — Bender et al. 26 (16): 4166 — Journal of Neuroscience

Dan Feldman’s group at UCSD has found that different “sides” of STDP (ie. LTP vs. LTD) at cortical synapses might be mediated through distinct signalling pathways. The major finding was that LTD was induced independent of NMDA receptors. Rather, LTD required mGluRs and VGCCs.

There are many questions here. The most interesting to think about is, Are we going to find different STDP rules all over the brain? And, if so, what will be the commond ground between them?

Here’s the abstract:

Many cortical synapses exhibit spike timing-dependent plasticity (STDP) in which the precise timing of presynaptic and postsynaptic spikes induces synaptic strengthening [long-term potentiation (LTP)] or weakening [long-term depression (LTD)]. Standard models posit a single, postsynaptic, NMDA receptor-based coincidence detector for LTP and LTD components of STDP. We show instead that STDP at layer 4 to layer 2/3 synapses in somatosensory (S1) cortex involves separate calcium sources and coincidence detection mechanisms for LTP and LTD. LTP showed classical NMDA receptor dependence. LTD was independent of postsynaptic NMDA receptors and instead required group I metabotropic glutamate receptors and calcium from voltage-sensitive channels and IP3 receptor-gated stores. Downstream of postsynaptic calcium, LTD required retrograde endocannabinoid signaling, leading to presynaptic LTD expression, and also required activation of apparently presynaptic NMDA receptors. These LTP and LTD mechanisms detected firing coincidence on ~25 and ~125 ms time scales, respectively, and combined to implement the overall STDP rule. These findings indicate that STDP is not a unitary process and suggest that endocannabinoid-dependent LTD may be relevant to cortical map plasticity.

Inferring network activity on a MEA from pairwise correlations

Weak pairwise correlations imply strongly correlated network states in a neural population : Nature

Very few MEA studies make it into Nature, so this definitely got my attention.

Often in neuroscience we are confronted with a small sample measurement of a few neurons from a large population. Although many have assumed, few have actually asked: What are we missing here? What does recording a few neurons really tell you about the entire network?

Using an elegant prep (retina on a MEA viewing defined scenes/stimuli), Segev, Bialek, and students show that statistical physics models that assume pairwise correlations (but disregard any higher order phenomena) perform very well in modeling the data. This indicates a certain redundancy exists in the neural code. The results are also replicated with cultured cortical neurons on a MEA.

Some key ideas from the paper are presented after the jump. Continue reading

I know what you're attending to!

Neuron : Dynamics of Parietal Neural Activity during Spatial Cognitive Processing

Here’s John Lisman’s review of this paper (from Georgopoulos’s group)… I don’t think I can say it better than him:

If ever there was a paper that would bring tears to one’s eyes, this is it: a previously hidden mental process has now become subject to experimental study. The mental process is the covert movement of attention, the selective focussing of attention to subregions of the visual field, but without eye movement. The movements of covert attention were hypothesized based on psychophysics, but the authors can now follow it using a vector field derived from a population of neurons in the parietal cortex. The monkey has been trained to use covert attentional shifts to solve a maze task. The major finding is that the vector derived from the population of parietal cells follows in time the path through the maze, as the monkey solves the maze.

From the abstract:

We found that the direction of the followed path could be recovered from neuronal population activity.

Yet another scary but cool result…

Tools for analyzing dendrites

From the Apr 20 issue of Neuron: Integrative Properties of Radial Oblique Dendrites in Hippocampal CA1 Pyramidal Neurons (or, for those who want just the N&V’s summary: Dendritic Enlightenment: Using Patterned Two-Photon Uncaging to Reveal the Secrets of the Brain’s Smallest Dendrites)

The technology is essentially high-speed two photon uncaging of glutamate, but the authors have used it here to create “realistic” patterns of dendritic input in an attempt to see just how dendritic arithmetic works. Although I haven’t read the paper closely, they claim to work out the spatiotemporal parameters underlying dendritic spike generation for pyramidal neurons.

A related methodology paper from a recent J. Neurophys. also uses fast acousto-optic deflectors and two-photon but for imaging purposes. It’s more descriptive about the setup and techniques for those interested in doing this type of work.

Social isolation delays the positive effects of running on adult neurogenesis

Social isolation delays the positive effects of running on adult neurogenesis – Nature Neuroscience

From the Apr 9, Nature Neurosci:

Social isolation delays the positive effects of running on adult neurogenesis
Alexis M Stranahan, David Khalil & Elizabeth Gould

Social isolation can exacerbate the negative consequences of stress and increase the risk of developing psychopathology. However, the influence of living alone on experiences generally considered to be beneficial to the brain, such as physical exercise, remains unknown. We report here that individual housing precludes the positive influence of short-term running on adult neurogenesis in the hippocampus of rats and, in the presence of additional stress, suppresses the generation of new neurons. Individual housing also influenced corticosterone levels—runners in both housing conditions had elevated corticosterone during the active phase, but individually housed runners had higher levels of this hormone in response to stress. Moreover, lowering corticosterone levels converted the influence of short-term running on neurogenesis in individually housed rats from negative to positive. These results suggest that, in the absence of social interaction, a normally beneficial experience can exert a potentially deleterious influence on the brain.