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Let’s get straight to business: the best burger at the Society for Neuroscience’s annual meeting, when it is held in Washington DC like this year, is served meters away from the Convention center, in a dark, narrow bar recalling the ones that you can find all over Brooklyn: The Passenger. It’s just the right size, with two thin patties that are cooked medium-rare, american cheese sandwiched between them (I think), grilled onions, lettuce, and a special sauce. You get something that reminded me of the burger at Five Guys, but much more hand-crafted, while still keeping that fast-food burger satisfying taste. It comes with a pickle spear and potato chips (get the salt-and-vinegar flavor!). At $14, it’s quite expensive, but that burger really delivers.
Materials and Methods: The Passenger is in fact the only place I’ve eaten a burger in Washington, but if I can get an even better one anywhere near the Convention center, I’ll happily retract the present publication.
Now that I know where to satisfy my burger cravings in both DC and San Diego (that most welcoming city is the home of the best burger I’ve ever had, at Hodad’s), all I need is to find a place to go in Chicago and I’ll be covered for many SfN’s to come. Tips anyone?
I’m sure that you would like to improve on this terrible pun–feel free to chime in in the comments! And now let’s move beyond the acronym: this post is about a poster that was shown at #SfN14 on Monday morning, November 17, during the session on Executive function: Decision making.
358.21/SS34. Disrupting inhibition in posterior parietal cortex reduces decision accuracy. K. ODOEMENE, A. M. BROWN, M. T. KAUFMAN, A. K. CHURCHLAND
The authors, from Cold Spring Harbor Laboratory, NY, are interested in understanding how sensory information is used by the brain to inform decision making. They trained mice on a visual discrimination task in which the animals had to learn to recognize that a slowly flashing light was associated with a water reward in one location and a faster flash with a reward at another place. They then injected a viral vector encoding a protein known as a DREADD: a designer receptor exclusively activated by a designer drug (really, that acronym is awesome), into the posterior parietal cortex of both hemispheres. The DREADD here was designed to be expressed only in inhibitory interneurons and was meant to suppress their activity. Injecting the DREADD in itself did not alter the animals’ behavior in any way, since there is no ligand for that receptor in the mouse’s organism (in this case, the ligand was a derivative of clozapine that the authors took care to verify was not metabolized by the mice into clozapine itself, a widely-used anti-dopaminergic drug that would likely have altered performance). AFfter injection of the ligand, however, the mice became worse at performing the task. The authors checked that the mice were indeed attempting to perform the task, although they were a little slower than controls, suggesting that the behavioral effect was not due to a general inhibition of brain functions.
The next steps for the authors will include targeting the regions of cortex that are injected using intrinsic signal optical imaging (the posterior parietal cortex of mice, between the somatosensory and visual cortices, is likely a functionally heterogeneous area and it would be important to know whether the injected region is visual or something else) and electrophysiological recordings to find neural correlates of the perceptual and decision-making stages of the task and their alteration by the DREADD-ligand combination.
I liked discovering the DREADD approach, with which I was not familiar, and I am looking forward to reading more about the neural correlates of that experiment.
303.Poster session. Oscillations: EEG.
Monday, Nov 17, 2014, 8 AM-12 PM.
I really enjoy poster sessions and the unique opportunities for interacting with the authors that they offer. This morning, I spent some time at the session on brain oscillations as studied by EEG. Here are highlights from a couple of posters (three, actually) that I had the opportunity to discuss with their authors. My apologies to the presenters whose posters I did not cover. Note that any inaccuracy or outright misunderstanding in what follows is my responsibility alone!
303.03/C39. Phase dependency of long-range neuronal transmission in entrained neuronal networks: A combined tACS-TMS-EEG study. K. D. FEHÉR, Y. MORISHIMA.
303.05/C41. A method for removing tACS artifacts from EEG data. Y. MORISHIMA, K. D. FEHÉR.
The authors of these posters, from the University of Bern, Switzerland, have combined seemingly for the first time transcranial alternating current stimulation (tACS), a noninvasive approach to modulate brain rhythms, together with transcranial magnetic stimulation (TMS), which allows sending brief, sudden pulses of simulation to the cortex, and EEG recordings.
First of all, they had to find a way of removing the tACS artifact that was orders of magnitude larger than the actual brain signals in the EEG (poster C41). Their approach involved upsampling of the EEG signals so that the EEG sampling rate was a multiple of the tACS frequency, trigger timing adjustment , then moving-window average filter, and finally PCA. Using that method, the authors were able to retrieve clean EEG and visual evoked potentials.
The authors then investigated how the phase of ongoing brain oscillations, here imposed by the tACS (6 Hz delivered to both frontal and parietal areas using 2 stimulators), influenced brain responses to sudden, punctual stimulation delivered by TMS (poster C39). They found widespread dependence of TMS-evoked potentials on the phase of tACS when both frontal and partial cortex were stimulated in phase. Interestingly, effects were restricted to the posterior electrodes when the phases of stimulation of frontal and parietal cortex were opposed.
Their preliminary results confirm the importance of ongoing brain oscillations in modulating brain responses. The next steps according to the authors will include testing other frequencies of tACS, such as the gamma band.
303.23/C59. An automated seizure onset zone detector using high frequency oscillations. S. GLISKE, W. C. STACEY.
The authors of this poster, from the University of Michigan, were interested in high-frequency oscillations (HFOs), brief periods of oscillatory activity (generally between 80 and 200 Hz) recorded by intracranial EEG in patients suffering from severe epilepsy. It is thought that HFOs are a specific marker of the seizure onset zone (SOZ), the part of the brain where seizures originate from and that should be removed surgically to cure the patients from their epilepsy.
HFOs are hard to detect “visually” by browsing the EEG; therefore, algorithms to detect HFOs have been developed, but perform poorly because there are many “false” detections. The authors therefore developed a series of algorithms that would detect and label those artifacts, avoiding false positives. They tested their algorithm in clinically annotated intracranial EEG recordings from the intracranial EEG portal, a data-sharing initiative (ieeg.org), as well as in data from patients at their local institution.
They found that their automated algorithm detected localized HFOs in just over half of the patients (53%). In all those cases, the HFOs were included either in the SOZ, as labeled by expert clinicians, or in the surgically resected area. These two zones are collectively considered the gold standard for localizing the source of seizures in epilepsy surgery. Importantly, although the current study was retrospective, the algorithm is fast enough that it can be run in real-time as data are collected.
In conclusion, the authors presented a specific, albeit not very sensitive, approach to localizing the seizure onset zone using an automated high-frequency oscillation detector. The next steps according to the authors will include investigating whether HFO detection influences clinical decision making. The possibility to perform data analysis online will prove crucial in that respect.
#SfN14 highlights: Multimodal Investigation of Large-Scale Brain Dynamics: Combining fMRI and Intracranial EEG
007.Minisymposium. Multimodal Investigation of Large-Scale Brain Dynamics: Combining fMRI and Intracranial EEG – Biyu He.
Saturday, Nov 15, 2014, 1:30-4 PM
I made it to DC almost in time to attend all the talks of the mini-symposium on the multimodal investigation of large-scale brain dynamics through functional MRI and intracranial EEG (nice job, Megabus). Altogether, I found that the talks were of a very high technical level, and a good grasp of the analysis techniques generally employed in those studies (especially in intracranial EEG) definitely helped me follow the finer points made by the speakers.
Here are a few highlights from the session. My apologies to the speakers whose talks I did not cover. Note that any inaccuracy or outright misunderstanding in what follows is my responsibility alone!
7.03. Large-scale patterns of cortical rhythmic suppression in human cerebral cortex – Christopher Honey
In his talk, Dr. Honey, from the University of Toronto, presented results on the relationship between cortical low-frequency rhythms (think theta, alpha and low beta, or between 4 and 30 Hz) and high-gamma power (HGP, approximately 70 to 180 Hz), a non-rhythmic portion of the intracranial EEG’s power spectrum that is a good proxy for local neuronal firing. The data came from intracranial electrodes implanted in patients with epilepsy who were going to have surgery in an attempt to remove the focus of their seizures. When the patients were performing an audiovisual task (watching a movie), Honey observed an inverse relationship between the power of the low-frequency alpha rhythm and that of the high-gamma band in the occipital cortex. Similarly, he found anti-correlation between the perirolandic beta rhythm (an oscillation that is most intense when the patients were idling, as opposed to moving their hands for instance) and HGP. At a more global level, he noted that the frequency that was most strongly anti-correlated with HGP varied across cortical areas (it was mostly theta in the temporal lobe and a mixture of theta and low beta in the prefrontal cortex). Crucially, however, that frequency was also the same one that dominated the power spectrum of spontaneous oscillations. Honey found a similar relationship between the low frequencies that displayed the highest modulation of HGP (so-called cross-frequency phase-power coupling) and spontaneous oscillations. He therefore put forward the idea that these low-frequency cortical rhythms may provide pulsed inhibition of local cortical activity (suppressive rhythms). Intriguingly, Honey also observed maximal anti-correlations between the power of low-frequency rhythms and the BOLD signal (collected before the patients were implanted with electrodes), which serves as a reminder that HGP and BOLD probably reflect partly the same underlying neuronal mechanisms.
Note that a question that remains open is why are different cortical areas oscillating at different baseline frequencies. I wonder whether it reflect some basic periodic or rhythmic property of e.g. visual inputs to the occipital cortex or motor outputs from the motor cortex…
7.04. Cognitive electrophysiology of the human medial parietal cortex: Local and network dynamics – B. Foster
Dr. Foster, from Stanford University, focused on the parietal cortex, parts of which have often been observed to be more active when subjects were apparently “not doing much” in the functional MRI scanner (hence they were dubbed part of the so-called default mode network, DMN). It is also known that the parietal cortex–especially the medial aspect, the posterior cingulate cortex (PCC) and retrosplenial cortex (RSC)–also activate during the retrieval of autobiographic memories. Dr. Foster and colleagues therefore designed an intracranial EEG task that would allow disentangling the engagement of those cortical areas during autobiographical retrieval tasks as opposed to more general, non self-centered memory retrieval or arithmetic. He found that, indeed, the PCC and RSC were selectively activated by self-episodic and self-semantic retrieval tasks. Interestingly, the angular gyrus also showed activation, and the two areas displayed correlated activity across single trials, validating the idea that they are part of a coherent functional network during those tasks.
7.05. Cross-frequency coupling in the cortical columnar microcircuit – A. Maier
Dr. Maier, from Vanderbilt University (Nashville, TN), explored cross-frequency phase-power coupling using intracortical recordings across the layers of the cerebral cortex in monkeys (so-called laminar recordings). He found that HGP in the supra- and infra-granular layers of the cerebral cortex are coupled to the phase of alpha oscillations, whereas HGP in the granular layer (that receives feed-forward input from the thalamus) did not display such a relationship. Dr. Maier used current source density (CSD) analysis to determine that the infra-granular layers were likely responsible for the drops in firing rate throughout the thickness of the cortical column. Therefore, he hypothesized, layer 6 neurons might be responsible for transiently shutting down the propagation of feed-forward activity through the cortical column micro-circuit, allowing instead feed-back inputs (that mostly reach the supra- and infra-granular layers) to exert their influence.
7.07. Multimodal imaging of spatio-temporal dynamics in language processing – T. Thesen
Dr. Thesen, from New York University, focuses on the processing of both written and spoken language using a combination of functional MRI, magnetoencephalography (MEG, a technique that records very similar signals to EEG) and intracranial EEG in epilepsy patients. The first experiment that he presented was concerned with written language. Using strings of pseudo-letters vs. pseudo-words made up entirely of consonants vs. actual words, he showed that there was a spatial gradient in the complexity of responses, ranging from specific to real letters vs. pseudo-letters in more posterior parts of the occipito-temporal cortex to specific to real words vs. pseudo-words in more anterior parts of that visual processing stream. Interestingly, Dr. Thesen’s use of electrophysiological techniques also revealed a temporal gradient, in that letter-specific responses started earlier after the appearance of the stimuli than word-specific responses.
In a second study, Dr. Thesen took advantage of the well-characterized McGurk effect (an audiovisual illusion caused by mismatched auditory and visual speech syllables–check out this Youtube video for an example!). When contrasting the response of the brain to audiovisual syllables to the combination of audio-only or video-only stimuli, he found that multisensory effects appeared very early in the auditory cortex (40 ms after sound onset), then a bit later in the left superior temporal sulcus (80 ms), and later again in the left inferior frontal gyrus (120 ms). The very early multisensory effects in the auditory cortex point to a direct, feed-forward effect of visual stimuli through the visual cortex to the early auditory areas. Interestingly, Dr. Thesen’s data even point towards the role of pre-stimulus activity in the visual cortex in the multisensory effects observed in the auditory cortex.
Altogether, a very interesting symposium with talks of a very high technical level that presented for the most part unpublished results. The attendance looked great, with several people sitting on the floor behind the rows of chairs!
Dr. Thesen’s results in particular were very interesting to me, as my own research tackles very similar subjects using similar methods. Check out my poster, Tuesday afternoon, where I’ll be happy to tell you more about this fascinating subject! 623.06/DD4. Phase tracking of visual speech in the human auditory cortex revealed by intracranial EEG.
I’m happy to announce that I’ll be one of the Society for Neuroscience’s official bloggers during the 2014 Annual Meeting, starting this Saturday November 15 in Washington DC. What does it mean? Essentially, that the SfN links to my blog (I will also try and cross-post on the SfN’s own platform, NeurOnLine–see here, for instance). Note that I’m also an editor for the PLOS Neuroscience Community, and we’ve put together a group of bloggers and tweeters who will provide collaborative coverage of the conference. So, given the many sources of information about the meeting that are available to you, why should you read this blog at all? Here, I’ll try to tell you what I intend to write about, so that you can make up your mind (and perhaps also learn about that awesome poster session that you somehow missed when preparing your itinerary!).
I like studying brains in their working environment, the body, hence I’ll focus on in vivo studies. I will report mostly on human neuroscience, with some work in other mammals thrown in (I worked with mice and rats during my PhD). My interests range from sensory perception through multisensory integration to cognition. As someone with dual training in neuroscience and neurology, I’m always interested in work on diseases or in patients–particularly those suffering from epilepsy. My method of predilection is electrophysiology, and especially intracranial EEG in humans, therefore I’ll be reporting on various studies that use that approach. Also, video games and music are important to me, so you can expect that I’ll be keeping an eye on studies about either (or both: if your poster title is “Experienced players of Rock Star have better multisensory discrimination abilities: an EEG study”, give me a call!). Finally, I spend most of my time on the poster floors, because I appreciate the interaction with the authors that posters allow, and that you don’t get at a talk.
What follows is a tentative list of what I would like to attend:
Sunday 1-3 PM: The Neuroscience of Gaming (WCC 201). I’ll post something about this one for sure.
Sunday 1-5 PM: Functional mechanisms of attention 1 (posters RR16-RR40).
On Sunday afternoon, I also warmly recommend the Symposium on studying human cognition with intracranial EEG and electrical brain stimulation, but since I already saw half of the talks at Human Brain Mapping 2014 this summer, I’ll pass this time.
Monday 8-12 AM: Oscillations: EEG (posters C37-C59). I’m especially happy to announce my colleague David Groppe’s poster, Electrocorticographic oscillatory connectivity predicts low frequency resting state functional magnetic resonance imaging connectivity. The man has a blog, too, and an excellent one at that! His presentation time is 10 AM.
Monday 8-12 AM: Multisensory and Temporal Factors in Cross-Modal Processing (posters DD8-DD25).
Also on Monday morning at 8 AM, I’ll try to visit poster M6, An EEG methodology to localize the irritative cortices in a preclinical model of focal epilepsy, by the group of J. Riera from Miami, and poster VV17, Elucidating brain network dynamics with resting-state fMRI and electrocorticography, from J. Parvizi’s team in Stanford. That’s going to mean a lot of walking, but hey, SfN is work!
Monday 3:15-4:25 PM: Cellular and Molecular Mechanisms of Explicit Learning in the Hippocampus – Roger A. Nicoll (WCC Hall D). The large SfN lectures are often extremely good–if you attended last year’s meeting in San Diego, you might remember the stellar presentation given by Doris Tsao. I’m very much looking forward to hearing Dr. Nicoll review long-term potentiation (LTP), our best candidate for the neural substrates of memory.
Tuesday 8-12 AM: Auditory Processing: Temporal, Frequency, and Spectral Processing-Perception (posters FF2-FF12).
Tuesday 1-5 PM: Multisensory: Cross-Modal Processing in Humans, Audio-Visual (posters CC35-DD11). I’ll be presenting my own poster, Phase tracking of visual speech in the human auditory cortex revealed by intracranial EEG. Yay! My presentation time is 2 PM.
Another poster on which I worked will be presented by my PI, Ashesh Mehta, Tuesday at 3 PM (SS18): Failure of the default mode network to deactivate precedes attentional lapses: An intracranial EEG study.
Also on Tuesday afternoon are interesting poster sessions on Human Studies of Epilepsy (posters L10-O1) and Auditory Processing: Human Studies of Perception, Cognition, and Action (posters CC7-CC34). I probably won’t have the time to check those out in detail, but once you are done visiting my poster, you might want to give them a look!
Wednesday 1-4 PM: Predictive Coding: Human Cognition (WCC 152A).
Two of my colleagues, Ido Davidesco and Corey Keller, will present their work, A causal role of the fusiform face area in face perception, on Wednesday at 4 PM (poster II19) (you’ll have to postpone that early flight back home, I’m afraid).
Now, all work and no play makes Jack a dull boy: you can expect the odd post about the commercial exhibition, the bus ride to DC, the social events, the best burger/ramen/pizza within 5 blocks of the convention center…
Here I briefly introduce one of the sessions I will blog about at SfN 2014, together with a short interview of Dr. Adam Gazzaley, one of the speakers at the session. The definitive version of this post was originally published on November 11 2014 on the PLOS Neuroscience Community website, where I serve as an editor.
ME08. The Neuroscience of Gaming. Social Issues Roundtable
Sunday, Nov 16, 2014, 1:00 PM — 3:00 PM. WCC 201
Featured speaker: Adam Gazzaley
One of the sessions that I’m most looking forward to at the SfN’s 2014 annual meeting is the Roundtable on the Neuroscience of Gaming. Why? Well, I started playing video games since I was in primary school, and they have been part of my life ever since. The Roundtable will bring together four speakers with varied backgrounds and expertise:
- Daniel Greenberg is the president of Media Rez, a software and game development studio based in Washington DC whose goal is to develop games that support behavior change in health and learning.
- Adam Gazzaley directs a cognitive neuroscience lab at the University of California in San Francisco that focuses, among others, on developing custom-made video games to improve cognitive functions.
- Mark Griffiths, from Nottingham Trent University, in the UK, specializes in behavioral addictions such as gambling and video gaming addictions.
- Martha Farah, who heads a cognitive neuroscience lab the University of Pennsylvania, will focus on the ethical and social aspects of using neuroscience in games.
I’m particularly interested in hearing about Dr. Gazzaley’s work. I’ve been thinking for a while that video games, in addition to being a great form of entertainment (and a cultural artefact!), represent fantastic tools to probe the function of the brain. Think about it: you are being exposed to complex, multisensory stimuli (obviously visual and auditory, but also tactile through vibrating controllers for instance), to which you have to respond by specific motor commands in a precise temporal window. The whole thing is orders of magnitude more engrossing than a typical psychophysical experiment, yet the basic principles remain. If you are able to intervene in the design of the game to have the player perform a task in which you’re interested, retrieve from the system when game events are happening, and synchronize that with measurements of brain activity, you can use video games as a very powerful scientific tool.
Well, Dr. Gazzaley and his team are doing precisely that — and more, since (among others) they are also adding non-invasive brain stimulation to their armamentarium. If you would like to know more about Dr. Gazzaley’s previous and current work, look to his study on how training on a custom-designed video game improved cognitive abilities in older adults, which was published by Nature last year (it was also highlighted on the cover, and it’s a very good one, too). More recently, Dr. Gazzaley was interviewed in a New York Times Magazine article on the controversy surrounding the “brain training” industry. He is also among the signatories of a recent consensus paper from the scientific community on the same issue. We can expect to hear more about this fascinating subject during the Roundtable.
Five Questions to: Adam Gazzaley
What, in your view, is the one most exciting finding that neuroscience has produced?
Evidence describing the anatomy and physiology of neuroplasticity.
If you could use a magic wand to improve one aspect of how research is conducted, what would you do?
The convergence of different perspectives and methodologies on the same issue would be more common.
What aspect of your research work do you prefer?
Working as a team with a group of intelligent and inspired people.
Is your career similar to what you had in mind as an undergraduate?
Similar, but more involved with health that I ever imagined.
What advice would you give an undergraduate neuroscience major (or recent graduate) about how best to advance in the field?
Search what you love to do, and don’t be afraid to think different.
I would like to thank Dr. Gazzaley for taking the time to answer my questions. I hope that I have convinced you to attend the Social Issues Roundtable on the neuroscience of gaming — but in case you missed the live session, I’ll blog about it, so keep watching this space!