Friday events are in Mellon Institute, CMU
Saturday talks are in 120B Lawrence Hall, Pitt
Poster Session and Dinner are in the Assembly Room and Ballroom, William Pitt Union, Pitt
FRIDAY, May 4, 2018
|5:30–8:30 PM||Student/Post Doc Data Blitz – Dinner – Social
328 & 348 Mellon Institute (Social Room & Conference Room)
SATURDAY, May 5, 2018
|9:00 AM||WELCOME – Faculty Organizers
Avniel Ghuman, Neurosurgery, Pitt
Sandy Kuhlman, Biological Sciences, CMU
120B Lawrence Hall, Pitt
McCLELLAND AWARDS (Student)
|9:10-9:40 AM||Uday Jagadisan
Bioengineering, University of Pittsburgh
Removal of inhibition uncovers latent movement potential during preparation (abstract)
|9:40-10:10 AM||Elliot Collins
Psychology, Carnegie Mellon
Numerosity representation is encoded in human subcortex (abstract)
STRICK AWARDS (Postdoc)
Neuroscience, University of Pittsburgh
Learning and attention reveal a general relationship between population activity and behavior (abstract)
|11:00-11:30 AM||Brian Coffman
Psychiatry, University of Pittsburgh
Reduced auditory segmentation potentials in first-episode schizophrenia (abstract)
|11:30 AM-1:30 PM||Lunch / Free Time
Please pick up a box lunch in the Lawrence Hall lobby. Seating is available in the Lower Lounge of the William Pitt Union
|1:30-2:00 PM||Entertainment / Community Building
120B Lawrence Hall, Pitt
|2:00-2:30 PM||Panel Discussion – Quantitative Analysis of Behavior
Avniel Ghuman, Neurological Surgery, Pitt
George Wittenberg, Neurology, Pitt
Eric Yttri, Biological Sciences, CMU
Moderator: Nathan Urban, Pitt
|2:45-3:15 PM||John Anderson, Richard King Mellon Professor Psychology and Computer Science
Psychology & Computer Science, Carnegie Mellon University
Combining Space and Time in the Mind (abstract)
|3:15-3:45 PM||Fabio Ferrarelli, Assistant Professor
Psychiatry, University of Pittsburgh
Are sleep spindle deficits a biomarker of Schizophrenia? (abstract)
|3:45-4:15 PM||Colleen McClung, Professor
Psychiatry and Translational Science, University of Pittsburgh
Circadian genes, rhythms, and the biology of psychiatric disorders (abstract)
|4:30-5:30 PM||Keynote: Leslie Griffith, M.D., Ph.D.
Nancy Lurie Marks Professor of Neuroscience,
Director, Volen National Center for Complex Systems
Sleep and memory in Drosophila melanogaster(abstract)
|5:30 PM||Poster Session
Assembly Room, William Pitt Union
Ballroom, William Pitt Union
|7:30-8:30 PM||Poster Session Continues – Winners Announced|
I will describe how we have combined hidden semi-Markov models (HSMM) and multi-voxel pattern matching (MVPA) and to discover sequences of mental states. I will provide evidence on the accuracy this HSMM-MVPA method in an experiment where we have access to ground truth about what the mental states are. I will describe analyses of how the success of this method varies with signal-to-noise ratio in the experimental data, power of the experiment, number of states to be recovered, and duration of the states.
Sensory perceptual deficits in schizophrenia are present before emergence of psychotic symptoms, persist throughout life, and are related to functional outcome. Impairments in perceptual processes that rely on the coordination of sensory and cognitive systems, such as sequence learning, may play a fundamental role in the pathophysiology of schizophrenia. We recently discovered the auditory segmentation potential (ASP), a brainwave that indexes auditory sequence grouping, and we demonstrated that this brainwave is not only impaired in schizophrenia, but also in individuals at their first episode of psychosis, where ASP was reduced by 40%. Further, ASP source activity within the brain was reduced specifically within midcingulate cortex (MCC), an area linked to aberrant perceptual organization, negative symptoms, and cognitive dysfunction in schizophrenia. This suggests that ASP may be useful as an early index of schizophrenia-related MCC dysfunction and may serve as a viable biomarker of disease presence.
Certain numerical abilities appear to be relatively ubiquitous in the animal kingdom, including the ability to recognize and differentiate relative quantities. This skill is present in human adults and children, as well as in nonhuman primates and, perhaps surprisingly, is also demonstrated by lower species such as mosquitofish and spiders, despite the absence of cortical computation available to primates. This ubiquity of numerical competence suggests that representations that connect to numerical tasks are likely subserved by evolution-arily conserved regions of the nervous system. Here, we test the hypothesis that the evaluation of relative numerical quantities is subserved by lower-order brain structures in humans. Using a monocular/dichoptic paradigm, across four experiments, we show that the discrimination of displays, consisting of both large (5–80) and small (1–4) numbers of dots, is facilitated in the monocular, subcortical portions of the visual system. This is only the case, however, when observers evaluate larger ratios of 3:1 or 4:1, but not smaller ratios, closer to 1:1. This profile of competence matches closely the skill with which newborn infants and other species can discriminate numerical quantity. These findings suggest conservation of ontogenetically and phylogenetically lower-order systems in adults’ numerical abilities. The involvement of subcortical structures in representing numerical quantities provokes a reconsideration of current theories of the neu-ral basis of numerical cognition, inasmuch as it bolsters the cross-species continuity of the biological system for numerical abilities.
Schizophrenia (SCZ) is a leading cause of disability worldwide, thus making the early identification of biomarkers for this disorder a critical research priority. In recent work, we found that individuals with chronic SCZ had a striking deficit in sleep spindles. A hallmark of Stage 2 NREM Sleep, spindles are short (0.5-2 s), waxing/waning oscillations in the 12-16 Hz range. By investigating individual spindle parameters, we established marked deficits in spindle amplitude, duration, and density in chronic SCZ patients relative to healthy and psychiatric control groups. Here, we present data from an ongoing study where we extended these findings to first-break psychosis (FEP) patients. Specifically, we performed sleep high density (hd)-EEG recordings in twenty FEP and twenty healthy controls (HC), and several sleep spindle parameters were calculated and compared across groups. Spindles, and especially spindle density, were reduced in FEP with SCZ, but not in FEP with other diagnoses, relative to HC. A reduction in spindle density was found in a fronto-central area and predicted the severity of SCZ patients’ negative symptoms. Altogether, the present findings indicate that abnormalities in sleep spindles are present at the beginning of psychosis, and that spindle deficits are specifically implicated in the neurobiology of SCZ, for which they may represent a trait biomarker. Building on these findings, we are currently investigating spindle abnormalities in youth at Clinical High Risk (CHR), a unique population enriched for precursors of major psychiatric disorders, such as SCZ, which will help assessing whether spindle abnormalities predate and predict the onset of this disorder.
Sleep is known to affect memory formation and recall in both humans and animals. The molecular and cellular mechanisms underlying this interaction are obscure. In Drosophila, the cellular basis of memory formation is well-described. Associative memory is formed in the mushroom body (MB) neuropil where sensory information and valence information converge. Long-term memory (LTM) formation requires the activity of an additional modulatory input from a pair of cells called the DPMs. Blockade of DPM output in a short window after training blocks LTM formation, but spares short-term memory. Several years ago, while investigating the cellular basis of GABAergic regulation of sleep we discovered that the DPMs were GABAergic and that their activation was strongly sleep-promoting (Haynes et al., 2015). I will describe ongoing work that addresses the connectivity of DPMs in the MB circuit and its role in memory consolidation.
The motor system prepares for movements well in advance of their execution. In the gaze control
system, the dynamics of preparatory neural activity have been well described by stochastic
accumulation-to-threshold models. However, it is unclear whether this activity has features
indicative of a hidden movement command. We explicitly tested whether preparatory neural activity
in premotor neurons of the primate superior colliculus has ‘motor potential’. We removed downstream
inhibition on the saccadic system using the trigeminal blink reflex, triggering saccades at
earlier-than-normal latencies. Accumulating low-frequency activity was predictive of eye movement
dynamics tens of milliseconds in advance of the actual saccade, indicating the presence of a latent
movement command. We also show that reaching a fixed threshold level is not a necessary condition
for movement initiation. The results bring into question extant models of saccade generation and
support the possibility of a concurrent representation for movement preparation and generation.
Nearly all people suffering from psychiatric disorders have significant disruptions in circadian rhythms and the sleep/wake cycle. Furthermore, disruptions to circadian rhythms including shift work, overseas travel, and irregular social schedules tend to precipitate or exacerbate mood and psychotic episodes. However, the role of the genes that control circadian rhythms in the development of these disorders has remained unclear. This seminar will summarize recent data from our lab using human postmortem tissue to understand how molecular rhythms in specific brain regions, and cell types within those regions, are altered in subjects with psychiatric diseases like bipolar disorder and schizophrenia. Moreover, I will discuss our work in mouse models which implicates the circadian system as a vital regulator of neuronal signaling and communication between circuits in the brain that control mood and reward. I will discuss the molecular, cellular and electrophysiological changes that might underlie the regulation of mood and switch to different mood states with disruption of the circadian gene function or the sleep/wake cycle. This combination of human and rodent studies provides better understanding of how circadian genes in multiple regions of the brain contribute to the development and progression of psychiatric diseases.
Both attention and perceptual learning improve performance on visual tasks, but they do so on very different timescales and are generally studied using different tasks. Both processes change how visual information is encoded in visual cortex, and trial-to-trial response variability that is shared among the neuronal population is a leading candidate for the aspect of neural code that limits perception. Indeed, we found that when we recorded from populations of V4 neurons in two rhesus monkeys as they practiced a task that cued attention, there was a single, robust relationship between changes in correlated variability and changes in behavioral performance, whether those changes occurred quickly with attention or slowly with learning. This correlated variability completely accounted for the choice-predictive activity in the V4 neuronal populations. Thus, changes in correlated variability may underlie all processes that improve perception, regardless of how long it takes any one process to affect performance.