Colloquium Series
Colloquia will generally be on Tuesdays, once per month. They will usually be held on the 3rd floor of Hagey Hall (HH) and exceptions will be noted. Abstracts will be posted as available.
Here is a link for past events, colloquia, and speakers.
- November 27, 2008 - Hugh Wilson (York), HH 138, 4:00 p.m.
- December 11, 2008 - William Hutchison (Toronto), HH 334, 3:30 p.m.
- February 5, 2009 - Mark Goldman (Davis), HH 373, 2:30 p.m.
- March 18, 2009 - A. David Redish (Minnesota), HH 373, 2:30 p.m.
- April 8, 2009 - Waterloo Brain Day (4 Speakers), PAS 2083
- May 6, 2009 - Vinod Goel (York), HH 334, 3:30 p.m.
Date:
Nov.
27,
2008
Location:
HH
138
Time:
4:00
p.m.
Speaker:
Hugh
Wilson
(York
University,
Ontario
Research
and
Development
Challenge
Fund
(ORCDF)
Professor
of
Spatial
and
Computational
Vision)
Title:
Perceptual
Oscillations
and
Waves
in
Vision
Abstract: When the two eyes are presented with mutually incompatible stimuli, such as orthogonal gratings, the cortex defaults to an oscillation, termed binocular rivalry, between the monocular inputs. Not only is rivalry a rich area for studying nonlinear dynamics in the cortex, but it also serves to elucidate a range of neuronal interactions. This talk will discuss the minimal physiological requirements for binocular rivalry and their relationship to both traveling rivalry waves and hierarchic levels of cortical processing. Additional topics will include the link between rivalry and stereopsis, rivalry hysteresis, and short term perceptual storage in rivalry. Finally, a generalization of rivalry that may provide insights into visual decision making will be discussed.
Date:
Dec.
11,
2008
Location:
HH
334
Time:
3:30
p.m.
Speaker:
William
Hutchison
(Toronto)
Title:
Oscillations
and
Synaptic
Plasticity
in
the
Basal
Ganglia
of
Movement
Disorders
Patients
Abstract: The dopamine precursor drug (L-DOPA) is standard therapy for the amelioration of Parkinson's disease (PD) symptoms, but long-term administration can lead to disabling motor fluctuations and L-dopa-induced dyskinesias. The enhancing effects of dopamine on synaptic plasticity of glutamatergic corticostriatal synapses (basal ganglia input) have been studied in rat brain slices, and Picconi et al (2002) have shown that dyskinesia may result from a selective impairment of the reversal of LTP induced by high frequency trains of stimuli by using low frequency trains. In contrast, little is known of the effects of dopamine on plasticity of synapses in substantia nigra pars reticulata (SNr, basal ganglia output), receiving dense GABAergic input from striatum, glutamatergic input from subthalamic nucleus (STN) as well as dopaminergic inputs via ventral dendrites of SN compacta neurons. This region is important since surgical intervention for movement disorders target the basal ganglia output structures (globus pallidus internus, GPi) or nuclei that project heavily to these outputs such as the subthalamic nucleus. My talk will describe a dual microelectrode stimulation technique to measure short term increases and decreases in amplitudes of evoked field potentials in SNr and GPi during deep brain stimulation operations for PD or dystonia, and present evidence that the field is primarily GABAergic in nature. The work will show that bidirectional plasticity can be demonstrated in both GPi and SNr, and L-DOPA has a powerful enhancing effect on the SNr plasticity, similar to the effects observed for excitatory synapses at the basal ganglia input. I will also briefly discuss the effects of L-DOPA on pathological oscillations in the basal ganglia and how they might interact with spiking neurons to produce aberrant synaptic plasticity in movement disorders.
Date:
Feb.
5,
2009
Location:
HH
373
Time:
2:30pm
Speaker:
Mark
Goldman
(University
of
California,
Davis)
Title:
Modeling
the
Mechanisms
Underlying
Memory-related
Neural
Activity
Abstract: Persistent neural activity, or the sustained discharge of action potentials long after the removal of a transiently presented stimulus, has been identified as a neural correlate of short-term memory in a wide variety of brain regions. This talk will present theoretical models of the neural mechanisms underlying persistent neural activity in a variety of systems. Experimental tests of these models will be discussed in the context of a particularly well-characterized system exhibiting such activity: the oculomotor neural integrator of the vertebrate brainstem, which is responsible for converting eye movement commands into persistent signals that encode the position of the eyes.
Date:
Mar.
18,
2009
Location:
HH
373
Time:
2:30
p.m.
Speaker:
A.
David
Redish
(Minnesota)
Title:
The
Identification
of
Covert
(cognitive)
Variables
in
Hippocampal
Neural
Activity,
Evidence
for
Active
Processing
of
Representations
Abstract: A complete description of neural coding should enable the prediction of spiking activity. As has been well-studied for decades, rodent hippocampal pyramidal cells show strong spatial firing correlations (known as the place field of the cell). Although the animal's position can be reconstructed from the firing of a relatively small number of these "place cells", hippocampal neural activity is more variable than predicted from the spatial position of the animal alone. Using new analyses applied to large-ensemble simultaneous neural recordings, we will show that this excess variability can be accounted for by identifiable, covert switching between multiple spatial maps. In addition to excess variability during normal, running behaviors, excess spiking is seen at specific times (while resting at feeders, while actively looking around at decision-points). We will show that this excess spiking is also accountable by other, identifiable, covert signals. The structure within these covert signals provide first steps towards a quantifiable description of cognition.
Date:
Wed.,
Apr.
30,
2009
**CANCELLED**
Location:
HH
334
Time:
3:30
p.m.
Speaker:
David
Terman,
Mathematical
Biosciences
Institute
&
Ohio
State
University
Title:
A
Data-driven
Computational
Model
of
Subthalamic
Nucleus
Deep
Brain
Stimulation
Abstract: The delivery of high-frequency stimulation has become a widely used therapeutic option for the treatment of Parkinson's disease (PD). The mechanisms underlying the effectiveness of deep brain stimulation (DBS), however, remain unclear. Studies have shown that pathological rhythmicity emerges in certain subsets of cells within the basal ganglia in Parkinsonism. Therefore, DBS for PD may work by eliminating such pathological signals. Recent experimental results, however, suggest that neurons directly downstream from stimulated regions may in fact be activated by DBS. These results support the alternative idea that DBS works by replacing pathological rhythms with regularized firing activity. Here, we present a computational implementation of this idea. Our simulations and analysis demonstrate a mechanism by which pathological oscillatory inhibition from the internal segment of the globus pallidus (GPi) to thalamocortical (TC) cells could compromise the fidelity of TC relay of excitatory signals, whereas elimination of the pathological oscillations within this inhibitory signal could restore TC cells' relay capabilities. We use GPi spike trains recorded from normal control monkeys and from parkinsonian monkeys with or without DBS of the subthalamic nucleus region as the source of inhibitory inputs to our model TC cells. Our results show that there is a significant decline in the ability of the TC cells to relay the excitatory stimuli when they are exposed to GPi signals recorded under parkinsonian conditions in the absence of DBS or with sub-therapeutic DBS, defined by its failure to induce a therapeutic effect on motor symptoms, relative to GPi data recorded from normal monkeys. Moreover, relay effectiveness is restored to non-parkinsonian levels by GPi signals recorded under parkinsonian conditions in the presence of therapeutic DBS, which induced a measurable improvement in motor symptoms.
Date:
Tues.,
May
6,
2009
Location:
HH
334
Time:
3:30
p.m.
Speaker:
Vinod
Goel,
Psychology,
York
University
Title:
Towards
a
Cognitive
Neuroscience
of
Rational
Thought
Abstract: Considerable progress has been made over the past decade in our understanding of the neural basis of logical reasoning. Unsurprisingly these data are telling us that the brain is organized in ways not anticipated by cognitive theory. In particular, they're forcing us to confront the possibility that there may be no unitary reasoning system in the brain (be it mental models or mental logic). Rather, the evidence points to a fractionated system that is dynamically configured in response to certain task and environmental cues. I will review three lines of demarcation including (a) systems for heuristic and formal processes (with evidence for some degree of content specificity in the heuristic system), (b) conflict detection/resolution systems, and (c) systems for dealing with certain and uncertain inferences; and then offer a tentative account of how the systems might interact to facilitate logical reasoning. Sensitivity to data generated by neuroimaging and patient methodologies will move us beyond the sterility of mental models vs. mental logic debate and further the development of cognitive theories of reasoning.