August 28, 2006
First day of classes
September 8, 2006
-- ICS Town Meeting
September 15, 2006 (SLC)
-- SLC Colloquium Series Kick Off
September 29, 2006 (SLC)
-- SLC Student Presentations
October 13, 2006
-- Kate Siek
Computer Science, University of Colorado
Title: "Sanitized Prototypes and Cargo Pants: Design and Evaluation of an Assistive Application for Dialysis Patients"
October 20, 2006
-- Allan Collins
Education and Social Policy, Northwestern University
Title: "The Second Educational Revolution: From Apprenticeship to Schooling to Lifelong Learning."
November 3, 2006
-- Charles Anderson
Washington University, St. Louis
Title: "Population Coding in Monkey Primary Visual Cortex."
With redundant neuronal population coding, the number of neurons. Allocated to represent each feature is proportional to its signal to noise ratio . We applied this hypothesis to obtain the spatial frequency dependence of the signal-to-noise-ratio conveyed by the retinal/LGN ganglion cells from the measured distribution of the preferred spatial frequencies of cortical cells in monkey primary visual cortex, V1, as measured by J. Cavanaugh and W. Bair  in the Movshon lab. The results quantitatively demonstrate that both ganglion cells and cortical cells in V1 utilize highly redundant codes, i.e. hundreds of neurons per degree of freedom, to represent image data. The analysis unifies a diverse set of anatomical and neurophyisiological facts about the early visual system and demonstrates many commonly held hypotheses are wrong. For example, that the image data is whitened by the center surround receptive field of ganglion cells. More generally, these results provide strong, quantitative, support that highly redundant coding forms the basis of the neuronal code for most neurobiological systems and rules out most sophisticated spike coding schemes.
 Eliasmith C and Anderson CH, "Neural Engineering", MIT PRESS 2003.
 Cavanaugh JR, Bair W, and Movshon JA (2002), Selectivity and
spatial distribution of signals from the receptive field surround in
macaque V1 neurons, J Neurophysiol. 88: 2547-56.
November 10, 2006
-- Robert Rupert
Philosophy Department, University of Colorado
Title: "Distributed Cognition, the Human Mind, and the Human Cognitive System"
November 17, 2006
-- Anu Sharma
SLHS, University of Colorado
Title: "A Critical Period for the Development of the Central Auditory Pathways."
Anu Sharma, Ph.D and Phillip M. Gilley, Ph. D
Speech Language and Hearing Science, University of Colorado at Boulder
We are investigating critical periods for the development, deterioration and plasticity of the human central auditory pathways in normal hearing children and in deaf children who regain hearing after being fitted with cochlear implants. Our measure of central auditory maturation and development is the latency, morphology and topography of the Cortical Auditory Evoked Potential (CAEP). We record CAEPs using 64 channel high density EEG recordings, standardized low resolution electromagnetic brain tomography (sLORETA) and dipole source analyses. Experiments with congenitally deaf children fit with cochlear implants have allowed us to establish the existence of and time limits of a critical period development of the central auditory pathways. In a series of experiments using CAEPs as a measure, we have found that the central auditory pathways are maximally plastic for a period of 3.5 years. If stimulation is delivered within that period CAEP latencies reach age-normal values within 3-6 months following the onset of stimulation with an implant. However, if stimulation is withheld for more that 7 years, we find that plasticity in the central pathways is greatly reduced. In late-implanted children, CAEP latencies decrease significantly over a period of approximately one month following the onset of stimulation then remain constant or change very slowly over months and years. The loss of central auditory plasticity in congenitally deaf children implanted after age 7 years is correlated with relatively poor development of oral speech and language skills. We suppose this link is, in fact, causal. Animal models suggest that primary auditory cortex may be functionally disconnected from higher-order auditory cortex, due to restricted development of inter- and intra- cortical connections, in late implanted children. This would account for late-implanted children who 'hear' via a cochlear implant but who experience very slow development of speech and language skills. Another aspect of plasticity which works against late-implanted children is the re-organization of higher order cortex by other function (e.g., vision). The hypothesis of cortical re-organization in children deprived of sound for a long time provides an account for the oral language-learning difficulties of children who receive a cochlear implant after the end of the critical period.
November 24, 2006
-- Happy Thanksgiving
December 15, 2006
-- ICS Holiday Gathering