Event Time and Location: Wednesday, October 18th @ 3PM in Steinman Hall Rm 402

Dr. Qi Wang (Department of Biomedical Engineering, Columbia University), Top-down and bottom-up modulation of neural coding in the somatosensory thalamus.

Abstract: The transformation of sensory signals into spatiotemporal patterns of neural activity in the brain is critical in forming our perception of the external world. Physical signals, such as light, sound, and force, are transduced to neural electrical impulses, or spikes, at the periphery, and these spikes are subsequently transmitted to the neocortex through the thalamic stage of the sensory pathways, ultimately forming the cortical representation of the sensory world. The bottom-up (by external stimulus properties) or top-down (by internal brain state) modulation of coding properties of thalamic relay neurons provides a powerful means by which to control and shape information flow to cortex. My talk will focus on two topics. First, I will show that sensory adaptation strongly shapes thalamic synchrony and dictates the window of integration of the recipient cortical targets, and therefore switches the nature of what information about the outside world is being conveyed to cortex. Second, I will discuss how the locus coeruleus – norepinephrine (LC-NE) system modulates thalamic sensory processing. Our data demonstrated that LC activation increased the feature sensitivity, and thus information transmission while decreasing their firing rate for thalamic relay neurons. Moreover, this enhanced thalamic sensory processing resulted from modulation of the dynamics of the thalamorecticulo-thalamic circuit by LC activation. Taken together, an understanding of the top-down and bottom-up modulation of thalamic sensory processing will not only provide insight about neurological disorders involving aberrant thalamic sensory processing, but also enable the development of neural interface technologies for enhancing sensory perception and learning.

Event Time and Location: Thursday 10/19 at noon in CDI 3.352

Forouzan Farahani will lead a discussion of causal inference on paper:
“Dendritic integration: 60 years of progress”

Understanding how individual neurons integrate the thousands of synaptic inputs they receive is critical to understanding how the brain works. Modeling studies in silico and experimental work in vitro, dating back more than half a century, have revealed that neurons can perform a variety of different passive and active forms of synaptic integration on their inputs. But how are synaptic inputs integrated in the intact brain? With the development of new techniques, this question has recently received substantial attention, with new findings suggesting that many of the forms of synaptic integration observed in vitro also occur in vivo, including in awake animals. Here we review six decades of progress, which collectively highlights the complex ways that single neurons integrate their inputs, emphasizing the critical role of dendrites in information processing in the brain.

Event Time and Location: Thursday 10/12 at noon in CDI 3.352

Lukas Hirsch will lead a discussion of causal inference, including the attached paper:
“Nonlinear causal discovery with additive noise models ”

The discovery of causal relationships between a set of observed variables is a fun damental problem in science. For continuous-valued data linear acyclic causal models with additive noise are often used because these models are well under-stood and there are well-known methods to fit them to data. In reality, of course, many causal relationships are more or less nonlinear, raising some doubts as to the applicability and usefulness of purely linear methods. In this contribution we show that the basic linear framework can be generalized to nonlinear models. In this extended framework, nonlinearities in the data-generating process are in fact a blessing rather than a curse, as they typically provide information on the underlying causal system and allow more aspects of the true data-generating mechanisms to be identified. In addition to theoretical results we show simulations and some simple real data experiments illustrating the identification power provided by non-linearities

Event Time and Location: Wednesday, October 11th @ 3PM in Steinman Hall Rm 402

Joshua Jacobs, Ph.D. (Department of Biomedical Engineering, Columbia University), Single-neuron and field-potential activity underlying human spatial navigation and memory.

Abstract: The ability to remember spatial environments is critical for everyday life. To understand, with a high spatial and temporal precision, how the brain supports navigation and forms spatial memories, we examined direct brain recordings from neurosurgical patients as they played our virtual-navigation video game. We found several novel signals that reveal the neural basis of human spatial memory and differentiate us from simpler animals. Humans have several types of neurons that represent a person’s current spatial location, including place, grid, and path-invariant cells, which show that the neural coding of spatial location is supported by multiple medial-temporal subregions that play complementary roles. In addition I will describe our work identifying the neural basis of spatial memory encoding in humans. We found two types of memory-related signals in the human MTL: theta oscillations and broadband power spectrum shifts. In key ways these signals differ significantly from patterns seen in animals, in particular with human memory-related theta occurring at a slower frequency than would be expected from earlier work. We also examine interactions between single-cell and network oscillatory activity. An emerging theme from our work is that in terms of spatial cognition the human brain has both shared and distinctive characteristics compared with animal models.

Event Time and Location: Wednesday, September 27, 2017, 3PM, Steinman Hall 402

George McConnell, PhD (Stevens Institute of Technology), Why Random Patterns of Deep Brain Stimulation Less Effectively Treat Parkinson’s Disease: Insights from In Vivo Studies

Abstract: Deep Brain Stimulation (DBS) of the subthalamic nucleus effectively treats several motor symptoms of Parkinson’s disease (PD), however, the mechanisms of action of DBS are unknown. Random temporal patterns of DBS are less effective than regular DBS, but the neural basis for this dependence on temporal pattern of stimulation is unclear. We quantified behavior and single-unit neuronal activity in parkinsonian rats to test the hypothesis that the ineffectiveness of irregular DBS is caused by a failure to mask low-frequency oscillatory activity. Irregular DBS relieved symptoms less effectively than regular DBS, even when delivered at a high average rate. The reduced effectiveness of random DBS paralleled a failure to suppress low-frequency oscillatory activity and suggest that long pauses during random DBS are responsible for the reduced effectiveness, because these pauses enable the propagation of low-frequency oscillatory activity. These results demonstrate a correlation between efficacy of DBS, temporal regularity of stimulus trains, and changes in neuronal oscillatory activity in the basal ganglia, highlighting the importance of considering temporal patterns – as opposed to simply the rate – of both stimulation and neuronal firing in studying the mechanisms of DBS for neurological disorders.

I recently graduated Yeshiva University High School for Boys in Washington Heights, New York.  After taking a gap year to study abroad, I look forward to attending Yeshiva University, where I plan on majoring in biology.