Matthew I. Banks

Matthew Banks
Associate Professor, Department of Anesthesiology
(608) 261-1143


Ph.D. University of Wisconsin- Madison

Lab Website:

Research Focus:

GABAA Receptors and the Dynamics of Cortical Inhibitory Circuits

Research Strengths:

Membrane Excitability and Synaptic Transmission; Neural Circuits

Research Description:

Sensory and cognitive information is represented in the neocortex in the spatiotemporal firing patterns of cells within neural networks.  Research in my lab focuses on how these firing patterns arise (circuitry and stimulus coding), how they are altered upon changes in awareness (e.g. upon loss of consciousness (LOC) induced by general anesthetics), and the causal relationship between these changes in stimulus representation and changes in awareness. Current theories of the neural basis of sensory awareness suggest that neocortex is constantly comparing expected with observed sensory information.  This comparison arises through the integration of ascending inputs from the sensory periphery via 'core' thalamo-cortical (TC) inputs with descending/modulatory cortico-cortical (CC) and 'matrix' TC inputs within the same or other sensory modalities. There is indirect evidence indicating that this integrative process is disrupted in slow wave sleep and upon anesthesia LOC. Although integration of ascending and descending/modulatory inputs to the column is widely believed to be a critical component of sensory awareness and likely a target for general anesthetics, there are several fundamental unanswered questions that motivate our research program.

(1) How does this integration process occur, and what is the net effect on activity in the column? For example, do descending/modulatory inputs have a net excitatory or inhibitory effect? Are specific cell subpopulations targeted? Is the integration primarily at the single cell or network level? At what level(s) in the cortical hierarchy is this integrative process critical, and how does this change with stimulus and task demands?

(2) What do general anesthetics do to this integrative process and what is the mechanism of their effect? Is there a causal relationship between these effects and LOC? Are effects at some level(s) in the cortical hierarchy more important for producing LOC? Do all agents that cause LOC share a common effect on columnar processing?

To answer these questions, we use auditory cortex in mice and rats as a model system, and we apply optogenetic, imaging and electrophysiological techniques in an acute slice preparation, and electrophysiological and behavioral techniques in vivo. In vivo, we record from the entire cortical column or from multiple loci in the same layer using multielectrode arrays, and we selectively activate core TC versus matrix TC/descending CC inputs using simple auditory versus visual stimuli (which trigger multimodal responses in auditory regions), respectively. In brain slices, we can ask detailed questions about synaptic physiology, cellular properties and network activity, and we can selectively activate core TC versus matrix TC and CC input pathways. As for experiments in vivo, we can record from the entire column at once using multichannel electrodes or calcium imaging, and we can use optognetic techniques to activate specific afferent pathways and to control activity in selected subpopulations of cortical cells.


Please see PubMed for most recent publications