When:
Friday, October 11, 2024
12:00 PM - 1:00 PM CT
Where: Ward Building, 5-230, 303 E. Chicago Avenue, Chicago, IL 60611 map it
Audience: Faculty/Staff - Student - Post Docs/Docs - Graduate Students
Contact:
Jenna Ward
(815) 529-6182
Group: Department of Neuroscience Seminars
Category: Lectures & Meetings
The Department of Neuroscience Welcomes Dr. Arlette Kolta
Arlette Kolta is a Full Professor at the Faculty of Dentistry at the University of Montreal and has a second affiliation to the Department of Neuroscience. She is also the director of the Interdisciplinary Center for Brain and Learning (CIRCA).
Abtract:
Several functions, motor or sensory, rely on the ability of neurons to modify their discharge pattern to faithfully encode the characteristics of a sensory stimulus or to reflect a rhythmic motor control for example. Changes in firing pattern often involve particular ion channels and are intimately related to the function of the circuit. Astrocytes are increasingly acknowledged as key regulators of neural activity, through release of gliotransmitters which effects on synaptic and network functions are increasingly understood. However, their contribution to neuronal computations is still poorly addressed.
Our work has revealed how by modifying the extracellular Ca2 + concentration through release of a calcium-binding protein (S100b), astrocytes can act directly on or near neuronal Na+ channels, a largely unexplored form of communication between astrocytes and neurons. This mechanism is likely to be involved in many functions given the ubiquitous distribution of these channels and astrocytes across the brain. Indeed, we have shown it to be involved in rhythmogenesis in a brainstem sensory-motor circuit that generates jaw movements, in input integration and axonal plasticity in cortical layer 5 pyramidal neurons and in ectopic firing and excitability changes of primary afferent neurons in chronic pain.
The S100β-dependent mechanism adds up to the previously reported conventional gliotransmitters. Beyond increasing our understanding of how astrocytes contribute to neuronal computations, our findings will help to understand the role of S100β which is abnormally regulated after trauma and in many neurological disorders including epilepsy, depression, Parkinson’s, and Alzheimer’s diseases. We propose that abnormal S100β control may have a wide impact by leading to abnormal extracellular ionic environment, abnormal neural activities, and thus pathological states.