26th of November 2009

 Lecture: Circuits that regulate cortical plasticity

Dr. Patrick Kanold, an associate professor at University of Maryland, will give the lecture Circuits that regulate cortical plasticity on the 10th of December 2009 at 4 pm. The lecture will be held at Reykjavík University, Kringlunni 1 room K5.

Kringlan 1, stofa K5

Klukkan 16:00, 10, desember 2009

 

Circuits that regulate cortical plasticity

Patrick Kanold PhD

Assistant Professor, Biology, University of Maryland, College Park (www.kanold.org)

CAREER

Instructor, Neurobiology, Harvard Medical School, 2005-2007


Post-Doctoral, 
Neurobiology, Harvard Medical School, 2000-2005 
Mentor: 
Carla Shatz


Ph.D., 
Biomedical Engineering, Johns Hopkins University, 2000 
Mentors: 
Eric Young, Paul Manis


Dipl.Ing. (MSE), 
Electrical Engineering, Technische Universitaet Berlin, Germany, 1994

 

ABSTRACT

 

One of the hallmarks of the young brain is its ability to be sculpted by experience especially during critical periods in development. However, the mechanisms underlying this early learning process and how they relate to learning processes in adult are unknown.

The young brain is structurally different from the adult brain and contains additional circuits that are formed by subplate neurons (SPNs). These neurons are among the earliest born cortical neurons; they reside in the white matter and disappear during development. After the critical period ends – when SPNs are no longer present - only limited plasticity is present. Thus SPNs might participate in types of synaptic plasticity that occur only during the critical period.

To elucidate the developmental role of SPNs, we study SPNs and their associated circuits in vitro in thalamocortical slices. We find that in rodent SPNs receive functional excitatory inputs from the thalamus shortly after birth, and that thalamic input to SPN is capable of inducing action potentials in SPNs. We also find that SPNs provide functional input to neurons in developing layer 4. Thus, SPNs are tightly integrated into the developing thalamocortical circuit providing input to the eventual targets of thalamic projections. These results suggest that SPNs are a reliable relay of early spontaneous and sensory evoked activity and can thereby regulate cortical development and plasticity.

Using a combination of ablation experiments and computational models, we find that SPNs are required for the functional maturation of the cortical columnar organization, the development of intracortical inhibitory circuits, and the outcome of plasticity during the critical period. Together these results show that SPNs act like a "teacher" helping thalamic neurons to make strong and precise connections to their cortical target neurons. By relaying thalamic input and controlling the balance of excitation and inhibition, SPNs can influence the correlations between thalamic and cortical activity and thereby synaptic plasticity. Thus, premature loss of SPNs can lead to developmental abnormalities manifested in altered cortical processing.

While SPNs die over development limited plasticity remains and this plasticity can be engaged by attention. We use in vivo 2-photon imaging to investigate the influence of attention and find that top-down circuits provide excitation to layer 4 and that this excitation can cause receptive field plasticity. Thus top-down circuits in the adult might play roles similar to SPNs in development.

Together, this work provides a framework of life-long learning and demonstrates that large-scale plasticity during the critical period is the product of a complex and dynamically changing circuit in which SPNs play a key role in the adult.

 

Each national member society can submit one application. 

For more details, see the Call for Proposals.

FENS

European Journal of Neuroscience