Postnatal Maturation and Experience-Dependent Plasticity of Inhibitory Circuits in Barrel Cortex
Sensory experience drives the refinement of sensory maps in developing adult sensory cortices (Wiesel and Hubel 1974; Stryker 1978; Crair et al. 1998; Feldman and Brecht 2005). Tremendous progress has been made toward understanding the process of maturation of excitatory networks. Cortical inhibition has also been shown to play a vital role in the regulation of critical periods for sensory plasticity (Hensch 2005). However, it is unclear whether neocortical inhibitory networks exhibit experience-dependent postnatal maturation. In my laboratory, we employ the so-called “barrel cortex” (Woolsey and Van der 1970) that, represents the individual whiskers on the snout of rodents. The map exhibits plasticity throughout life, in that under- or over-stimulation of a whisker is reflected by contraction or expansion, respectively, of the barrel representing it in the primary somatosensory cortex (Simons and Land 1987). This review focuses on the mechanisms underlying activity-dependent regulation of neocortical inhibitory circuits and the roles of inhibition in somatosensory cortical map plasticity during postnatal development. The focus will be placed on the following questions related to experience-dependent plasticity of neocortical inhibitory networks. (1) How do intrinsic and synaptic properties of inhibitory circuits in barrel cortex change during postnatal maturation? (2) How does sensory stimulation or deprivation affect the maturation of inhibitory circuits? (3) Does the maturation of neocortical inhibitory circuits proceed in an activity-dependent manner or do they develop independently of sensory inputs? (4) What are the molecular and cellular mechanisms that underlie the activity-dependent or -independent maturation of inhibitory networks?
KeywordsGABAA Receptor Sensory Experience Excitatory Neuron Intracortical Inhibition Sensory Deprivation
I thank Chunzhao Zhang, Yuanyuan Jiao, Leah Selby and Andrew Young for their help and excellent assistance in all studies described in this chapter. I thank Dr. Yuchio Yanagawa at the Department of Genetic and Behavioral Neuroscience, Gunma University Graduate School of Medicine for the generous gift of GAD67-GFP mouse. My work is supported by NIH. Most of work dealing with the properties of excitatory neurons and excitatory synapses in the barrel cortex could not be cited here due to the focus of this book on the GABAergic system. I apologize to my colleagues for such necessary omissions.
- Lau D, Vega-Saenz de Miera EC, Contreras D, Ozaita A, Harvey M, Chow A, Noebels JL, Paylor R, Morgan JI, Leonard CS, Rudy B (2000) Impaired fast-spiking, suppressed cortical inhibition, and increased susceptibility to seizures in mice lacking Kv3.2 K+ channel proteins. J Neurosci 20:9071–9085PubMedGoogle Scholar