Development and critical period plasticity of the barrel cortex

Abstract

In primary sensory neocortical areas of mammals, the distribution of sensory receptors is mapped with topographic precision and amplification in proportion to the peripheral receptor density. The visual, somatosensory and auditory cortical maps are established during a critical period in development. Throughout this window in time, the developing cortical maps are vulnerable to deleterious effects of sense organ damage or sensory deprivation. The rodent barrel cortex offers an invaluable model system with which to investigate the mechanisms underlying the formation of topographic maps and their plasticity during development. Five rows of mystacial vibrissa (whisker) follicles on the snout and an array of sinus hairs are represented by layer IV neural modules ('barrels') and thalamocortical axon terminals in the primary somatosensory cortex. Perinatal damage to the whiskers or the sensory nerve innervating them irreversibly alters the structural organization of the barrels. Earlier studies emphasized the role of the sensory periphery in dictating whisker-specific brain maps and patterns. Recent advances in molecular genetics and analyses of genetically altered mice allow new insights into neural pattern formation in the neocortex and the mechanisms underlying critical period plasticity. Here, we review the development and patterning of the barrel cortex and the critical period plasticity.

Figure 1

Schematic diagram illustrating the timing of arrival of afferents along the whisker-barrel pathway and emergence of axonal and cellular patterns.

Figure 2

Schematic diagram illustrating the classical structural plasticity in the barrel cortex following row C whisker lesions or infraorbital nerve transection. These effects are only seen when peripheral lesions are performed up to postnatal day 3. The patterns and deficits are routinely assessed by histochemical stains such as succinic dehydrogenase or cytochrome oxidase histochemistry or with immunohistochemistry for TCA markers such as 5-HTT or vesicular glutamate transporter 2 or by Nissl or Golgi stains for neuronal and dendritic organization.