No abstract

⎯Optogenetics is a rapidly developing new technique that combines optical methods with techniques that are used in molecular biology. It can be used for monitoring various optical processes in cells and controlling their activity using light. The technique is based on bacterial opsin expression in mammalian neurons. In this review, the use of optogenetics for controlling the activity of specific neuronal populations in different regions of the human brain is considered in detail. The paper also presents information on light-sensitive proteins, genetically encoded optical instruments, and their use for activation or inhibition of neurons and investigation of the causal relationship between neural networks and pathological symptoms.

The aim of the study is to identify new gene mutations causing cerebral cortex malformations in mice. Materials and Methods. To identify genes causing cerebral cortex malformations, chemical mutagenesis was carried out using N-ethyl-N-nitrosourea as a mutagen. A total of 141 male C3H mice aged 8 weeks were injected with the mutagen in order to induce mutations in spermatogonial stem cells. After a period of sterility, the animals were used in three-generation backcross scheme. Satb2-LacZ reporter mice were involved in this strategy to label the neurons forming the corpus callosum. Results. The animal phenotype displaying primary microcephaly and 6 mutant lines demonstrating audiogenic epilepsy have been described. The phenotypes of these mutants will be further presented and discussed.

The neocortex is stereotypically organized into layers of excitatory neurons arranged in a precise parallel orientation. Here we show that dynamic adhesion both preceding and following radial migration is essential for this organization. Neuronal adhesion is regulated by the Mowat-Wilson syndrome-associated transcription factor Zeb2 (Sip1/Zfhx1b) through direct repression of independent adhesion pathways controlled by Neuropilin-1 (Nrp1) and Cadherin-6 (Cdh6). We reveal that to initiate radial migration, neurons must first suppress adhesion to the extracellular matrix. Zeb2 regulates the multipolar stage by transcriptional repression of Nrp1 and thereby downstream inhibition of integrin signaling. Upon completion of migration, neurons undergo an orientation process that is independent of migration. The parallel organization of neurons within the neocortex is controlled by Cdh6 through atypical regulation of integrin signaling via its RGD motif. Our data shed light on the mechanisms that regulate initiation of radial migration and the postmigratory orientation of neurons during neocortical development.