Karl Peter Giese

TL;DR: It is demonstrated that unwanted variance dominates the signal in transcriptional studies of learning and memory and the removal of unwanted variance through normalization is introduced as a necessary step for the analysis of genome-wide transcriptional Studies in the context of brain and behavior.

TL;DR: The connections between GSK3β and Cdk5 are summarized, implications for AD hypotheses are discussed and recent evidence from p25 transgenic mice suggests that there is a dynamic crosstalk: during aging or prolonged overactivation of Cdk3β activity may alter in favor of AD pathogenesis.

TL;DR: In this paper, the role of altered neuronal excitability in mammalian learning and memory was investigated using Kv beta 1.1-deficient mice, which is a regulatory subunit with a restricted expression pattern in the brain, and it confers fast inactivation on otherwise noninactivating K(+) channel subunits.

TL;DR: It is shown that, in mice with deficient autophosphorylation of αCaMKII, the spatial tuning of place fields is initially similar to that of wild-type mice, but completely fails to show the experience-dependent increase over days, and place field reproducibility in the mutants, although impaired, does showThe progressive improvement in spatial coding in new hippocampal place cell maps depends on the existence of two molecularly dissociable, experience- dependent processes.

TL;DR: The role that gene targeting and other transgenic techniques have had in the study of mammalian learning and memory is described, focusing especially on the hippocampus, a brain structure that is thought to be central to the processing and temporary storage of complex information.