Specifically, diabetic mice exhibit decreased expression of CaMKIV (calcium/calmodulin-dependent protein kinase IV) in the hippocampus and altered CREB expression in the amygdala and hypothalamus, suggesting that disruptions in this neurotrophic signaling cascade contribute to the emergence of anxiety-like behavior in the STZ-induced diabetic model [81]. This evidence concerns the gene CAMK4 and Anxiety.