Stimulation of the Sigma-1 Receptor and the Effects on Neurogenesis and Depressive Behaviors in Mice

• Published in: Advances in experimental medicine and biology Vol. 964; pp. 201 - 211
• Main Authors: Fukunaga, Kohji, Moriguchi, Shigeki
• Format: Book Chapter Journal Article
• Language: English
• Published: Switzerland Springer International Publishing AG 01.01.2017; Springer International Publishing
• Series: Advances in Experimental Medicine and Biology
• Subjects: Animals; BDNF; Behavior, Animal - physiology; Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism; CaMKII; CaMKIV; Depression - metabolism; Hippocampus - metabolism; Humans; Ligands; Medical research; Mice; Neurogenesis - physiology; Proteins; Proto-Oncogene Proteins c-akt - metabolism; Receptors, sigma - metabolism; Sigma-1 Receptor; Signal Transduction - physiology; Depression; CaMKII; BDNF; Neurogenesis; Sigma-1 receptor; CaMKIV
• ISBN: 9783319501727; 3319501720
• ISSN: 0065-2598; 2214-8019
• DOI: 10.1007/978-3-319-50174-1_14

Sigma-1 receptor (Sig-1R) is molecular chaperone regulating calcium efflux from the neuronal endoplasmic reticulum to mitochondria. Recent studies show that Sig-1R stimulation antagonizes depressive-like behaviors in animal models, but molecular mechanisms underlying this effect remain unclear. Here, we focus on the effects of Sig-1R ligands on hippocampal neurogenesis and depressive-like behaviors. Sig-1R stimulation also enhances CaMKIIcalmodulin-dependent kinase II (CaMKII)/CaMKIVCalcium/calmodulin-dependent protein kinase IV (CaMKIV) and protein kinase B (Akt) activities in hippocampus. Therefore, we discuss the fundamental roles of Sig-1R, CaMKIIcalmodulin-dependent kinase II (CaMKII)/CaMKIVCalcium/calmodulin-dependent protein kinase IV (CaMKIV) and protein kinase B (Akt) signaling in amelioration of depressive-like behaviors following Sig-1R stimulation.