Glycogen synthase kinase-3β/β-catenin signaling in the rat hypothalamus during the estrous cycle

• Published in: Journal of neuroscience research Vol. 90; no. 5; pp. 1078 - 1084
• Main Authors: Barrera-Ocampo, Alvaro, Gutierrez-Vargas, Johanna, Garcia-Segura, Luis Miguel, Cardona-Gómez, Gloria Patricia
• Format: Journal Article
• Language: English
• Published: Hoboken Wiley Subscription Services, Inc., A Wiley Company 01.05.2012
• Subjects: Analysis of Variance; Animals; beta Catenin - metabolism; Disks Large Homolog 4 Protein; Estrous Cycle - physiology; Female; Glycogen Synthase Kinase 3 - metabolism; Glycogen Synthase Kinase 3 beta; GSK3β; Hypothalamus - metabolism; Immunoprecipitation; Intracellular Signaling Peptides and Proteins - metabolism; Membrane Proteins - metabolism; Phosphorylation; PI3K; PSD95; Rats; Rats, Wistar; Signal Transduction - physiology; synapsin I; Synapsins - metabolism; β-catenin
• ISSN: 0360-4012; 1097-4547
• DOI: 10.1002/jnr.22816

During the estrous cycle, a remodeling of synapses on somas and dendritic spines occurs in the rat hypothalamic arcuate nucleus. The synaptic remodeling is known to be induced by estradiol, but the molecular mechanisms involved still have not been fully clarified. β‐Catenin is known to regulate synaptic plasticity, so we have assessed possible modifications of β‐catenin in the rat mediobasal hypothalamus during the estrous cycle. Our findings indicate that β‐catenin expression is increased during proestrus and estrus in comparison with diestrus day. This increase was accompanied by an enhanced phosphorylation of Akt in Ser473 and of glycogen synthase kinase‐3β (GSK3β) in Ser9. Also, the association of β‐catenin with the synaptic protein PSD95 was increased during these same stages of the estrous cycle, whereas the levels of synapsin I were significantly decreased in proestrus. These findings suggest that Akt/GSK3β/β‐catenin signaling is involved in the synaptic modifications that occur in the basal hypothalamus during the estrous cycle. © 2012 Wiley Periodicals, Inc.