Decreased expression of spine-associated Rap guanosine triphosphatase-activating protein (SPAR) in glutamate-treated primary hippocampal neurons

Abstract

Spine-associated Rap guanosine triphosphatase-activating protein (SPAR) is an important regulator of activity-dependent remodeling of synapses. It is also critically involved in both mature dendritic spine formation and the maintenance of spine maturity. Glutamate is a major neurotransmitter of the brain, and is involved in all aspects of cognitive function, as it is the primary transmitter utilized by the cortical and hippocampal pyramidal neurons. Glutamate has also been associated with neuronal dendritic spine damage. The precise molecular mechanisms underlying dendritic spine damage following glutamate-induced neurotoxicity remain unknown. In the current study, we measured mRNA and protein expression levels of SPAR and serum-inducible kinase (SNK) in primary hippocampal neurons following glutamate treatment. Expression of SPAR and SNK was altered by glutamate treatment, indicating that the SPAR and SNK signaling pathways may be involved in the damage to dendritic spines in hippocampal neurons following excitotoxicity induced by glutamate.