Reelin supplementation recovers synaptic plasticity and cognitive deficits in a mouse model for Angelman syndrome

The European Journal of Neuroscience
Whitney R HethornE J Weeber

Abstract

The Reelin signaling pathway is implicated in processes controlling synaptic plasticity and hippocampus-dependent learning and memory. A single direct in vivo application of Reelin enhances long-term potentiation, increases dendritic spine density and improves associative and spatial learning and memory. Angelman syndrome (AS) is a neurological disorder that presents with an overall defect in synaptic function, including decreased long-term potentiation, reduced dendritic spine density, and deficits in learning and memory, making it an attractive model in which to examine the ability of Reelin to recover synaptic function and cognitive deficits. In this study, we investigated the effects of Reelin administration on synaptic plasticity and cognitive function in a mouse model of AS and demonstrated that bilateral, intraventricular injections of Reelin recover synaptic function and corresponding hippocampus-dependent associative and spatial learning and memory. Additionally, we describe alteration of the Reelin profile in tissue from both the AS mouse and post-mortem human brain.

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Related Concepts

Reln protein, rat
Metazoa
Insula of Reil
Structure of Subiculum Hippocampi
Injections, Intraventricular
Nerve Tissue Proteins
Serine Endopeptidases
Cell Adhesion Molecules, Neuronal
Extracellular Matrix Proteins
Angelman Syndrome

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