Huntingtin is critical both pre- and postsynaptically for long-term learning-related synaptic plasticity in Aplysia.

ABSTRACT: Patients with Huntington's disease exhibit memory and cognitive deficits many years before manifesting motor disturbances. Similarly, several studies have shown that deficits in long-term synaptic plasticity, a cellular basis of memory formation and storage, occur well before motor disturbances in the hippocampus of the transgenic mouse models of Huntington's disease. The autosomal dominant inheritance pattern of Huntington's disease suggests the importance of the mutant protein, huntingtin, in pathogenesis of Huntington's disease, but wild type huntingtin also has been shown to be important for neuronal functions such as axonal transport. Yet, the role of wild type huntingtin in long-term synaptic plasticity has not been investigated in detail. We identified a huntingtin homolog in the ma

SUBMITTER: Choi YB 

PROVIDER: S-EPMC4108396 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature