Premium
Aggregate formation and the impairment of long‐term synaptic facilitation by ectopic expression of mutant huntingtin in Aplysia neurons
Author(s) -
Lee JinA,
Lim ChaeSeok,
Lee SeungHee,
Kim Hyoung,
Nukiobuyuki,
Kaang BongKiun
Publication year - 2003
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2003.01650.x
Subject(s) - aplysia , huntingtin , facilitation , neuroscience , ectopic expression , neural facilitation , mutant , chemistry , microbiology and biotechnology , biology , inhibitory postsynaptic potential , excitatory postsynaptic potential , biochemistry , gene
Huntington's disease (HD) is caused by an expansion of a polyglutamine (polyQ) tract within huntingtin (htt) protein. To examine the cytotoxic effects of polyQ‐expanded htt, we overexpressed an enhanced green fluorescent protein (EGFP)‐tagged N‐terminal fragment of htt with 150 glutamine residues (Nhtt150Q‐EGFP) in Aplysia neurons. A combined confocal and electron microscopic study showed that Aplysia neurons expressing Nhtt150Q‐EGFP displayed numerous abnormal aggregates (diameter 0.5–5 µm) of filamentous structures, which were formed rapidly (approximately 2 h) but which were sustained for at least 18 days in the cytoplasm. Furthermore, the overexpression of Nhtt150Q‐EGFP in sensory cells impaired 5‐hydroxytryptamine (5‐HT)‐induced long‐term synaptic facilitation in sensori‐motor synapses without affecting basal synaptic strength or short‐term facilitation. This study demonstrates the stability of polyQ‐based aggregates and their specific effects on long‐term synaptic plasticity.