Altered distribution of striatal activity-dependent synaptic plasticity in the 3-nitropropionic acid model of Huntington's disease.
Huntington's disease (HD) is a neurodegenerative disorder characterized by involuntary choreiform movements, neuropsychiatric disturbances and cognitive decline. The hyperkinetic phenomenology has commonly been attributed to a disturbance of the basal ganglia function, mainly the neostriatum, but its pathophysiology mechanisms remain unclear. Activity-dependent long-term changes in synaptic efficacy, such as long-term potentiation (LTP) and long-term depression (LTD), are widely considered to be the cellular models for acquisition and storage of information in neuronal networks. Both LTP and LTD have been described at the corticostriatal pathway and they might be probably involved not only in physiological motor behavior processing but also in disease states affecting that pathway. Systemic injection of 3-nitropropionic acid (3-NP) induces excitotoxic striatal lesions and abnormal movements in rodents, resembling those seen in HD. We examined synaptic plasticity in dorsolateral striatum slices prepared from both control and 3-NP-treated rats by recording extracellular field potentials. Our results reinforce the idea that both forms of activity-dependent synaptic plasticity can be recorded at the dorsolateral region of striatum by the same stimulating protocol in control rats and suggest that 3-NP-induced striatal lesions may be associated with suppression of LTD expression in the sensorimotor striatum.
Dalbem
André
A
Neuroscience Laboratory, Instituto de Pesquisas Biomédicas (Biomedical Research Institute), Hospital São Lucas, Pontifícia Universidade Católica do Rio Grande do Sul, Porto Alegre, RS, Brazil.
Silveira
Carine Volkweis
CV
Pedroso
Michele Franzen
MF
Breda
Ricardo Vaz
RV
Werne Baes
Cristiane Von
CV
Bartmann
Ana Paula
AP
da Costa
Jaderson Costa
JC
D000818:Animals; D003342:Corpus Striatum / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology*; D004195:Disease Models, Animal; D004791:Enzyme Inhibitors / Q000633:toxicity; D006816:Huntington Disease / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology*; D007150:Immunohistochemistry; D008297:Male; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology*; D009574:Nitro Compounds; D009924:Organ Culture Techniques; D011422:Propionates / Q000633:toxicity; D051381:Rats; D017208:Rats, Wistar; D013569:Synapses / Q000187:drug effects / Q000502:physiology*
D004791:Enzyme Inhibitors; D009574:Nitro Compounds; D011422:Propionates; C015392:3-nitropropionic acid