Behavioral Consequences following Aav Mediated Hippocampal Eaac1 Knockdown

نویسندگان

  • Katie Marie Coombs
  • Michael Babcock
  • Carl A. Fox
  • Christy Weeden
  • Damon McNeil
  • Khena Bullshields
چکیده

The neuronal glutamate transporter EAAC1 (EAAT3) is present in hippocampal neurons to prevent excessive glutamate accumulation. Glutamate receptor-dependent synaptic plasticity is important for learning and memory. The present study investigates behavior associated with blocking the glutamate transporter EAAC1. To manipulate EAAC1 function, rats were intrahippocampally injected with a adeno-associated viral (AAV) vector encoding an EAAC1 antisense mRNA sequence or an AAV empty cassette. Twenty-eight days following surgery, rats were tested in a delayed matching-toplace (DMTP) watermaze task to examine spatial memory, which is hippocampaldependent. Rats treated with EAAC1 antisense exhibited shorter latencies to locate the target platform relative to controls (p < 0.05). These data indicate that microinfusion of AAV encoding EAAC1 antisense significantly altered performance on task involving glutamate transmission and the hippocampus.

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تاریخ انتشار 2007