Journal
NEUROIMAGE
Volume 15, Issue 3, Pages 633-639Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1006/nimg.2001.1045
Keywords
-
Ask authors/readers for more resources
Long-term potentiation (LTP), a model of activity-dependent synaptic plasticity, involves the persistent enhancement of excitatory neurotransmission. Several recent studies have suggested a critical role for nitric oxide (NO) production in hippocampal LTP. However, increase in NO production in living tissue has not yet been directly demonstrated. We used 1,2-diaminoanthraquinone (DAQ) to demonstrate NO production in rat brain slices in relation to induction of LTP. DAQ was found to be without neurotoxic effects and it neither influenced normal evoked field potential amplitudes nor did it affect induction of LTP in comparison to controls. We found that DAQ-induced fluorescence is elevated within a limited area of about 40,000 mum(2) during LTP induction in the hippocampal area CA1. Furthermore, we could demonstrate that application of the NO-synthetase inhibitor L-NAME inhibits the induction of LTP in area CA1 and causes a strong reduction of DAQ induced fluorescence. Our results are consistent with the hypothesis that NO can serve as a retrograde messenger during induction of LTP in the hippocampus. (C) 2002 Elsevier Science (USA).
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available