The development of a reliable methodology for documentation of the role of NO in neural behavior is a very tantalizing prospect. NO has been implicated in some neural functions in vitro and evidence for its presence in the LGN is fairly strong, but to date the degree and nature of its impact on the transmission of neural signals remains elusive. In conjunction with others, the PI has developed a new and unique system for quantifiable delivery of NO at specific sites, a sine qua non for establishment of the neural activity of the compound. If successful, the completion of this work has a good likelihood of yielding a breakthrough in this regard. The criticisms of the last submission centered around the problem that the proposed program was too ambitious for available resources and not well-focused. On the whole the PI has responded directly to the critiques. The inclusion of a seasoned research associate will help to insure progress, and with the elimination of the in vivo electrophysiology the scope of the investigation is more realistic. It is not clear whether the move to cat (as opposed to rat) is the best approach, inasmuch as the bulk of the work would appear to concentrate on in vitro studies, and use of rat tissue is rather more proven in this context. The risk may be balanced by the direct utility of the results for future electrophysiological work in the cat. Perhaps the greatest risk is the possibility of failure to find any significant effect of NO on signal transmission, despite the suggestions documented in the background studies. For this reason, reduction of the grant period to four years is suggested.
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