In　the　present　study,　the　effect　of　chronic　fatigue　stress　on　the　neuronal　nitric　oxide　synthase　(nNOS)　in　the　rat　nucleus　accumbens　(NAc)　was　assessed　in　order　to　explore　the　neurobiology　mechanism　of　central　fatigue　stress,　especially　the　role　of　the　NAc　in　central　fatigue.　In　the　experiment,　adult　male　Wistar　rats　were　forced　to　swim　till　exhaustion　every　day　for　4　weeks.　Immunohistochemistry　was　used　for　measurement　of　the　nNOS-positive　neurons　associated　with　the　image　manipulation.　Our　results　showed　that　a　long-time　exposure　to　chronic　forced　swim　stress　increased　the　number　of　nNOS　immunoreactive-positive　neurons　in　the　rat　NAc　(106.7%,　P　＜　0.001),　distributed　area　(150.2%,　P　＜　0.001)　and　gray　degree　value　(11.3%,　P　＜　0.01).　The　results　indicate　that　nitric　oxide　(NO)/nNOS　may　be　involved　in　the　formation　of　the　fatigue　stress,　and　that　NO　may　play　a　role　in　the　regulation　of　stress　in　the　NAc.　The　up-regulation　of　NO/nNOS　during　the　exposure　to　long-time　swim　stress　is　likely　to　be　one　of　the　results　of　brain　damage　and　psychiatric　disorder　induced　by　NO　overproduction.