Recent　studies　have　demonstrated　that　noradrenaline　acting　in　the　ventrolateral　orbital　cortex　(VLO)　can　potentially　reduce　allodynia　induced　by　spared　nerve　injury　(SNI),　and　this　effect　is　mediated　by　alpha(2)　adrenoceptor.　The　present　study　examined　the　effect　of　the　alpha　1　adrenoceptors　in　the　VLO　on　allodynia　induced　by　SNI　in　the　rats.　The　mechanical　paw　withdrawal　threshold　(PWT)　was　measured　using　von　Frey　filaments.　Microinjection　of　selective　alpha　1　adrenoceptor　agonist　methoxamine　(20,　50,100　mu　g　in　0.5　mu　l)　into　the　VLO,　contralateral　to　the　site　of　nerve　injury,　increased　PWT　in　a　dose-dependent　manner.　This　effect　was　antagonized　by　pre-microinjection　of　the　selective　alpha　1　adrenoceptor　antagonist　benoxathian　into　the　same　VLO　site,　and　blocked　by　electrolytic　lesion　of　the　ventrolateral　periaqueductal　gray　(PAG).　Furthermore,　pre-administration　of　non-selective　glutamate　receptor　antagonist　kynurenic　acid,　phospholipase　C　(PLC)　inhibitor　U73122,　and　protein　kinase　C　(PKC)　inhibitor　chelerythrine　to　the　VLO　also　blocked　methoxamine-induced　inhibition　of　allodynia.　These　results　suggest　that　activation　of　alpha　1　adrenoceptors　in　the　VLO　can　potentially　reduce　allodynia　induced　by　SNI.　This　effect　may　be　direct　excitation　of　the　VLO　neurons,　via　PLC-PKC　signaling　pathway,　projecting　to　the　PAG　or　facilitating　glutamate　release　and　then　indirectly　exciting　the　VLO　output　neurons　projecting　to　the　PAG,　leading　to　activation　of　the　PAG-brainstem　descending　inhibitory　system　which　depresses　the　nociceptive　transmission　at　the　spinal　cord　level.　(C)　2016　Elsevier　Ltd.　All　rights　reserved.