x il ins ▁( H x ), ▁H x A 3 ▁( i . e . ▁ 8 R / S - h ydro xy - 1 1 , 1 2 - ox ido - 5 Z , 9 E , 1 4 Z - e icos atri eno ic ▁acid ) ▁and ▁H x B 3 ▁( i . e . ▁ 1 0 R / S - h ydro xy - 1 1 , 1 2 - ox ido - 5 Z , 8 Z , 1 4 Z - e icos atri eno ic ▁acid ) ▁( see ▁He po x il in # P ain ▁per ception ) ▁directly ▁activ ate ▁TR PA 1 ▁and ▁thereby ▁contribute ▁to ▁the ▁hyper al ges ia ▁and ▁tact ile ▁all od yn ia ▁responses ▁of ▁m ice ▁to ▁skin ▁infl amm ation . ▁In ▁this ▁animal ▁model ▁of ▁pain ▁per ception , ▁the ▁he po x il ins ▁are ▁released ▁in ▁sp inal ▁cord ▁and ▁directly ▁activ ate ▁TR PA ▁( and ▁also ▁TR P V 1 ) ▁re cept ors ▁to ▁augment ▁the ▁per ception ▁of ▁pain . ▁ 1 2 S - H p ET E , ▁which ▁is ▁the ▁direct ▁prec ursor ▁to ▁H x A 3 ▁and ▁H x B 3 ▁in ▁the ▁A LO X 1 2 ▁path way , ▁may ▁act ▁only ▁after ▁being ▁converted ▁to ▁these ▁he po x il ins . ▁The ▁epo x ide , ▁ 4 , 5 - ep ox y