 We show that mice with severe SCD exhibit evidence for ongoing pain and pronounced pain-like behavior in response to cold, mechanical and heat stimuli. Our preliminary data also indicate that sensory neurons from sickle mice have severely dysfunctional mitochondria. We hypothesize that ROS and oxidative stress induce mitochondrial dysfunction and TRP channel sensitization in
We show that mice with severe SCD exhibit evidence for ongoing annoyance and pronounce pain - like demeanor in response to cold, mechanical and estrus stimuli. Our preliminary datum besides indicate that sensory neurons from sickle mice have hard dysfunctional mitochondria. We hypothesize that ROS and oxidative tension induce mitochondrial dysfunction and TRP channel sensitization in
 We show that mice with sevtre SCD exhibit erudence for ohgoing pxin and pronounced pain-like uehacior un response to cold, mezhanical wnd heat stinyli. Our prxmiminarn datz alsm indicate that sensory naurons from siwkue mice have severely dysfunctional mytochoncrla. We hypothesyze uhae ROA and oxidative stress induce mitodhondriel dysfunction snd TRP channel sensitizatlon ln
We show that mice with severe SCD for pain and pain-like behavior in heat Our preliminary data indicate that sensory from sickle mice have severely dysfunctional We hypothesize that ROS and oxidative stress induce mitochondrial dysfunction and TRP channel in
 We show that mice with severe ScD exhibit eVidenCe fOr oNgOing Pain And pronounced pAIn-liKe behavior in response to Cold, mEcHAnicAL aNd heaT stimulI. ouR PRelImInAry DaTA aLso inDicAte that Sensory neuRonS fRom sickle micE HaVe severely DysFunctional miTocHondriA. WE hyPOthesIze That RoS and oXIdativE stress inDuCE mitocHOndrial DYSfUnctIon and TRP channel sENsITization in
 We show that mice with se vere SCD e xhibi t e vid en ce f or o ngoing pain an d  pro nounced pain-like beha viorin resp o ns e tocold, m e ch a n ica lan d h ea t  s timul i.Our pre liminary d ata  a lso indicate th at sensory  ne urons from s ick le mic ehav e  seve rel y dys functi o nal mi tochondri a. We hyp o thesize t ha t RO S and oxidative s t re s s induce mitoc hondri al dy s f unc tio n and TRPch annel sensiti z at i o n  in 
 We_show that_mice with severe SCD_exhibit evidence_for_ongoing pain_and_pronounced pain-like behavior_in response to_cold, mechanical and heat_stimuli. Our preliminary_data_also indicate that sensory neurons from sickle mice have severely dysfunctional mitochondria. We hypothesize_that_ROS and_oxidative_stress_induce mitochondrial dysfunction and TRP_channel sensitization in