title: Exposure to intermittent nociceptive stimulation under pentobarbital anesthesia disrupts spinal cord function in rats.
abstract: BACKGROUND
  Spinal cord plasticity can be assessed in spinal rats using an instrumental learning paradigm in which subjects learn an instrumental response, hindlimb flexion, to minimize shock exposure. Prior exposure to uncontrollable intermittent stimulation blocks learning in spinal rats but has no effect if given before spinal transection, suggesting that supraspinal systems modulate nociceptive input to the spinal cord, rendering it less susceptible to the detrimental consequences of uncontrollable stimulation.
  
  
  OBJECTIVE
  The present study examines whether disrupting brain function with pentobarbital blocks descending inhibitory systems that normally modulate nociceptive input, making the spinal cord more sensitive to the adverse effect of uncontrollable intermittent stimulation.
  
  
  METHODS
  Male Sprague-Dawley rats received uncontrollable intermittent stimulation during pentobarbital anesthesia after (experiment 1) or before (experiment 2) spinal cord transection. They were then tested for instrumental learning at a later time point. Experiment 3 examined whether these manipulations affected nociceptive (thermal) thresholds.
  
  
  RESULTS
  Experiment 1 showed that pentobarbital had no effect on the induction of the learning deficit after spinal cord transection. Experiment 2 showed that intact rats anesthetized during uncontrollable intermittent stimulation failed to learn when later transected and tested for instrumental learning. Experiment 3 found that uncontrollable intermittent stimulation induced an antinociception in intact subjects that was blocked by pentobarbital.
  
  
  CONCLUSIONS
  The results suggest a surgical dose of pentobarbital (50 mg/kg) suppresses supraspinal (experiment 2) but not spinal (experiment 1) systems that modulate nociceptive input to the spinal cord by blocking the antinociception that is induced by this input (experiment 3).
authors.affiliation: Psychology Department, Texas A&M University, College Station, TX 77843-4235, USA. swashburn@tamu.edu
authors.forename: Stephanie N
authors.initials: SN
authors.lastname: Washburn
authors.forename: Brianne C
authors.initials: BC
authors.lastname: Patton
authors.forename: Adam R
authors.initials: AR
authors.lastname: Ferguson
authors.forename: Kara L
authors.initials: KL
authors.lastname: Hudson
authors.forename: James W
authors.initials: JW
authors.lastname: Grau
mesh_terms: D000818:Animals; D001522:Behavior, Animal; D003216:Conditioning, Operant / Q000187:drug effects; D004597:Electroshock; D006614:Hindlimb; D006993:Hypnotics and Sedatives / Q000494:pharmacology*; D008297:Male; D009473:Neuronal Plasticity / Q000187:drug effects* / Q000502:physiology; D009619:Nociceptors / Q000187:drug effects*; D010146:Pain / Q000188:drug therapy; D010147:Pain Measurement; D017288:Pain Threshold; D010424:Pentobarbital / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013116:Spinal Cord / Q000187:drug effects* / Q000502:physiology; D013119:Spinal Cord Injuries / Q000503:physiopathology
chemical_list: D006993:Hypnotics and Sedatives; D010424:Pentobarbital