title: Ensemble encoding of nociceptive stimulus intensity in the rat medial and lateral pain systems.
abstract: BACKGROUND
  The ability to encode noxious stimulus intensity is essential for the neural processing of pain perception. It is well accepted that the intensity information is transmitted within both sensory and affective pathways. However, it remains unclear what the encoding patterns are in the thalamocortical brain regions, and whether the dual pain systems share similar responsibility in intensity coding.
  
  
  RESULTS
  Multichannel single-unit recordings were used to investigate the activity of individual neurons and neuronal ensembles in the rat brain following the application of noxious laser stimuli of increasing intensity to the hindpaw. Four brain regions were monitored, including two within the lateral sensory pain pathway, namely, the ventral posterior lateral thalamic nuclei and the primary somatosensory cortex, and two in the medial pathway, namely, the medial dorsal thalamic nuclei and the anterior cingulate cortex. Neuron number, firing rate, and ensemble spike count codings were examined in this study. Our results showed that the noxious laser stimulation evoked double-peak responses in all recorded brain regions. Significant correlations were found between the laser intensity and the number of responsive neurons, the firing rates, as well as the mass spike counts (MSCs). MSC coding was generally more efficient than the other two methods. Moreover, the coding capacities of neurons in the two pathways were comparable.
  
  
  CONCLUSIONS
  This study demonstrated the collective contribution of medial and lateral pathway neurons to the noxious intensity coding. Additionally, we provide evidence that ensemble spike count may be the most reliable method for coding pain intensity in the brain.
authors.affiliation: Neuroscience Research Institute and Department of Neurobiology, Peking University Health Science Center, Beijing, China.
authors.forename: Yang
authors.initials: Y
authors.lastname: Zhang
authors.forename: Ning
authors.initials: N
authors.lastname: Wang
authors.forename: Jin-Yan
authors.initials: JY
authors.lastname: Wang
authors.forename: Jing-Yu
authors.initials: JY
authors.lastname: Chang
authors.forename: Donald J
authors.initials: DJ
authors.lastname: Woodward
authors.forename: Fei
authors.initials: F
authors.lastname: Luo
mesh_terms: D000200:Action Potentials / Q000502:physiology*; D000818:Animals; D001522:Behavior, Animal; D002452:Cell Count; D004566:Electrodes; D006179:Gyrus Cinguli / Q000473:pathology / Q000503:physiopathology; D007834:Lasers; D020645:Mediodorsal Thalamic Nucleus / Q000473:pathology / Q000503:physiopathology; D009434:Neural Pathways; D059225:Nociception / Q000502:physiology*; D009619:Nociceptors / Q000378:metabolism* / Q000473:pathology; D010146:Pain / Q000473:pathology / Q000503:physiopathology*; D010812:Physical Stimulation; D051381:Rats; D013003:Somatosensory Cortex / Q000473:pathology / Q000503:physiopathology; D020651:Ventral Thalamic Nuclei / Q000473:pathology / Q000503:physiopathology