title: Functional plasticity in primate somatosensory thalamus following chronic lesion of the ventral lateral spinal cord.
abstract: The long-term consequences of thoracic spinothalamic tract lesion on the physiological properties of neurons in the ventral posterior lateral nucleus of the thalamus in monkeys were assessed. Neurons responding to both compressive and phasic brush stimuli (multireceptive neurons), but not brush-specific (low-threshold) neurons, in the partially deafferented thalamus showed increased spontaneous activity, increased responses evoked by cutaneous stimuli and larger mean receptive field size than the same types of cells in the thalamus with intact innervation. The spike train properties of both the spontaneous and evoked discharges of cells were also altered so that there was an increased incidence of spike-bursts in cells of deafferented thalamus. These changes were widespread in the thalamus, and included cells in both the fully innervated forelimb representation and the partially denervated hindlimb representation ipsilateral to the lesion. The spontaneous and evoked spike trains in the ipsilateral thalamus also show increased frequency of both spike-burst and non-burst events compared to the intact thalamus. These results indicate that chronic spinothalamic tract lesion produces widespread changes in the physiological properties of a discrete cell population of the thalamus.The findings in this study indicate that the thalamic processing of somatosensory information conveyed by the lemniscal system is altered by transection of the spinothalamic tract. This change in sensory processing in the thalamus would result in altered cortical processing of innocuous somatosensory inputs following deafferentation and so possibly contribute to the generation of the central pain syndrome.
authors.affiliation: Department of Neurosurgery, The Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
authors.forename: H R
authors.initials: HR
authors.lastname: Weng
authors.forename: J I
authors.initials: JI
authors.lastname: Lee
authors.forename: F A
authors.initials: FA
authors.lastname: Lenz
authors.forename: A
authors.initials: A
authors.lastname: Schwartz
authors.forename: C
authors.initials: C
authors.lastname: Vierck
authors.forename: L
authors.initials: L
authors.lastname: Rowland
authors.forename: P M
authors.initials: PM
authors.lastname: Dougherty
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000818:Animals; D002908:Chronic Disease; D003714:Denervation / Q000009:adverse effects; D005073:Evoked Potentials, Somatosensory / Q000502:physiology*; D006930:Hyperalgesia / Q000473:pathology / Q000503:physiopathology; D008251:Macaca / Q000033:anatomy & histology / Q000502:physiology* / Q000601:surgery; D009473:Neuronal Plasticity / Q000502:physiology*; D009474:Neurons / Q000145:classification / Q000473:pathology / Q000502:physiology*; D010146:Pain / Q000473:pathology / Q000503:physiopathology; D010812:Physical Stimulation; D013133:Spinothalamic Tracts / Q000473:pathology / Q000503:physiopathology* / Q000601:surgery; D014110:Touch / Q000502:physiology; D020651:Ventral Thalamic Nuclei / Q000473:pathology / Q000503:physiopathology*