title: Sensory enrichment after peripheral nerve injury restores cortical, not thalamic, receptive field organization.
abstract: Sensory perception can be severely degraded after peripheral injuries that disrupt the functional organization of the sensory maps in somatosensory cortex, even after nerve regeneration has occurred. Rehabilitation involving sensory retraining can improve perceptual function, presumably through plasticity mechanisms in the somatosensory processing network. However, virtually nothing is known about the effects of rehabilitation strategies on brain organization, or where the effects are mediated. In this study, five macaque monkeys received months of enriched sensory experience after median nerve cut and repair early in life. Subsequently, the sensory representation of the hand in primary somatosensory cortex was mapped using multiunit microelectrodes. Additionally, the primary somatosensory relay in the thalamus, the ventroposterior nucleus, was studied to determine whether the effects of the enrichment were initiated subcortically or cortically. Age-matched controls included six monkeys with no sensory manipulation after median nerve cut and regeneration, and one monkey that had restricted sensory experience after the injury. The most substantial effect of the sensory environment was on receptive field sizes in cortical area 3b. Significantly greater proportions of cortical receptive fields in the enriched monkeys were small and well localized compared to the controls, which showed higher proportions of abnormally large or disorganized fields. The refinements in receptive field size and extent in somatosensory cortex likely provide better resolution in the sensory map and may explain the improved functional outcomes after rehabilitation in humans.
authors.affiliation: Department of Psychology, 301 Wilson Hall, Vanderbilt University, Nashville TN 37203, USA. sherre.l.florence@vanderbilt.edu
authors.forename: S L
authors.initials: SL
authors.lastname: Florence
authors.forename: L A
authors.initials: LA
authors.lastname: Boydston
authors.forename: T A
authors.initials: TA
authors.lastname: Hackett
authors.forename: H T
authors.initials: HT
authors.lastname: Lachoff
authors.forename: F
authors.initials: F
authors.lastname: Strata
authors.forename: M M
authors.initials: MM
authors.lastname: Niblock
mesh_terms: D000818:Animals; D001931:Brain Mapping; D003714:Denervation / Q000009:adverse effects; D005073:Evoked Potentials, Somatosensory / Q000502:physiology; D006987:Hypesthesia / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D008253:Macaca mulatta; D009416:Nerve Regeneration / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology*; D009474:Neurons / Q000166:cytology / Q000502:physiology; D010465:Perception / Q000502:physiology; D059348:Peripheral Nerve Injuries; D010525:Peripheral Nerves / Q000473:pathology / Q000503:physiopathology; D010812:Physical Stimulation / Q000379:methods; D020127:Recovery of Function / Q000502:physiology*; D013003:Somatosensory Cortex / Q000166:cytology / Q000502:physiology*; D014110:Touch / Q000502:physiology*; D020651:Ventral Thalamic Nuclei / Q000166:cytology / Q000502:physiology*