title: Contribution of GABAergic cortical circuitry in shaping somatosensory evoked scalp responses: specific changes after single-dose administration of tiagabine.
abstract: OBJECTIVE
  To determine whether conventional as well as high-frequency somatosensory evoked potentials (SEPs) to upper limb stimulation are influenced by GABAergic intracortical circuitry.
  
  
  METHODS
  We recorded SEPs from 6 healthy volunteers before and after a single-oral administration of tiagabine. Conventional low-frequency SEPs have been obtained after stimulation of the median nerve, as well as after stimulation of the first phalanx of the thumb, which selectively involves cutaneous finger inputs. Median nerve SEPs have been further analyzed after digital narrow-bandpass filtering, to selectively examine high-frequency responses. Lastly, in order to explain scalp SEP distribution before and after tiagabine administration, we performed the brain electrical source analysis (BESA) of raw data.
  
  
  RESULTS
  After tiagabine administration, conventional scalp SEPs showed a significant amplitude increase of parietal P24, frontal N24 and central P22 components. Similarly, BESA showed a significant strength increase of the second peak of activation of the first two perirolandic dipoles, which are likely to correspond to the N24/P24 and P22 generators. By contrast, no significant changes of high-frequency SEPs were induced by drug intake.
  
  
  CONCLUSIONS
  Our findings support the view that both N24/P24 and P22 SEP components are probably generated by deep spiny cell hyperpolarization, which is strongly increased by inhibitory inputs from GABAergic interneurons. By considering the clear influence of inhibitory circuitry in shaping these SEP components, conventional scalp SEP recording could be useful in the functional assessment of the somatosensory cortex in different physiological and pathological conditions. By contrast, intrinsic firing properties of the cell population generating high-frequency SEP responses are unaffected by the increase of recurrent GABAergic inhibition.
authors.affiliation: Department of Neurology, Catholic University, Policlinico A. Gemelli, L.go A. 00168 Rome, Italy. drestuccia@rm.unicatt.it
authors.forename: D
authors.initials: D
authors.lastname: Restuccia
authors.forename: M
authors.initials: M
authors.lastname: Valeriani
authors.forename: E
authors.initials: E
authors.lastname: Grassi
authors.forename: G
authors.initials: G
authors.lastname: Gentili
authors.forename: S
authors.initials: S
authors.lastname: Mazza
authors.forename: P
authors.initials: P
authors.lastname: Tonali
authors.forename: F
authors.initials: F
authors.lastname: Mauguière
mesh_terms: D000328:Adult; D005073:Evoked Potentials, Somatosensory / Q000187:drug effects* / Q000502:physiology; D018755:GABA Agonists / Q000008:administration & dosage* / Q000009:adverse effects; D006801:Humans; D008297:Male; D018482:Muscle, Skeletal / Q000294:innervation; D009475:Neurons, Afferent / Q000502:physiology; D009557:Nipecotic Acids / Q000008:administration & dosage* / Q000009:adverse effects; D011434:Proprioception / Q000187:drug effects / Q000502:physiology; D013003:Somatosensory Cortex / Q000502:physiology*; D000078308:Tiagabine; D005680:gamma-Aminobutyric Acid / Q000502:physiology*
chemical_list: D018755:GABA Agonists; D009557:Nipecotic Acids; D005680:gamma-Aminobutyric Acid; D000078308:Tiagabine