title: Development from primary to augmenting responses in the somatosensory system.
abstract: The development from primary to augmenting responses of somatosensory (SI) cortical area to low-frequency stimulation of the ventrobasal (VB) thalamus or white matter (WM) beneath SI in VB-lesioned preparations was studied by field potential analysis and extracellular unit recording. Compared to the major postsynaptic components of the primary field response, which reverse at 0.25--0.35 mm and whose sink extends from 0.6 to 1.8 mm, the augmenting potential reverses more superficially (0.1--0.15 mm) and its large depth-negativity is located in layers III and IV (0.4--1 mm). Augmentation is visible by the second shock of a 10/sec train; it grows from a late (15--20 msec) depth-negative wave in conjunction with the decrement of the early rapid components of the primary response. Out of 47 neurons that responded to the first shock in the 10/sec VB or WM train with early (less than 5 msec) discharges, 23 fulfilled stringent criteria for augmentation at the second shock: greater than 100% increased discharge probability and greater than 100% increased mean latency of response. The necessary condition for the generation of an augmented potential is a given temporal relation between the evoking stimulus and the declining phase of inhibition or the onset of rebound in the preceding response. The augmented potential cannot appear if the stimulus is delivered following the rebound of the preceding response. Not only this finding, but the similarity between the depth-profiles of the rebound and augmenting potential suggest that the same elements are responsible for both events. While the patterns of augmenting responses to WM stimulation in VB-lesioned preparations differ slightly from thalamically evoked augmenting waves, the intrinsic cortical organization is sufficient for the development of a primary potential into augmenting responses.
mesh_terms: D000818:Animals; D002415:Cats; D004558:Electric Stimulation; D005071:Evoked Potentials; D009433:Neural Inhibition; D009434:Neural Pathways / Q000502:physiology; D009474:Neurons / Q000502:physiology; D013003:Somatosensory Cortex / Q000502:physiology*; D009435:Synaptic Transmission; D013787:Thalamic Nuclei / Q000502:physiology; D013788:Thalamus / Q000502:physiology*