Reticular influences on primary and augmenting responses in the somatosensory cortex.
The effects of brief, conditioning trains of high-frequency pulses to the midbrain reticular formation (RF) on primary and augmenting responses of somatosensory (SI) cortex were investigated. Testing stimulation was applied to the ventrobasal (VB) thalamus or to the white matter (WM) beneath SI in VB-lesioned animals. The RF-elicited EEG activation was associated with increased firing rates of SI neurons, enhanced probability of early synaptic discharges to VB or WM stimuli, and significantly reduced duration of the suppressed firing period following an afferent VB or WM volley. The diminished latency of the postinhibitory rebound under RF stimulation had the consequence that, within 10/sec shock-train, the second stimulus was delivered following completion of the rebound component and, instead of an augmented potential, generated a field response of primary-type. The dependence of the RF-induced change in augmenting potentials upon the sharpening effect exerted on the preceding inhibitory-rebound sequence was corroborated by analyzing the RF influence on neurons with different time-course of recovery from inhibition. The replacement of augmenting potentials by primary responses under RF stimulation is advanced as the mechanism behind the obliteration of spontaneously developing 'type I' spindle-waves during EEG arousal. The demonstration of RF influences on SI responses to WM stimulation in VB-lesioned animals points out the cortical level of the effects. The reticulo-thalamo-cortical pathways underlying these influences are discussed.
D000818:Animals; D002415:Cats; D003344:Cortical Synchronization; D005071:Evoked Potentials; D008636:Mesencephalon / Q000502:physiology; D009433:Neural Inhibition; D009434:Neural Pathways / Q000502:physiology; D009474:Neurons / Q000502:physiology; D012154:Reticular Formation / Q000502:physiology*; D013003:Somatosensory Cortex / Q000502:physiology*; D009435:Synaptic Transmission; D013787:Thalamic Nuclei / Q000502:physiology