Differences in cutaneous sensory response properties of single somatosensory cortical neurons in awake and halothane anesthetized rats.

The major aim of this study was to investigate the effect of halothane anesthesia on different latency components of cutaneous sensory responses of single units in the primary somatosensory (SI) cortex of rats. Quantitative studies of computer generated post-stimulus time histograms were used to determine whether the increase in "nonspecific" properties often observed in the SI cortices of awake animals were attributable to a generally increased sensory responsiveness of these cells or to a selective increase of certain "nonspecific" components of their sensory response. Sensory "specificity" was investigated here by measuring the size of cutaneous receptive fields of single cells and testing their ability to follow high stimulus frequencies. Histograms generated by repetitive touch stimulation of the forepaw in awake animals were divisible into the following different latency components: (1) a short latency excitatory response which was often divisible into two peaks (E1a and E1b), and occasionally (2) a post-excitatory inhibitory phase (I1) and/or (3) a long latency excitatory peak (E2). In anesthetized animals spontaneous discharge rates were lower and the proportion of cells exhibiting either pure inhibition or post-excitatory inhibition was increased. By contrast, the longer latency excitatory components (E1b and E2) were weaker and were seen much less frequently than in the awake situation. In nine cells tested in the awake state and then again in the anesthetized state the magnitude, receptive field size, and ability to follow high frequencies of the E1a peak was slightly reduced. The E1b and E2 peaks seen in the awake state, on the other hand, were completely abolished by anesthesia. In awake animals the E1b and E2 phases exhibited relatively "nonspecific" physiological properties. This was indicated by the facts that: (1) the cutaneous receptive fields of the E1a peak were slightly smaller than those of the E1b peaks and much smaller than those of the E2 peaks, and (2) the E1a peak was able to follow higher frequencies of touch stimulation than the E1b or E2 peaks. It is concluded therefore that although halothane anesthesia slightly depressed the short latency response component (E1a) exhibiting highly sensory properties, its main effect was to depress the longer latency excitatory components (E1b and E2) which exhibited relatively "nonspecific" properties.