Ketamine increases and decreases the power of baseline and evoked Υ oscillations, respectively.
Top left: Experimental design showing the 3 principal neuronal elements of the somatosensory thalamocortical system (CT, corticothalamic; ECoG, electrocorticogram; TC, thalamocortical; TRN, thalamic reticular nucleus). The experiments were made in non-anesthetized head-restrained rats under control (cont) and ketamine (keta; 2.5 mg/kg, subcutaneous) conditions. Sensory-evoked potentials were recorded following contralateral natural-like mechanical stimulation of a few vibrissae with a piezo bender actuator. Bottom: Time-frequency-power graph of the ECoG for each condition (sensory stimulus given at 0 ms). The Z values (frequency power) are in color code. Up right: Quantitative and statistical analysis (*, t-test, p< 0.0001) show that ketamine administration increases the power of basal Υ oscillations and decreases the power of evoked Υ oscillations. The averaged power of the basal Υ oscillations is measured during the 100-ms epoch before the sensory stimulation (45 trials, 3 rats). The power of the sensory-evoked Υ oscillations is directly measured from the average sensory-evoked potential (12 values from the post-stimulus 100-ms epoch from 3 rats per condition). This finding complements clinical data and has mechanistic importance since it provides evidence in support of the hypothesis of the existence of multiple generators of Υ oscillations. Adapted from Kulikova et al., first published online in Eur. J. Neurosci. :29 AUG 2012 (DOI: 10.1111/j.1460-9568.2012.08263.x.)