Contributions of GABAergic and glutamatergic mechanisms to isoflurane-induced suppression of thalamic somatosensory information transfer.

Indications for a pivotal role of the thalamocortical network in producing the state of anesthesia have come from in vivo animal studies as well as imaging studies in humans. We studied possible synaptic mechanisms of anesthesia-induced suppression of touch perception in the rat's thalamus. Thalamocortical relay neurons (TCNs) receive ascending and descending glutamatergic excitatory inputs via NMDA and non-NMDA receptors (AMPAR) and are subjected to GABA(A)ergic inhibitory input which shapes the sensory information conveyed to the cortex.

Increased responsiveness of cortical neurons in contrast to thalamic neurons during isoflurane-induced EEG bursts in rats.

The neuronal mechanisms underlying the electroencephalographic (EEG) burst-suppression pattern are not yet understood, however, they are generally attributed to interactions within thalamocortical networks. In contrast, we report that the sensory cortex and the thalamus are disconnected, with thalamic sensory processing being unaffected by cortical EEG bursts. We studied the activity of single neurons of the somatosensory thalamocortical system in rats during burst-suppression EEG induced by the volatile anesthetic, isoflurane.