Propofol and ketamine increase the activity of certain potassium channels (TASK-3 and SK3, respectively), while pentobarbital and ketamine decrease the activity of SK1 channels. These effects were observed in Xenopus oocytes expressing seven types of potassium channels. Molecular docking simulations identified specific amino acid residues where each anesthetic binds: propofol to Q126 of TASK-3, ketamine to S290 of SK1 and S467 of SK3, and pentobarbital to S330 and T358 of SK1. Because these potassium channels help regulate respiration, heart rhythm, and blood vessel dilation, the findings suggest a molecular basis for the cardiovascular and respiratory side effects of intravenous general anesthetics.
In early schizophrenia, attention and perception problems are linked to brain structure and chemistry abnormalities, as well as disrupted brain rhythms in corticothalamic networks. The drug ketamine, which blocks NMDA receptors, mimics these symptoms. In lightly anesthetized rats, a single psychotomimetic dose of ketamine (2.5 mg/kg, subcutaneous) transiently increased baseline beta/gamma oscillations but decreased sensory-induced beta/gamma oscillations. It also disrupted information transfer in the somatosensory thalamus and cortex and reduced sensory-induced thalamocortical connectivity in the broadband gamma range. These findings support the hypothesis that NMDA receptor antagonism disrupts the transfer of perceptual information in the somatosensory cortico-thalamo-cortical system.