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The level of arousal in mammals is correlated with metabolic state and specific patterns of cortical neuronal responsivity. In particular, rhythmic transitions between periods of high activity (up phases) and low activity (down phases) vary between wakefulness and deep sleep/anesthesia. Current opinion about changes in cortical response state between sleep and wakefulness is split between neuronal network-mediated mechanisms and neuronal metabolism-related mechanisms. Here, we demonstrate that slow oscillations in network state are a consequence of interactions between both mechanisms. Specifically, recurrent networks of excitatory neurons, whose membrane potential is partly governed by ATP--modulated potassium ([K.sub.ATP]) channels, mediate response-state oscillations via the interaction between excitatory network activity involving slow, kainate receptor-mediated events and the resulting activation of ATP-dependent homeostatic mechanisms. These findings suggest that [K.sub.ATP] channels function as an interface between neuronal metabolic state and network responsivity in mammalian cortex. glutamate | slow-wave oscillation | potassium channel | rhythm

Metabotropic glutamate receptors (mGluRs) in hippocampus are involved in the formation of long-term potentiation (LTP) and depotentiation. The mGluRs are essential to trigger LTP when slices are in a deconditioned state. The mGluRs trigger a molecular switch that removes the need for mGluR stimulation during LTP induction.