Seminar Series

Different involvement of neocortical high- and low-gamma rhythms in spike-pattern replay following sensory stimulation in in vitro models of wake as sleep state

Adaptation to repeated sensory inputs is a critical component governing cognitive performance. In awake state, plastic changes to stimulation result in a reduction of the cortical response in the gamma band (‘repetition suppression’) and an increase in temporal precision of neuronal outputs (‘sharpening’) for familiar stimuli. For novel stimuli an increase in the gamma band cortical response is seen (repetition enhancement). These processes are well documented but it is not clear how they occur mechanistically. Using in vitro models of repeated, ascending input to primary auditory cortex we can show that both suppression and enhancement of neuronal outputs occurs concurrently in a lamina-specific manner. Both phenomena are associated with elevated local field potential gamma power in the low- but not high-subband. This dichotomy appears to relate to two different profiles of synaptic plasticity: In superficial layers, enhanced neuronal outputs correlated with plasticity of excitatory synapses onto excitatory neurons; In deep layers, suppressed neuronal outputs correlated with plasticity of inhibitory synapses onto excitatory neurons. In contrast to the role of low-gamma rhythms in the reorganisation of spike-patterns in the awake state, subsequent generation of delta rhythms (to model NREM3/4 sleep) resulted in spike replay only for neurons previously active and phase-locked to high-gamma rhythms. These findings will be discussed in relation to memory consolidation and what may constitute an error signal in cortex.