Transient neocortical gamma oscillations induced by neuronal response modulation In this paper a mean field model of spatiotemporal electroencephalographic activity in the neocortex is used to computationally study the emergence of neocortical gamma oscillations as a result of neuronal response modulation. It is shown using a numerical bifurcation analysis that gamma oscillations emerge robustly in the solutions of the model and transition to beta oscillations through coordinated modulation of the responsiveness of inhibitory and excitatory neuronal populations. The spatiotemporal pattern of the propagation of these oscillations across the neocortex is illustrated by solving the equations of the model using a finite element software package. Thereby, it is shown that the gamma oscillations remain localized to the regions of neuronal modulation. Moreover, it is discussed that the inherent spatial averaging effect of commonly used electrocortical measurement techniques can significantly alter the amplitude and pattern of fast oscillations in neocortical recordings, and hence can potentially affect physiological interpretations of these recordings.

Interactions between stimulievoked cortical activity and spontaneous low frequency oscillations measured with neuronal calcium Abstract   Spontaneous brain activity has been widely used to map brain connectivity. The interactions between taskevoked brain responses and the spontaneous cortical oscillations, especially within the low frequency range of xe2x88xbc0.1xe2x80xafHz, are not fully understood. Trialtotrial variabilities in brainu0027s response to sensory stimuli and the ability for brain to detect under noisy conditions suggest an appreciable impact of the brain state. Using a multimodality imaging platform, we simultaneously imaged neuronal Ca2 and cerebral hemodynamics at baseline and in response to singlepulse forepaw stimuli in ratu0027s somatosensory cortex. The high sensitivity of this system enables detection of responses to very weak and strong stimuli and real time determination of low frequency oscillations without averaging. Results show that the ongoing neuronal oscillations inversely modulate Ca2 transients evoked by sensory stimuli. High intensity stimuli reset the spontaneous neuronal oscillations to an unpreferable excitability following the stimulus. Cerebral hemodynamic responses also inversely interact with the spontaneous hemodynamic oscillations, correlating with the neuronal Ca2 transient changes. The results reveal competing interactions between spontaneous oscillations and stimulationevoked brain activities in somatosensory cortex and the resultant hemodynamics.