Thus, the initial spikes in a response to cortical input may already be part of a gamma-synchronized response (Fries et al., 2001). While a pure selleck rate code may be feasible as means to provide an initial cortical representation of sensory stimuli, one cannot rule out an interaction with gamma rhythms as a temporal code here either. Many different modes of gamma rhythm generation can be experimentally induced
(Whittington et al., 2011), but none of the known manifestations truly behave as a “clock” for principal cell spike timing. Principal cell inputs to interneurons are vital to drive the observed rhythm and changes in principal cell spike behavior can alter the gamma rhythm on a period by period basis (Whittington et al., 1995). The main differences lie in the way fast spiking interneurons are recruited into the population rhythm by principal cells—they can be recruited by tonic excitation through glutamate overspill at synapses activating metabotropic receptors, convergence onto excitatory synapses on interneurons of ectopic action potentials generated in principal cell axons, or conventional somatic spike generation. Persistent, highly frequency-inert gamma rhythms associate with sparse somatic spiking (Miller, 1996) in
superficial neocortex. Gamma rhythms can also be generated in hippocampus that are associated with high spike rates in individual neurons (an order of magnitude greater than in persistent gamma rhythms) and are considerably more frequency—and thus spike rate—variable (Whittington et al., 1997). In neocortex, spike rates are closely related to gamma rhythm generation BTK inhibitor (in conjunction with slower changes in membrane potential (Mazzoni et al., 2010), with gamma rhythms being the single most important determinant of spike-density function (Rasch et al., 2008). But many in vivo studies show sensory-induced spike rate changes that peak at mean rates from way above the classical
gamma band frequency (e.g., Zinke et al., 2006). If it is assumed that spike timing is precisely determined by the trains of GABAergic inhibition that are the signature of population gamma rhythms, then how is this possible? One explanation for these data is that there are at least two gamma rhythm generators in neocortex. First, a persistent rhythm provides relatively rigid temporal structure despite low principal cell spike rates and low population gamma frequencies (ca. 40 Hz). Such a rhythm has been documented in superficial layers of primary sensory and association cortices (Cunningham et al., 2004; Ainsworth et al., 2011; Figure 5), where spike rates favor sparse coding (Wolfe et al., 2010). Such a scheme is particularly evident in local representations of sensory stimuli (Ohiorhenuan et al., 2010) where input increases quiescence but also increases temporally brief periods of common (population) activity. This sparseness has been proposed to be due to increases in surround inhibition (Haider et al.