To better understand population phenomena in thalamocortical neuronal ensembles, we have constructed a preliminary network model with 3,560 multicompartment neurons (containing soma, branching dendrites, and a portion of axon). Types of neurons included superficial pyramids (with regular spiking [RS] and fast rhythmic bursting [FRB] firing behaviors); RS spiny stellates; fast spiking (FS) interneurons, with basket-type and axoaxonic types of connectivity, and located in superficial and deep cortical layers; low threshold spiking (LTS) interneurons, which contacted principal cell dendrites; deep pyramids, which could have RS or intrinsic bursting (IB) firing behaviors, and endowed either with nontufted apical dendrites or with long tufted apical dendrites; thalamocortical relay (TCR) cells; and nucleus reticularis (nRT) cells. To the extent possible, both electrophysiology and synaptic connectivity were based on published data, although many arbitrary choices were necessary. In addition to synaptic connectivity (by AMPA/kainate, NMDA, and GABA(A) receptors), we also included electrical coupling between dendrites of interneurons, nRT cells, and TCR cells, and--in various combinations--electrical coupling between the proximal axons of certain cortical principal neurons. Our network model replicates several observed population phenomena, including 1) persistent gamma oscillations; 2) thalamocortical sleep spindles; 3) series of synchronized population bursts, resembling electrographic seizures; 4) isolated double population bursts with superimposed very fast oscillations (>100 Hz, "VFO"); 5) spike-wave, polyspike-wave, and fast runs (about 10 Hz). We show that epileptiform bursts, including double and multiple bursts, containing VFO occur in rat auditory cortex in vitro, in the presence of kainate, when both GABA(A) and GABA(B) receptors are blocked. Electrical coupling between axons appears necessary (as reported previously) for persistent gamma and additionally plays a role in the detailed shaping of epileptogenic events. The degree of recurrent synaptic excitation between spiny stellate cells, and their tendency to fire throughout multiple bursts, also appears critical in shaping epileptogenic events.

Beta2 frequency (20 -30 Hz) oscillations appear over somatosensory and motor cortices in vivo during motor preparation and can be coherent with muscle electrical activity. We describe a beta2 frequency oscillation occurring in vitro in networks of layer V pyramidal cells, the cells of origin of the corticospinal tract. This beta2 oscillation depends on gap junctional coupling, but it survives a cut through layer 4 and, hence, does not depend on apical dendritic electrogenesis. It also survives a blockade of ␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors or a blockade of GABA A receptors that is sufficient to suppress gamma (30 -70 Hz) oscillations in superficial cortical layers. The oscillation period is determined by the M type of K ؉ current.gap junction ͉ intrinsic bursting ͉ layer 5 ͉ M current ͉ neocortex T he mammalian neocortex generates a broad range of electroencephalogram rhythms concurrently in the awake behaving state. Some rhythms are strongly associated with sensory processing (the gamma band; ref. 1), whereas others are associated with cortical outputs (the beta band; ref.2). Here we show an in vitro model of concurrent but independently generated gamma (30-70 Hz) rhythms in layer rhythms in layer V somatosensory cortex. The beta2 rhythm occurred robustly in layer V intrinsically bursting (IB) neurons, in the form of bursts admixed with spikelets, and single action potentials. It was blocked by reducing gap junction conductance with carbenoxolone and was unaffected by blockade of synaptic transmission sufficient to ablate the layer II͞III gamma rhythm. It also could be seen in the absence of synaptic transmission with axonal excitability enhanced with 4-aminopyridine, suggesting a nonsynaptic rhythm mediated by axonal excitation. A network model, based on the hypothesis of electrical coupling via axons, is consistent with this hypothesis. The frequency of this network beta2 rhythm was set by the magnitude of M current in IB neurons. Our data suggest the possibility that a normally occurring cortical network oscillation involved in motor control could be generated largely or entirely by nonsynaptic mechanisms.Electroencephalogram beta oscillations, particularly those in the higher beta2 frequency range, have been recorded over premotor, supplementary motor, somatosensory, and other parietal cortical areas, in rats (3), monkeys (2, 4, 5), and humans (6). The oscillations are associated with sensory cues requiring sustained motor response and occur during the anticipatory period leading up to directed movement after such a sensory cue. The origin of these in vivo beta rhythms is unclear; however, pyramidal tract neurons (lying in layer V; ref. 7) and motor cortex local field potentials exhibit coherence at beta2 frequencies with hand and forearm electromyographic activity, in monkeys performing a precision grip task (8, 9), suggesting that beta2 oscillations originate in layer V in vivo. In addition, layer V neurons form a major input pathway to basal ganglia, which also demonstrate ...

Basic cellular and network mechanisms underlying gamma frequency oscillations (30 -80 Hz) have been well characterized in the hippocampus and associated structures. In these regions, gamma rhythms are seen as an emergent property of networks of principal cells and fast-spiking interneurons. In contrast, in the neocortex a number of elegant studies have shown that specific types of principal neuron exist that are capable of generating powerful gamma frequency outputs on the basis of their intrinsic conductances alone. These fast rhythmic bursting (FRB) neurons (sometimes referred to as ''chattering'' cells) are activated by sensory stimuli and generate multiple action potentials per gamma period. Here, we demonstrate that FRB neurons may function by providing a large-scale input to an axon plexus consisting of gap-junctionally connected axons from both FRB neurons and their anatomically similar counterparts regular spiking neurons. The resulting network gamma oscillation shares all of the properties of gamma oscillations generated in the hippocampus but with the additional critical dependence on multiple spiking in FRB cells.G amma frequency oscillations are readily recordable from scalp and depth electroencephalogram electrodes placed over or in the neocortex of humans and laboratory animals. They occur spontaneously at low amplitude or transiently at larger amplitudes in response to sensory stimuli (1, 2). Their role in processing of sensory information has been proposed to involve the establishment of a temporal framework within which longrange synchronization of individual neuronal elements coding for specific sensory events can occur (3). Qualitatively similar oscillations also occur in the hippocampus (4) and entorhinal cortex (5), where their generation can be ascribed to the phasic or tonic (or a combination of both) excitation of fast spiking (FS) interneurons, the outputs of which, in turn, provide a temporal framework for controlling the outputs of principal cells (6, 7).Although much is known of the mechanisms underlying gamma oscillations in the archicortex and entorhinal cortex, relatively little evidence is available to suggest a mechanism (or mechanisms) involved in generating neocortical gamma oscillations. What is known is that specific neurons exist within the neocortical mantle that are capable of generating outputs within the gamma frequency range on the basis of intrinsic properties alone (in the absence of influences from local networks). Such neurons exhibit fast rhythmic bursting (FRB), with interburst frequencies of 20 Hz and upward, in response to depolarizing current injection alone (8-10). These FRB neurons (sometimes called ''chattering cells'') have also been shown to participate in visually evoked gamma (25-70 Hz) oscillations in vivo (8), with the FRB cells morphologically identified as spiny layer II͞III pyramidal neurons. Other principal neocortical neurons also possess the ability to generate activity within the gamma band on the basis of intrinsic properties alone in layer IV ...