In the CNS, activity of individual neurons has a small but quantifiable relationship to sensory representations and motor outputs. Coactivation of a few 10s to 100s of neurons can code sensory inputs and behavioral task performance within psychophysical limits. However, in a sea of sensory inputs and demand for complex motor outputs how is the activity of such small subpopulations of neurons organized? Two theories dominate in this respect: increases in spike rate (rate coding) and sharpening of the coincidence of spiking in active neurons (temporal coding). Both have computational advantages and are far from mutually exclusive. Here, we review evidence for a bias in neuronal circuits toward temporal coding and the coexistence of rate and temporal coding during population rhythm generation. The coincident expression of multiple types of gamma rhythm in sensory cortex suggests a mechanistic substrate for combining rate and temporal codes on the basis of stimulus strength.

Rhythmic activity in populations of cortical neurons accompanies, and may underlie, many aspects of primary sensory processing and short-term memory. Activity in the gamma band (30 Hz up to > 100 Hz) is associated with such cognitive tasks and is thought to provide a substrate for temporal coupling of spatially separate regions of the brain. However, such coupling requires close matching of frequencies in co-active areas, and because the nominal gamma band is so spectrally broad, it may not constitute a single underlying process. Here we show that, for inhibition-based gamma rhythms in vitro in rat neocortical slices, mechanistically distinct local circuit generators exist in different laminae of rat primary auditory cortex. A persistent, 30 – 45 Hz, gap-junction-dependent gamma rhythm dominates rhythmic activity in supragranular layers 2/3, whereas a tonic depolarization-dependent, 50 – 80 Hz, pyramidal/interneuron gamma rhythm is expressed in granular layer 4 with strong glutamatergic excitation. As a consequence, altering the degree of excitation of the auditory cortex causes bifurcation in the gamma frequency spectrum and can effectively switch temporal control of layer 5 from supragranular to granular layers. Computational modeling predicts the pattern of interlaminar connections may help to stabilize this bifurcation. The data suggest that different strategies are used by primary auditory cortex to represent weak and strong inputs, with principal cell firing rate becoming increasingly important as excitation strength increases.

Local field potentials (LFPs) sampled with extracellular electrodes are frequently used as a measure of population neuronal activity. However, relating such measurements to underlying neuronal behaviour and connectivity is non-trivial. To help study this link, we developed the Virtual Electrode Recording Tool for EXtracellular potentials (VERTEX). We first identified a reduced neuron model that retained the spatial and frequency filtering characteristics of extracellular potentials from neocortical neurons. We then developed VERTEX as an easy-to-use Matlab tool for simulating LFPs from large populations (>100,000 neurons). A VERTEX-based simulation successfully reproduced features of the LFPs from an in vitro multi-electrode array recording of macaque neocortical tissue. Our model, with virtual electrodes placed anywhere in 3D, allows direct comparisons with the in vitro recording setup. We envisage that VERTEX will stimulate experimentalists, clinicians, and computational neuroscientists to use models to understand the mechanisms underlying measured brain dynamics in health and disease.Electronic supplementary materialThe online version of this article (doi:10.1007/s00429-014-0793-x) contains supplementary material, which is available to authorized users.

Lesions of primary visual cortex (V1) lead to loss of conscious visual perception with significant impact on human patients. Understanding the neural consequences of such damage may aid the development of rehabilitation methods. In this rare case of a Rhesus macaque (monkey S), likely born without V1, the animal’s in-group behaviour was unremarkable, but visual task training was impaired. With multi-modal magnetic resonance imaging, visual structures outside of the lesion appeared normal. Visual stimulation under anaesthesia with checkerboards activated lateral geniculate nucleus of monkey S, while full-field moving dots activated pulvinar. Visual cortical activation was sparse but included face patches. Consistently across lesion and control monkeys, functional connectivity analysis revealed an intact network of bilateral dorsal visual areas temporally correlated with V5/MT activation, even without V1. Despite robust subcortical responses to visual stimulation, we found little evidence for strengthened subcortical input to V5/MT supporting residual visual function or blindsight-like phenomena.

Repeated presentations of sensory stimuli generate transient gamma-frequency (30-80 Hz) responses in neocortex that show plasticity in a task-dependent manner. Complex relationships between individual neuronal outputs and the mean, local field potential (population activity) accompany these changes, but little is known about the underlying mechanisms responsible. Here we show that transient stimulation of input layer 4 sufficient to generate gamma oscillations induced two different, lamina-specific plastic processes that correlated with lamina-specific changes in responses to further, repeated stimulation: Unit rates and recruitment showed overall enhancement in supragranular layers and suppression in infragranular layers associated with excitatory or inhibitory synaptic potentiation onto principal cells, respectively. Both synaptic processes were critically dependent on activation of GABA B receptors and, together, appeared to temporally segregate the cortical representation. These data suggest that adaptation to repetitive sensory input dramatically alters the spatiotemporal properties of the neocortical response in a manner that may both refine and minimize cortical output simultaneously.gamma rhythms | habituation | GABA B receptor | sensory processing | synaptic plasticity G amma-frequency (30-80 Hz) neuronal-population activity is a near-ubiquitous property of cortical responses to all modalities of sensory input (1). It is a feature of the temporal organization of outputs from neuronal ensembles and plays a critical role in intercortical communication and short-term memory (2). However, gamma-frequency responses are not stereotyped; they are powerfully influenced by neuromodulatory state and the nature of the cognitive task associated with sensory presentations. In particular they show plasticity, manifesting as changing local field potential power, frequency, spatial extent, and altered neuronal spike rates and spike-field coherences (3, 4). This plasticity is particularly overt on repeated presentation of familiar or novel discrete sensory stimuli (5-7).Understanding the processes underlying this plasticity is further complicated by the mechanistic inhomogeneity of brain rhythms within the gamma band. Both the lower (30-50 Hz) and higher (51-80 Hz) subbands are generated by fast spiking interneuronal recruitment into local circuit activity (8). However, in general they originate in different primary sensory cortical laminae and manifest in different cognitive states (9). In addition, although a repetition-related suppression of neuronal response has been most frequently described, notable examples have reported enhancements of both broadband gamma-frequency population activity (10) and discrete neuronal outputs (spikes) (11). Why enhancement or suppression is observed remains unclear. However, the direction of observed plasticity in the sensory gamma-frequency response can be influenced by task (12), stimuli (13), and the pattern of ongoing neuronal activity (5).Plasticity in the gamma-related cortical ...

Damage following traumatic brain injury or stroke can often extend beyond the boundaries of the initial insult and can lead to maladaptive cortical reorganisation. On the other hand, beneficial cortical reorganisation leading to recovery of function can also occur. We used resting state FMRI to investigate how cortical networks in the macaque brain change across time in response to lesions to the prefrontal cortex, and how this reorganisation correlated with changes in behavioural performance in cognitive tasks. After prelesion testing and scanning, two monkeys received a lesion to regions surrounding the left principal sulcus followed by periodic testing and scanning. Later, the animals received another lesion to the opposite hemisphere and additional testing and scanning. Following the first lesion, we observed both a behavioural impairment and decrease in functional connectivity, predominantly in frontal-frontal networks. Approximately 8 weeks later, performance and connectivity patterns both improved. Following the second lesion, we observed a further behavioural deficit and decrease in connectivity that showed little recovery. We discuss how different mechanisms including alternate behavioural strategies and reorganisation of specific prefrontal networks may have led to improvements in behaviour. Further work will be needed to confirm these mechanisms.

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Human functional magnetic resonance imaging (fMRi) typically employs the blood-oxygen-leveldependent (BoLD) contrast mechanism. in non-human primates (nHp), contrast enhancement is possible using monocrystalline iron-oxide nanoparticles (Mion) contrast agent, which has a more temporally extended response function. However, using BoLD fMRi in nHp is desirable for interspecies comparison, and the BOLD signal's faster response function promises to be beneficial for rapid event-related (reR) designs. Here, we used reR BoLD fMRi in macaque monkeys while viewing realworld images, and found visual responses and category selectivity consistent with previous studies. However, activity estimates were very noisy, suggesting that the lower contrast-to-noise ratio of BoLD, suboptimal behavioural performance, and motion artefacts, in combination, render reR BoLD fMRi challenging in nHp. previous studies have shown that reR fMRi is possible in macaques with Mion, despite Mion's prolonged response function. to understand this, we conducted simulations of the BoLD and Mion response during reR, and found that no matter how fast the design, the greater amplitude of the Mion response outweighs the contrast loss caused by greater temporal smoothing. We conclude that although any two of the three elements (reR, BoLD, nHp) have been shown to work well, the combination of all three is particularly challenging.