Rat Primary Visual Cortex Research Articles

Visual Deprivation Suppresses L5 Pyramidal Neuron Excitability by Preventing the Induction of Intrinsic Plasticity

In visual cortex monocular deprivation (MD) during a critical period (CP) reduces the ability of the deprived eye to activate cortex, but the underlying cellular plasticity mechanisms are incompletely understood. Here we show that MD reduces the intrinsic excitability of layer 5 (L5) pyramidal neurons and enhances long-term potentiation of intrinsic excitability (LTP-IE). Further, MD and LTP-IE induce reciprocal changes in K(v)2.1 current, and LTP-IE reverses the effects of MD on intrinsic excitability. Taken together these data suggest that MD reduces intrinsic excitability by preventing sensory-drive induced LTP-IE. The effects of MD on excitability were correlated with the classical visual system CP, and (like the functional effects of MD) could be rapidly reversed when vision was restored. These data establish LTP-IE as a candidate mechanism mediating loss of visual responsiveness within L5, and suggest that intrinsic plasticity plays an important role in experience-dependent refinement of visual cortical circuits.

A single spiking neuron that can represent interval timing: analysis, plasticity and multi-stability

The ability to represent interval timing is crucial for many common behaviors, such as knowing whether to stop when the light turns from green to yellow. Neural representations of interval timing have been reported in the rat primary visual cortex and we have previously presented a computational framework describing how they can be learned by a network of neurons. Recent experimental and theoretical results in entorhinal cortex have shown that single neurons can exhibit persistent activity, previously thought to be generated by a network of neurons. Motivated by these single neuron results, we propose a single spiking neuron model that can learn to compute and represent interval timing. We show that a simple model, reduced analytically to a single dynamical equation, captures the average behavior of the complete high dimensional spiking model very well. Variants of this model can be used to produce bi-stable or multi-stable persistent activity. We also propose a plasticity rule by which this model can learn to represent different intervals and different levels of persistent activity.

Expression of immediate-early genes in primary visual cortex of rat early after acute optic nerve injury

To investigate the differential expression of immediate-early genes c-jun and c-fos in primary visual cortex of rat early after acute optic nerve injury and the relationship between immediate-early gene expression and injury degree of optic nerve. This was an factorial design of two factors. 55 male Sprague-Dawley rats were divided into groups randomized. Unilateral optic nerve crush injury or transection was performed in rats to obtain acute partial or complete monocular optic nerve injury models. Frozen sections through visual cortex were cut in normal rats and model rats respectively at 2 h, 1 d, 3 d, 1 week and 1 month after operation. Expression of c-Jun and c-Fos was detected in primary visual cortex by means of immunohistochemistry. Statistical comparisons were made using variance analysis of factorial design. Statistically significant different of c-Jun expression existed between optc nerve crash injury and transection models (F = 50.344, P = 0.000). Increased expression of c-Jun in primary visual cortex could be observed at 2 h postoperation, and reached peak value at 1d postoperation. The extent of increased c-Jun expression was much higher in optic nerve transection models than crush injury models. Statistically significant different of c-Fos expression existed between optc nerve crash injury and transection models (F = 62.232, P = 0.000) Decreased expression of c-Fos in primary visual cortex could be observed at 2 h postoperation in optic nerve crush injury models, and reached bottom at 3 d postoperation. The extent of decrease of c-Fos expression was lower in optic nerve transection models than crush injury models and transient increased expression could be observed at 2 h postoperation. The expression of immediate-early genes c-Jun and c-Fos changed shortly after optic nerve injury. They may act in opposite direction in the primary visual cortex.

Callosal contribution to ocular dominance in rat primary visual cortex

Ocular dominance (OD) plasticity triggered by monocular eyelid suture is a classic paradigm for studying experience-dependent changes in neural connectivity. Recently, rodents have become the most popular model for studies of OD plasticity. It is therefore important to determine how OD is determined in the rodent primary visual cortex. In particular, cortical cells receive considerable inputs from the contralateral hemisphere via callosal axons, but the role of these connections in controlling eye preference remains controversial. Here we have examined the role of callosal connections in binocularity of the visual cortex in naïve young rats. We recorded cortical responses evoked by stimulation of each eye before and after acute silencing, via stereotaxic tetrodotoxin (TTX) injection, of the lateral geniculate nucleus ipsilateral to the recording site. This protocol allowed us to isolate visual responses transmitted via the corpus callosum. Cortical binocularity was assessed by visual evoked potential (VEP) and single-unit recordings. We found that acute silencing of afferent geniculocortical input produced a very significant reduction in the contralateral-to-ipsilateral (C/I) VEP ratio, and a marked shift towards the ipsilateral eye in the OD distribution of cortical cells. Analysis of absolute strength of each eye indicated a dramatic decrease in contralateral eye responses following TTX, while those of the ipsilateral eye were reduced but maintained a more evident input. We conclude that callosal connections contribute to normal OD mainly by carrying visual input from the ipsilateral eye. These data have important implications for the interpretation of OD plasticity following alterations of visual experience.

Extracellular matrix regulates ocular dominance plasticity in the adult rat primary visual cortex

Degradation of extracellular matrix chondroitin sulphate proteoglycans (CSPGs) using Chondroitinase ABC (ChABC) is a promising strategy for the treatment of spinal cord injury, with potent effects on promoting functional recovery and anatomical repair in spinal injured animals. We have previously demonstrated that ChABC treatment prevents atrophy of corticospinal projection neurons following spinal injury in adult YFP-H mice. Here, we investigate whether ChABC-mediated repair of the cell body extends to rubrospinal projection neurons (RSNs), whether neuroprotective effects can be sustained long-term and importantly, whether delayed treatment with ChABC can reverse chronic atrophy. Adult YFP-H mice underwent unilateral rubrospinal tract transection and were treated with ChABC or a control enzyme, delivered either acutely post-injury or after a one month delay. Eight weeks following injury and control treatment, RSNs in the injured red nucleus, identified by YFP label and NeuN immunoreactivity, showed severe atrophy, with ~ 40% loss of mean cell area compared to uninjured neurons in the contralateral red nucleus. Both acute and delayed treatment with ChABC promoted a significant rescue of injured RSNs, restoring cell area to ~ 80% and ~ 70%, respectively, of that in uninjured neurons. Thus, we demonstrate for the first time that CSPG degradation in the injured spinal cord not only promotes sustained rescue of cell atrophy when delivered acutely but can also reverse chronic atrophy in descending projection neurons. Thus, modulation of the extracellular matrix can mediate neuroprotective effects both early and late after spinal cord injury.

FIND -- a unified framework for neural data analysis

The complexity of neurophysiology data has increased tremendously over the last years, especially due to the widespread availability of multi-channel recording techniques. With adequate computing power the current limit for computational neuroscience is the effort and time it takes for scientists to translate their ideas into working code. Advanced analysis methods are complex and often lack reproducibility on the basis of published descriptions. To overcome this limitation we develop FIND (Finding Information in Neural Data) as a platform-independent, open source framework for the analysis of neuronal activity data based onMatlab (Mathworks). Here, we outline the structure of the FIND framework and describe its functionality, our measures of quality control, and the policies for developers and users. Within FIND we have developed a unified data import from various proprietary formats, simplifying standardized interfacing with tools for analysis and simulation. The toolbox FIND covers a steadily increasing number of tools. These analysis tools address various types of neural activity data, including discrete series of spike events, continuous time series and imaging data. Additionally, the toolbox provides solutions for the simulation of parallel stochastic point processes tomodelmulti-channel spiking activity.We illustrate two examples of complex analyses with FIND tools: First, we present a time-resolved characterization of the spiking irregularity in an in vivo extracellular recording from a mushroom-body extrinsic neuron in the honeybee during odor stimulation. Second, we describe layer specific input dynamics in the rat primary visual cortex in vivo in response to visual flash stimulation on the basis of multi-channel spiking activity. © 2008 Elsevier Ltd. All rights reserved.

Short-term (2 to 5 h) dark exposure lowers long-term potentiation (LTP) induction threshold in rat primary visual cortex

Up- and down-regulation of synaptic strength (i.e., long-term potentiation, LTP, long-term depression) is thought to be the primary mechanism mediating experience-dependent plasticity of cortical networks. Recent evidence indicates that the expression of plastic changes at synapses itself is dynamic and regulated, at least in part, by the recent history of synaptic activity, a concept termed metaplasticity. Here, adult, urethane-anesthetized rats were exposed to light or dark conditions for various durations (1, 2, and 5 h) to influence activity levels in the retinal-dorsal lateral geniculate nucleus (dLGN)-primary visual cortex (V1) pathway. Field potentials, recorded in layer IV of V1, were evoked by light flashes to the retina or single pulse electrical stimulation of the dLGN. Brief (60 s) periods of high frequency (50 Hz) retinal light stimulation results in an increase in visual evoked potential (VEP) amplitude in animals exposed to complete darkness for 2 h, while VEP amplitude failed to show potentiation in animals maintained in darkness for shorter periods. Similarly, weak theta burst stimulation of the dLGN failed to induce LTP in animals maintained under continuous light, but elicited robust LTP after 5 h of dark exposure. These data demonstrate that induction thresholds for sensory- and electrically-induced LTP in the retino-geniculo-cortical pathway of adult rats are dynamically regulated by levels of preceding sensory stimulation. Importantly, such metaplastic adjustments of plasticity in V1 can occur over time-scales significantly shorter than previously recognized.

Age-Dependent Decline in Supragranular Long-Term Synaptic Plasticity by Increased Inhibition During the Critical Period in the Rat Primary Visual Cortex

Supragranular long-term potentiation (LTP) and depression (LTD) are continuously induced in the pathway from layer 4 during the critical period in the rodent primary visual cortex, which limits the use of supragranular long-term synaptic plasticity as a synaptic model for the mechanism of ocular dominance (OD) plasticity. The results of the present study demonstrate that the pulse duration of extracellular stimulation to evoke a field potential (FP) is critical to induction of LTP and LTD in this pathway. LTP and LTD were induced in the pathway from layer 4 to layer 2/3 in slices from 3-wk-old rats when FPs were evoked by 0.1- and 0.2-ms pulses. LTP and LTD were induced in slices from 5-wk-old rats when evoked by stimulation with a 0.2-ms pulse but not by stimulation with a 0.1-ms pulse. Both the inhibitory component of FP and the inhibitory/excitatory postsynaptic potential amplitude ratio evoked by stimulation with a 0.1-ms pulse were greater than the values elicited by a 0.2-ms pulse. Stimulation with a 0.1-ms pulse at various intensities that showed the similar inhibitory FP component with the 0.2-ms pulse induced both LTD and LTP in 5-wk-old rats. Thus extracellular stimulation with shorter-duration pulses at higher intensity resulted in greater inhibition than that observed with longer-duration pulses at low intensity. This increased inhibition might be involved in the age-dependent decline of synaptic plasticity during the critical period. These results provide an alternative synaptic model for the mechanism of OD plasticity.

FIND — A unified framework for neural data analysis

The complexity of neurophysiology data has increased tremendously over the last years, especially due to the widespread availability of multi-channel recording techniques. With adequate computing power the current limit for computational neuroscience is the effort and time it takes for scientists to translate their ideas into working code. Advanced analysis methods are complex and often lack reproducibility on the basis of published descriptions. To overcome this limitation we develop FIND (Finding Information in Neural Data) as a platform-independent, open source framework for the analysis of neuronal activity data based on Matlab (Mathworks). Here, we outline the structure of the FIND framework and describe its functionality, our measures of quality control, and the policies for developers and users. Within FIND we have developed a unified data import from various proprietary formats, simplifying standardized interfacing with tools for analysis and simulation. The toolbox FIND covers a steadily increasing number of tools. These analysis tools address various types of neural activity data, including discrete series of spike events, continuous time series and imaging data. Additionally, the toolbox provides solutions for the simulation of parallel stochastic point processes to model multi-channel spiking activity. We illustrate two examples of complex analyses with FIND tools: First, we present a time-resolved characterization of the spiking irregularity in an in vivo extracellular recording from a mushroom-body extrinsic neuron in the honeybee during odor stimulation. Second, we describe layer specific input dynamics in the rat primary visual cortex in vivo in response to visual flash stimulation on the basis of multi-channel spiking activity.

Differential Cholinergic Modulation of Ca2+ Transients Evoked by Backpropagating Action Potentials in Apical and Basal Dendrites of Cortical Pyramidal Neurons

The effect of the cholinergic agonist carbachol (CCh) on backpropagating action potential (bAP)-evoked Ca2+ transients in distal apical and basal dendrites of layer 2/3 pyramidal neurons in the primary visual cortex of rats was studied using whole cell recordings and confocal Ca2+ imaging. In the presence of CCh (20 microM), initial bAP-evoked Ca2+ transients were followed by large propagating secondary Ca2+ transients that were restricted to proximal apical dendrites < or =40 microm from the soma. In middle apical dendrites (41-100 microm from the soma), Ca2+ transients evoked by AP bursts at 20 Hz, but not by single APs, were increased by CCh without secondary transients. CCh failed to increase the bAP-evoked Ca2+ transients in distal apical dendrites (101-270 microm from the soma). In contrast, in basal dendrites, CCh increased Ca2+ transients evoked by AP bursts, but not by single APs, and these transients were relatively constant over the entire length of the dendrites. CCh further increased the enhanced bAP-evoked Ca2+ transients in the presence of 4-aminopyridine (200 microM), an A-type K+ channel blocker, in basal and apical dendrites, except in distal apical dendrites. CCh increased large Ca2+ transients evoked by high-frequency AP bursts in basal dendrites, but not in distal apical dendrites. CCh-induced increase in Ca2+ transients was mediated by InsP3-dependent Ca2+-induced Ca2+-release. These results suggest that cholinergic stimulation differentially increases the bAP-evoked increase in [Ca2+]i in apical and basal dendrites, which may modulate synaptic activities in a location-dependent manner.

Effects of visual experience on vascular endothelial growth factor expression during the postnatal development of the rat visual cortex.

The development of the cortical vascular network depends on functional maturation. External inputs are an essential requirement in the modeling of the visual cortex, mainly during the critical period, when the functional and structural properties of visual cortical neurons are particularly susceptible to alterations. Vascular endothelial growth factor (VEGF) is the major angiogenic factor, a key signal in the induction of vessel growth. Our study focused on the role of visual stimuli on the development of the vascular pattern correlated with VEGF levels. Vascular density and the expression of VEGF were examined in the primary visual cortex of rats reared under different visual environments (dark rearing, dark-rearing in conditions of enriched environment, enriched environment, and laboratory standard conditions) during postnatal development (before, during, and after the critical period). Our results show a restricted VEGF cellular expression to astroglial cells. Quantitative differences appeared during the critical period: higher vascular density and VEGF protein levels were found in the enriched environment group; both dark-reared groups showed lower vascular density and VEGF levels, which means that enriched environment without the physical exercise component does not exert effects in dark-reared rats.

Serotonin inhibits the induction of NMDA receptor-dependent long-term potentiation in the rat primary visual cortex

An increase in serotonin [5-hydroxytryptamine (5-HT)] levels in the rat visual cortex is correlated with the developmental decrease in long-term potentiation (LTP), and 5-HT may play an important role in the closure of the critical period by regulating LTP. The effect of 5-HT on the induction of N-methyl- d-aspartate receptor (NMDAR)-dependent and metabotropic glutamate receptor (mGluR)-dependent LTP in visual cortex slices from young rats was investigated. The field potential in layer II/III was recorded by stimulating the underlying layer IV. NMDAR-dependent LTP was induced in slices from 3-week-old rats by theta-burst stimulation (TBS) but not in slices from 5-week-old rats. However, LTP was induced in 5-HT-depleted slices from 5-week-old rats by incubation with para-chloroamphetamine (10 μM, 2 h), a 5-HT-depleting agent. The reinstated LTP in 5-HT-depleted slices was inhibited by the application of d-aminopentanoate, an NMDAR antagonist (50 μM) and 5-HT (10 and 30 μM). In contrast, the induction of mGluR-dependent LTP by weak TBS in disinhibited slices with picrotoxin (1 μM) in the bath was not affected by 5-HT application. The coapplication of 5-HT 1A and 5-HT 2 receptor agonists inhibited the induction of NMDAR-dependent LTP in 5-HT-depleted slices. 5-HT levels in the visual cortex increased with age. Based on these findings, we conclude that NMDAR-dependent LTP is specifically inhibited by coactivation of 5-HT 1A and 5-HT 2 receptors with the increase in 5-HT levels in the rat visual cortex at the end of the critical period.

Functional Role of the Fast Transient Outward K+CurrentIAin Pyramidal Neurons in (Rat) Primary Visual Cortex

A molecular genetic approach was exploited to directly test the hypothesis that voltage-gated K+ (Kv) channel pore-forming (alpha) subunits of the Kv4 subfamily encode the fast transient outward K+ current (IA) in cortical pyramidal neurons and to explore the functional role of IA in shaping action potential waveforms and in controlling repetitive firing in these cells. Using the biolistic gene gun, cDNAs encoding a mutant Kv4.2 alpha subunit (Kv4.2W362F), which functions as a dominant negative (Kv4.2DN), and enhanced green fluorescent protein (EGFP) were introduced in vitro into neurons isolated from postnatal rat primary visual cortex. Whole-cell voltage-clamp recordings obtained from EGFP-positive pyramidal neurons revealed that IA is selectively eliminated in cells expressing Kv4.2DN. The densities and properties of the other Kv currents are unaffected. In neurons expressing Kv4.2DN, input resistances are increased and the (current) thresholds for action potential generation are decreased. In addition, action potential durations are prolonged, the amplitudes of afterhyperpolarizations are reduced, and the responses to prolonged depolarizing inputs are altered markedly in cells expressing Kv 4.2DN. At low stimulus intensities, firing rates are increased in Kv4.2DN-expressing cells, whereas at high stimulus intensities, Kv4.2DN-expressing cells adapt strongly. Together, these results demonstrate that Kv4alpha subunits encode IA channels and that IA plays a pivotal role in shaping the waveforms of individual action potentials and in controlling repetitive firing in visual cortical pyramidal neurons.

Functional imaging with cellular resolution reveals precise micro-architecture in visual cortex

Neurons in the cerebral cortex are organized into anatomical columns, with ensembles of cells arranged from the surface to the white matter. Within a column, neurons often share functional properties, such as selectivity for stimulus orientation; columns with distinct properties, such as different preferred orientations, tile the cortical surface in orderly patterns. This functional architecture was discovered with the relatively sparse sampling of microelectrode recordings. Optical imaging of membrane voltage or metabolic activity elucidated the overall geometry of functional maps, but is averaged over many cells (resolution >100 microm). Consequently, the purity of functional domains and the precision of the borders between them could not be resolved. Here, we labelled thousands of neurons of the visual cortex with a calcium-sensitive indicator in vivo. We then imaged the activity of neuronal populations at single-cell resolution with two-photon microscopy up to a depth of 400 microm. In rat primary visual cortex, neurons had robust orientation selectivity but there was no discernible local structure; neighbouring neurons often responded to different orientations. In area 18 of cat visual cortex, functional maps were organized at a fine scale. Neurons with opposite preferences for stimulus direction were segregated with extraordinary spatial precision in three dimensions, with columnar borders one to two cells wide. These results indicate that cortical maps can be built with single-cell precision.

P.1.013 Measurement of monoaminergic activity by drugs acting on adrenergic α 2-receptors in rat hippocampus and primary visual cortex

P.1.013 Measurement of monoaminergic activity by drugs acting on adrenergic α 2-receptors in rat hippocampus and primary visual cortex

Selective reconfiguration of layer 4 visual cortical circuitry by visual deprivation

Visual deprivation during a developmental sensitive period markedly alters visual cortical response properties, but the changes in intracortical circuitry that underlie these effects are poorly understood. Here we use a slice preparation of rat primary visual cortex to show that 2 d of prior visual deprivation early in life increases the excitability of layer 4 circuitry. Slice recordings showed that spontaneous activity of layer 4 star pyramidal neurons increased 25-fold after 2 d of visual deprivation between postnatal days (P) 15 and P17. This effect was mediated by increased net excitatory and decreased net inhibitory synaptic drive. Paired recordings showed that excitatory connections between star pyramidal neurons doubled in amplitude, whereas inhibitory connections decreased or increased depending on the interneuron class. These effects reversed when vision was restored. This dynamic adjustment of the excitation-inhibition balance may allow the networks within layer 4 to maintain stable levels of activity in the face of variable sensory input.

Retinotopy within rat primary visual cortex using optical imaging

The purpose of this study was to determine the retinotopic organization of rat primary visual cortex (area 17) using optical imaging technology. Stimulating discrete regions of visual space resulted in localised changes in the remitted light during optical imaging of visual cortex in rat. From these localised changes, our results confirm previous electrophysiological studies on the location, size and organization of rat primary visual cortex. Small differences in the cortical magnification factor (CMF) were found between visual field areas with the highest CMF confined to the upper nasal region. No significant CMF differences were found within the horizontal and vertical visual field axes. No secondary visual areas were activated either anterior or medial to area 17 with the pattern stimuli used in the current study. However, there was evidence of activity to upper nasal stimulation on the posterior lateral extrastriate area. The location of area 17 from optical imaging activity was confirmed anatomically using conventional immunohistochemical techniques. This study shows the retinotopic organization of rat primary visual cortex and serves as a precursor before examining animal models of retinal degeneration and the effectiveness of potential therapies to stem retinal disease.

Neurotoxic lesion of anteromedial/posterior parietal cortex disrupts spatial maze memory in blind rats

The primary visual cortex of rats is surrounded laterally (in Oc2L) and medially (in Oc2M) by several peristriate visual areas. Previous studies from our laboratory demonstrated that bilateral lesions in Oc2L result in visual pattern discrimination deficit, and in failure to solve a conditional discrimination which requires figure–background association. In contrast, neurotoxic lesions of the rostral part of Oc2M (which contains the anteromedial and anterior peristriate visual areas, collectively referred to as AM complex) result in deficits in visuospatial discrimination, and in disruptions in visual tasks involving spatial memory. The objective of this study was to behaviorally test the role of AM complex in a spatial memory task in absence of visual cues. For this purpose, we analyzed memory retention of Lashley III maze in blind rats after bilateral ibotenate lesions in AM complex, or in the primary visual cortex (V1, Oc1), to test the hypothesis that AM complex is essential for this cognitive task. The results showed a significant loss of memory retention of the maze in rats with lesions in AM complex, but not in rats with lesions in V1. Furthermore, the retention loss in rats with AM complex lesions was positively and significantly correlated with the size of the lesion. The results indicate a critical role of AM complex in spatial memory mechanisms independent on visual cues. A probable homology of rat AM complex with the posterior parietal cortex of primates is discussed.

Coding with noisy neurons: stability of tuning curve estimation strongly depends on the analysis method

An important issue in the neurosciences is a quantitative description of the relation between sensory stimuli presented to an animal and their representations in the nervous system. A standard technique is the construction of a neural tuning curve, that is, a neuron’s average firing rate as a function of some parameter characterizing a family of stimuli. It is unavoidable that some of the response data are erroneously attributed to a cell, e.g., during spike sorting. However, the widely used method of statistical analysis based on the sample mean and least-squares approximation for the spike count can perform extremely badly if the noise distribution is not exactly normal, which is almost never the case in applications. Here, we present a method for constructing neural tuning curves that is especially suited for cases of high noise and the presence of outliers. Since it is usually not decidable if an outlier is faulty or not we limit the influence of far outlying points rather than try to identify and discard them. In contrast to traditional methods employing a point-by-point estimation of a tuning curve, we use all measured data from all different stimulus conditions at once in the construction. Given the measured data at only a finite number of stimulus conditions, a robust tuning curve is obtained that approximates the cell’s ideal tuning curve optimally in all stimulus conditions with respect to a given distance measure. A measure that assesses the quality of this fitting method with respect to the traditional least-squares fitting method and to a median-based fitting method is introduced. The reliability of inference with respect to the encoding accuracy that can be achieved by a population of neurons is demonstrated in both artificially generated and experimentally recorded data from rat primary visual cortex. While the data shown in this paper are responses to orientation stimuli, the method of tuning curve construction is also viable and maintains its optimality properties for the case in which the stimulus is defined on a finite interval.

Halothane augments event-related γ oscillations in rat visual cortex

Cortical γ oscillations have been associated with neural processes supporting cognition and the state of consciousness but the effect of general anesthesia on γ oscillations is controversial. Here we studied the concentration-dependent effect of halothane on γ (20–60 Hz) power of event-related potentials (ERP) in rat primary visual cortex. ERP to light flashes repeated at 5-s intervals was recorded with chronically implanted, bipolar, intracortical electrodes at selected steady-state halothane concentrations between 0 and 2%. γ-Band power was calculated for 0–1000, 0–300 and 300–1000 ms poststimulus periods and corresponding prestimulus (PS) periods. Multitaper power spectral analysis was used to estimate γ power from both single-trial and average ERP in order to differentiate between phase-locked (evoked) and non-phase-locked (induced) γ activities. Significant PS γ power was present at all halothane concentrations. Flash elicited an increase in γ power that lasted up to 1 s poststimulus at all halothane concentrations. Halothane at intermediate concentrations (0.5–1.2%) augmented both PS and ERP γ power two to four times relative to the waking baseline. γ Power was not different between waking and deeply anesthetized (2%) levels. γ Power reached maximum, as predicted by a Gaussian fit of power-concentration data, at halothane concentration (0.86%) similar to the concentration (0.73%) that abolished the righting reflex, a behavioral index of loss of consciousness. Evoked, i.e. stimulus-locked, γ power was present during the first 300 ms poststimulus but not later, and was approximately 50% of single-trial ERP γ power. Single-trial γ power was present also at 300–1000 ms poststimulus, reflecting ERP not phase-locked to the stimulus. In summary, these observations suggest that (1) γ activity is present in states ranging from waking to deep halothane anesthesia, (2) halothane does not prevent the transfer of visual input to striate cortex even at surgical plane of anesthesia, and (3) anesthetic-induced loss of consciousness, as reflected by the loss of righting reflex, is not correlated with a reduction in γ power. Variance with other studies may be due to an underestimation of γ power by ERP signal averaging as compared with single-trial analysis.