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1 Department of Psychology, University of Colorado, Boulder, CO 80309-0345, USA
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Abstract |
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(Received 7 September 2004;
accepted after revision 1 October 2004;
first published online 1 October 2004)
Corresponding author R. J. Staba: Department of Psychology, University of Colorado, Boulder, CO 80309-0345, USA. Email: staba{at}psych.colorado.edu
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Introduction |
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While the somatosensory P1/N1 is thought to be produced by sequential activation of supra- and infragranular pyramidal cells via excitatory synaptic connections between cell groups (Simons, 1978; Simons & Woolsey, 1979; Di et al. 1990; Agmon & Connors, 1991), the neural mechanisms of FOs are unclear. Unit recordings indicate that FOs are associated with rapid and time-locked population discharge of cortical pyramidal cells (Kandel & Buzsaki, 1997; Jones et al. 2000; Barth, 2003). While pyramidal cell action potentials (APs) cannot follow FO frequencies, FOs appear to define preferred latencies for firing of individual cells within a population (Jones et al. 2000; Barth, 2003). The cellular mechanism responsible for synchronizing this population response remains a major question. One possibility is that FOs reflect synchronized inhibitory drive imposed by GABAergic interneurones, similar to the generator of high frequency ripples in hippocampus (Buzsaki et al. 1992). This possibility is consistent with intracellular recordings indicating that fast spiking (FS) cells, thought to represent inhibitory interneurones, present phase-locked APs at FO frequencies in response to physiological stimulation (Jones et al. 2000). However, the role of inhibitory interneurones has been called into question by evidence that the GABAA receptor antagonist, bicuculline methiodide, fails to attenuate FOs and instead increases their duration along with development of epileptiform slow waves (Jones & Barth, 2002). This raises the distinct possibility that, instead of inhibition, FOs may be synchronized by excitatory interactions between pyramidal cells.
In this light, FOs may rely on excitatory interactions within the pyramidal population mediated by chemical synaptic transmission similar to that responsible for the P1/N1 slow wave. Previous studies have shown that epicortical GABA application effectively abolishes the N1 slow wave, while leaving the P1 intact, suggesting that GABA differentially suppresses intracortical synaptic excitation of infragranular pyramidal cells responsible for the N1 (Brailowsky & Knight, 1984; Toldi & Feher, 1985; Kaneko & Hicks, 1988). In the present study, we tested the hypothesis that FOs rely on an excitatory pathway similar to that responsible for the slow wave complex by recording laminar field potentials and single unit responses before and during GABA application in the rat PMBSF.
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Methods |
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All procedures were conducted within the guidelines established by the University of Colorado Institutional Animal Care and Use Committee. Adult male Sprague-Dawley rats (n = 28, 225–300 g) were anaesthetized using a mixture of ketamine HCl (64 mg kg–1), xylazine (13 mg kg–1) and acepromazine (2.1 mg kg–1), and placed on a regulated heating pad to maintain normal body temperature (37°C). A unilateral craniotomy was performed over the right hemisphere extending from bregma to lambda and from the midsagittal suture to the lateral aspect of the temporal bone, exposing a large area of parietotemporal cortex. The dura was reflected and the exposed cortex regularly wetted with Ringer solution containing (mM): NaCl 135, KCl 3, MgCl2 2 and CaCl2 2; pH 7.3 at 37°C. Anaesthesia levels were maintained throughout the experiment so that the eye blink and flexor withdrawal reflexes could barely be elicited. At the conclusion of the experiment, animals were killed with an overdose of anaesthesia without regaining consciousness.
Stimulation and recording
Vibrissa on the left mystacial pad were displaced 
300 µm in the ventrodorsal direction (0.3 ms duration at 1 Hz) using a laboratory-built solenoid (Jones & Barth, 1999; Barth, 2003). Field potential recordings were made using a laminar electrode consisting of a linear array of 24 platinum contacts (diameter, 40 µm; intercontact spacing, 100 µm) extending 2.3 mm beneath the cortical surface (Neurotrack KFT, Budapest, Hungary). The electrode was centrally positioned within the cortical barrel field and inserted perpendicular to the surface nearest areas generating maximum amplitude SEPs as determined from surface recordings using a 64-contact electrode array arranged in an 8 x 8 grid. For single unit recordings, a stabilizing pressure plate with central access hole for a microelectrode was positioned within the vibrissa/barrel field using the same techniques as used for laminar recordings. The pressure plate also had a single silver wire electrode mounted to the side of the access hole to monitor epicortical SEPs concurrently with unit responses. Fine tipped (1.5 µm; 20–30 M
) glass microelectrodes filled with Ringer solution were inserted through the pressure plate and advanced through the cortex in 2 µm increments until single units responding to stimulation of the vibrissa were isolated. Single unit isolation was verified visually by the presence of only one AP firing pattern with consistent amplitude and morphology. Laminar field potentials and unit recordings were referenced to a AgCl-coated electrode placed within the dorsal neck muscle. Field potentials were amplified (x 200), filtered (1–3000 Hz) and digitized at 10 kHz. Unit recordings were amplified (x 1000), filtered (300–3000 Hz) and also digitized at 10 kHz.
Data collection
For all experiments, single trial data (n
= 100) was recorded during three conditions: before GABA application; during GABA exposure; and 30 min after washout. GABA (50 mM; Sigma, St Louis, MO, USA) was dissolved in Ringer solution buffered with 5 mM Hepes that had a final pH of 7.3. GABA was applied to the cortical barrel field using a 4-mm2 pledget that was notched to surround the laminar electrode (n
= 10). The GABA-soaked pledget remained in place for 5 min during the recording of evoked responses. To verify that GABA was penetrating the infragranular lamina, in five animals cortical depth injections were made using a microinjection system (WPI Inc., Sarasota, FL, USA). From the cortical surface to a depth of 1 mm, and < 1 mm from the laminar electrode, GABA was injected at a rate of 23 nl s–1 for 5–10 s. In a separate series of animals used for single unit recordings (n
= 13), the access hole in the pressure plate was filled with GABA with time allowed for GABA to diffuse throughout the cortical barrel field. Recovery trials were recorded 30 min after GABA washout using Ringer solution.
Laminar analysis
For each animal, laminar field potentials were averaged across trials and digitally band-pass filtered to separately examine the slow wave (1–100 Hz) and FO (250–600 Hz). To better resolve the locations of extracellular current sinks and sources along the axis of the electrode array, spatially filtered current source density (CSD) (low pass cut-off, 1 Hz mm–1; Nicholson & Freeman, 1975; Rappelsberger et al. 1981; Mitzdorf, 1985) was calculated using the equation described by Mitzdorf (1985). This equation computes CSD as the second spatial derivative of potential measured in 100 µm increments along an axis perpendicular to the cortical surface. Preliminary inspection of the 24 CSD waveforms recorded from the laminar electrode revealed that the eight most distal contacts located within superficial white matter did not contribute additional information to the CSD profile. Subsequent analysis and illustration used the remaining 16 contacts spanning the cortical laminae.
Principal component analysis (PCA) was used to separate the independent sources of covariance in the CSD across the laminar electrode (Ruchkin et al. 1964; Barth et al. 1989). In the context of this study, the principal components represented distinct neuronal populations generating unique spatial patterns of CSD, covarying across multiple contacts of the laminar electrode. Component loadings reflected the weighted contribution of each neuronal population to the CSD at each electrode contact. Preliminary results indicated that the laminar patterns of component loadings were approximately dipolar. To simplify the model of activity underlying the evoked response, principal components were rigidly rotated so that their laminar loading patterns best reflected dipolar sources. Component loadings were derived from the baseline CSD only. Multiple regression was then used to calculate a linear combination of these component loadings that best fitted the time course of the evoked response at baseline and during application of GABA. Reconstructions of the spatiotemporal patterns of activity contributed by each principal component were computed by multiplying the spatial loading pattern (xn) by their respective temporal series of regression weights (Reg Wgts) (tn). A composite model of activity was computed by summing the spatiotemporal patterns of activity from the first two principal components, such that:
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The P1/N1 and FO amplitude were computed from the regression weights as the maximum/minimum peak and root-mean-square values, respectively. FO centre frequency was defined as the largest peak appearing in a 512-point fast Fourier transform of the bandpass filtered data. Comparison between the composite model and CSD profile was calculated as follows:
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Single units were initially segregated into groups according to the phase relationship between their vibrissa-evoked firing pattern and concurrently recorded surface FOs. In order to eliminate slight intertrial variations in FO latency that could obscure phase relationships between FOs and unit discharges, FOs and APs were phase-aligned by a ± 1.5 ms shift determined from the cross-correlation function computed between single trial FOs and grand averaged FOs for a given unit. Distinct temporal patterns of a single unit's discharge were additionally segregated using a K-means cluster algorithm (Hartigan & Wong, 1979). The grouping variable was the poststimulus latencies of unit responses. In this application, if all trials consisted of unit responses at the same poststimulus latencies, then a single cluster containing all trials would yield the minimum variance around the mean response latency. However, if unit response latencies differed systematically in subgroups of trials (i.e. occurring at the latency of the second FO wave in some trials, first and fourth FO waves on other trials, etc.) then trials clustered within each subgroup would yield a smaller within-group variance than if all trials were treated as a single group. The maximum number of permitted clusters was six. Changes in unit discharge during application of GABA were then quantified by computing the ratio of mean APs during baseline to those during the application of GABA for each isolated unit. Analysis of variance (ANOVA) and paired t tests were used to compare evoked responses across conditions and changes in AP discharge, respectively. Significance for all comparisons was set at P = 0.05.
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Results |
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300 µm beneath the cortical surface that attained maximum amplitude 15 ms following stimulus onset (Fig. 1C; Comp 1). Similarly, the second reconstruction revealed a current dipole reversing at 1100 µm with a poststimulus latency of 22 ms (Fig. 1C; Comp 2).
Figure 1D displays similar laminar analysis of the band pass filtered (250–600 Hz) FO (mean, 338 ± 60 Hz) that coincided with the SEP slow wave. Inspection of the CSD profile revealed a complex pattern of spatiotemporal activity that appeared as a series of waves propagating between the cortical depth and surface with no clear reversal in polarity in the depth. Unlike the slow wave response, the poststimulus latency of FOs was variable across animals and precluded the calculation of a grand average CSD profile. The example of Fig. 1D is therefore from a single animal. Similar to the analysis of the slow wave, results from PCA showed that FOs could be modelled by the activation of two spatially distinct cellular populations. Reconstructions of the first two principal components again suggested contributions from supra- and infragranular populations. Dipolar loading patterns of the two components were consistent across animals and reversed polarity 500 and 1000 µm below the cortical surface, respectively. Superimposition of regression weights show the variability in FO onset across animals. Yet, models of FOs, based on the patterns of activity from the first two principal components of the individual animals, accounted for 97 ± 1.6% of the variance in the CSD.
Application of exogenous GABA simplified the laminar profile of the vibrissa-evoked slow wave response (Fig. 2A), but had little effect on the generation of FOs (341 ± 58 Hz; Fig. 2B). GABA enhanced the P1 and largely suppressed the N1. Suppression of the N1 was consistently observed in all animals and occurred within 1 min of GABA exposure. During GABA application the evoked response began with a P1-like slow wave peaking at a slightly longer latency (18 ± 1.6 ms) and longer duration compared to the P1 before GABA application. Inspection of the CSD profile revealed that the evoked response was produced by a current sink distributed across the middle/deep cortical layers that was surrounded by a large source within superficial layers and a smaller source located within the deepest cortical layers (Fig. 2A). This pattern resembled the profile of activity that occurred during the time course of the P1 before GABA application (cf. Fig. 1C). However, the ensuing large polarity reversal of the sink-source pair within the depth, associated with the N1, was greatly diminished during GABA application.
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In contrast to the pronounced effects that GABA had on the P1/N1 complex, no differences were observed in the CSD of FOs during GABA exposure (Fig. 2B). Using the component loadings derived from the baseline pre-GABA period, reconstructions of the first two principal components revealed that contributions of the supra- and infragranular current dipoles to the FOs were virtually unchanged by GABA. Analysis comparing amplitude before and during GABA application found no difference in FO amplitude generated from either supragranular (RMS amplitude, 0.77 ± 0.37 versus 0.74 ± 0.37 µV mm–2, P = 0.9) or infragranular populations (0.88 ± 0.61 versus 0.86 ± 0.53 µV mm–2, P = 0.9). The regression model, based on pre-GABA component loadings, accounted for 96 ± 3.2% of the system variance during exposure to GABA.
Based on distinct firing patterns and the presence or absence of phase-locking between APs and FOs, the 33 units studied were segregated into four groups (Fig. 3A–D). The first group consisted of two cells that consistently responded with bursts of three to five APs at the same frequency and phase as concurrently recorded FOs (Fig. 3A). The phase relationship between temporal patterns of AP bursts and FOs varied across clusters of single trials (Fig. 3A; 
1–6) but each cluster contained multiple APs with interspike intervals matching the FOs. These two cells were also distinct in that GABA did not decrease their firing, and in this example, actually increased firing over baseline by 160%. It should be noted that these units also displayed APs with half amplitude widths of less than 0.5 ms, but this was not considered a reliable distinguishing feature as eight other cells showed the same characteristic, but without high frequency firing. The second group consisted of cells (n
= 12) that typically fired one to two APs with an interspike interval greater than, but at a multiple of, the FO period. Single trials clustered into subgroups that showed AP discharge at preferred latencies of the FOs (Fig. 3B). Three cells comprised a third group that typically fired a single AP at only one phase of the FOs (Fig. 3C). Finally, approximately half the cells recorded (n
= 16) fitted into a fourth group that typically fired two or more APs at interspike intervals exceeding the FO period and showing no locking to a consistent phase even after clustering of single trials (Fig. 3D). All units, except for the first group, exhibited a significant decrease in firing during GABA application compared to baseline (60 ± 6.5%, P
= 0.00007, n
= 31). Similar attenuation of unit firing during GABA exposure was observed when cells were separately analysed in the supragranular layers (60 ± 9.6%, P
= 0.001, n
= 10) and infragranular layers (60 ± 8.4%, P
= 0.00005, n
= 21), and differences between supra- and infragranular attenuation were not significant. Excluding the first group, there were no significant differences in GABA-dependent attenuation between cell groups.
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at 1 kHz) than cortical microelectrodes and therefore were assumed to reflect multiunit activity (MUA) as opposed to single units. Firing patterns of thalamic units displayed no apparent relationship to cortical FOs either before or after GABA application (Fig. 3E). MUA typically consisted of one to three rapid discharges at 5–7 ms poststimulus, before cortical FOs appeared. This was often followed by activity during and after cortical FOs emerged but revealed no phase-locking with the cortical signal. The temporal pattern of MUA was not changed in any of the thalamic units by the epicortical application of GABA. The second experiment examined whether gap junctions might be implicated in FO generation. Epipial slow waves and FOs were recorded from the PMBSF before and during the systemic administration of halothane, which is an anaesthetic known to close gap junctions (Terrar & Victory, 1988; Burt & Spray, 1989; Peinado et al. 1993). Halothane (1.5%) was administered to four additional animals for a period of 4–6 min following baseline recording. During this initial period, there was little effect on the amplitude of the slow wave (Fig. 4A; dark traces) compared to baseline recording (Fig. 4A; light traces). The RMS amplitude of the slow wave during halothane exposure was 91% that of baseline (P = 0.37). In contrast, concurrently recorded FO were attenuated by 70% (P = 0.0009) during halothane exposure (Fig. 4B; dark traces) compared to baseline (Fig. 4B; light traces). The differential effect of halothane on FO compared to the slow wave could be maintained for up to 1–3 min.
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Discussion |
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Laminar analysis of the slow wave closely resembles previous studies (Mitzdorf, 1987; Vaknin, 1989; Barth & Di, 1990; Di et al. 1990; Sukov & Barth, 1998), indicating thalamocortical activation of supra- and infragranular pyramidal cells producing the P1, followed by longer latency intracortical activation of infragranular pyramidal cells producing the N1. As previously shown in cat somatosensory cortex (Brailowsky & Knight, 1984), GABA suppresses the N1 with a reduced contribution from infragranular pyramidal cells. The simplest explanation for this effect is that GABA widely hyperpolarizes cortical neurones, resulting in an average reduction of firing to 60% of baseline. The resiliency of the P1 slow wave in the presence of GABA suggests that thalamocortical input is sufficient to evoke postsynaptic activity within supragranular cells, but that many of these cells fail to fire and thus fail to establish postsynaptic potentials in infragranular pyramidal cells. This possibility is consistent with evidence that suggests that thalamocortical transmission may be more reliable and efficient compared to intracortical synaptic transmission (Kharazia & Weinberg, 1994; Gil et al. 1999; see also Castro-Alamancos & Connors, 1997; Amitai, 2001).
Laminar analysis of FOs suggests that they too are produced by asynchronous activation of supra- and infragranular cells. This conclusion is supported by simultaneous field potential and multiunit recordings revealing neuronal discharge associated with individual cycles of FOs (Kandel & Buzsaki, 1997; Jones et al. 2000; Barth, 2003) and suggesting that cortical circuit interactions may contribute to FO generation. Data on higher frequency sigma-bursts observed in humans (Gobbele et al. 1998; Gobbele et al. 1999) and piglets (Ikeda et al. 2002) have suggested that an additional extra-cortical oscillatory component may also reside within the thalamus. However, rhythmic thalamic input does not appear to play a role in rat somatosensory cortex as FOs may be evoked during direct cortical stimulation with or without an intact thalamic VB (Staba et al. 2003), and are abolished during cortical cooling (Staba et al. 2003) or cortical application of kynurenic acid (Ikeda et al. 2002), despite intact, non-rhythmic thalamic input. This conclusion is also supported by the present results, indicating no rhythmic MUA in the VB corresponding to concurrently recorded cortical FOs.
While the laminar profile of FOs appears similar to that of the P1/N1 slow wave complex, FOs are unchanged by GABA, indicating that a distinct neural mechanism underlies their generation. It has been proposed that FOs may reflect excitatory interactions between cortical pyramidal cells (Jones et al. 2000; Jones & Barth, 2002; Barth, 2003) resulting in tightly synchronized population spikes. Recent evidence indicates that regular-spiking cells, presumably pyramidal cells (Connors & Gutnick, 1990), can discharge at preferred latencies that correspond with individual cycles of the oscillation (Jones et al. 2000; Barth, 2003). The responses of approximately half of the units studied here during baseline conditions were quite similar to those obtained with previous intracellular recording from regular-spiking cells. While no single pyramidal cell can fire at FO frequencies, coordinated AP firing within a population of pyramidal cells may generate coherent, small amplitude extracellular currents that could produce patterns in the laminar CSD similar to the patterns observed in the present study.
If FOs reflect synchronized population spikes in cortical pyramidal cells, the question remains how they persist in the presence of GABA, which substantially decreases cell firing and therefore intracortical transmission upon which the postsynaptic N1 slow wave relies. Simultaneous displacement of multiple vibrissae generates a synchronous thalamocortical volley, apparently of sufficient strength to overcome cellular hyperpolarization in a limited number of supra- and infragranular pyramidal cells, resulting in FOs without the accompanying large amplitude N1 slow wave. Yet, if FOs require circuit interactions between pyramidal cells that are based on excitatory synaptic transmission, it is unlikely that they would remain unchanged by GABA.
The present observation that the gap junction blocker, halothane, produces a marked attenuation of FOs compared to the slow wave, suggests the possibility that excitatory coupling giving rise to FOs is not based strongly on chemical synaptic transmission, and may occur instead through electrical coupling. Precedent for this suggestion does exist in studies of hippocampal ripple (200 Hz) oscillations. Modelling studies predict that high frequency activity, in the absence of chemical synaptic transmission, may occur through a network of hippocampal pyramidal cells electrically coupled by their axons (Traub et al. 1999). Simulations of ripple activity can be produced with a sparse connectivity between axons and low frequency of ectopic spike generation (Traub et al. 1999). Indeed, evidence from in vitro hippocampal studies shows that only a small proportion of principal neurones participate in each ripple, and ripples can be extinguished with halothane, indicating that they may emerge through a network of electrically coupled principal cells (Ylinen et al. 1995; Draguhn et al. 1998; Schmitz et al. 2001). If a similar mechanism is responsible for FOs in cortex, it could explain why FOs persist during partial suppression of pyramidal cell firing sufficient to eliminate the N1, yet, unlike the N1, are nearly extinguished by halothane.
However, analogies between somatosensory cortex and hippocampus must be made tentatively. While evidence exists for cortical gap junctions (Gutnick & Prince, 1981), more evidence is needed concerning electrical coupling between axons of cortical pyramidal cells. In contrast to pyramidal cells, there is strong evidence for electrical coupling between fast-spiking inhibitory cells in neocortex (Galarreta & Hestrin, 1999), which could serve to synchronize their discharge at FO frequencies. We identified only two units with high frequency firing patterns and phase-locking to the FOs that were similar to intracortical recordings of inhibitory interneurones responding to vibrissa stimulation (Jones et al. 2000). Inhibitory interneurones do receive direct excitatory thalamocortical input that would be expected to persist in the absence of intracortical excitatory drive, and when synchronized in sufficient numbers, could produce small dipolar field potentials in dendrites that radiate in a predominately vertical orientation (Jones & Hendry, 1984). Yet, while the present study indicates that the mechanism of FO generation is clearly different than that of the slow wave-evoked potential and may rely on gap junctions, the effect of GABA and halothane on both principal cells and interneurones must now be examined and characterized with intracellular recording techniques to determine their specific contribution to FOs in somatosensory cortex.
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