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Figure 1: AAV DIO ChR2-mCherry gives Cre-dependent and cell-type-specific expression of light-activated channels in vivo. a, AAV DIO ChR2-mCherry with Cre-dependent expression of ChR2 produced cell-type-specific targeting of light-activated channels. In the presence of Cre, ChR2-mCherry is inverted into the sense direction and expressed from the EF-1α (EEF1A1) promoter. ITR, inve pA, poly(A); WPRE, woodchuck hepatatis B virus post-transcriptional element. b, ChR2-mCherry was robustly expressed in PV+ interneurons in barrel cortex of adult PV-Cre mice. c, A corresponding injection in αCamKII-Cre mice resulted in exclusive labelling of excitatory neurons. d, e, ChR2-mCherry expression in PV-Cre mice was confined to cells expressing PV. e, PV+ cells with ChR2-mCherry expression and typical FS interneuron morphology. f, g, ChR2-mCherry expression in αCamKII-Cre mice is confined to neurons immuno-negative for PV. g, ChR2-mCherry-expressing cells with typical pyramidal neuron morphology. Scale bars: b, c, 100?m; d–g, 25?m.
In experiments targeting excitatory neurons, AAV DIO ChR2-mCherry was injected into the barrel cortex of adult CW2 (ref. 24) mice, which express Cre from the αCamKII (also known as Camk2a) promoter (‘αCamKII-Cre mice’), inducing recombination in excitatory neurons in cortex24. Robust ChR2-mCherry expression was observed in excitatory neurons in a laminar profile corresponding to the Cre expression pattern (Fig. 1c and Supplementary Fig. 4)24. At least 50% of the αCamKII+ neurons in layer 2/3 expressed ChR2-mCherry (913 of 1,638 cells in a total area of 8.4×106?m3) close to the injection site, covering an anterioposterior distance of 1,560±154.9μm (mean?±?s.d., n = 3). Immunohistochemical analysis revealed that 100±0% (mean±s.d., n = 4,024 ChR2-mCherry+ neurons, 4 animals) of the ChR2-mCherry-expressing neurons were immuno-negative for PV (Fig. 1f, g and Supplementary Fig. 2), and 100±0% expressed the neuronal marker NeuN (data not shown).
FS activation suppresses local sensory responses
We recorded light-activated FS and regular spiking (RS) single units in layers 2/3 and 4 of barrel cortex in PV-Cre (n = 64 FS cells in 15 animals) and αCamKII-Cre (n = 56 RS cells in 7 animals) mice. We did not observe light activation of layer 5 FS cells (n = 12 sites in 7 animals). Barrel cortex, which processes information from the rodent vibrissae (whiskers), was targeted as a well-defined model of basic sensory cortical function. In agreement with the immunohistological results, the action potential shapes of the neurons activated by light pulses were differentiated into two discrete populations based on mouse type: PV-Cre/FS and αCamKII-Cre/RS (P & 0.01; Fig. 2a).
Figure 2: Light-evoked activity in FS-PV+ inhibitory interneurons suppresses sensory processing in nearby excitatory neurons. a, Light-activated RS and FS cells recorded in layers 2/3 and 4 of barrel cortex in PV-Cre and αCamKII-Cre mice, respectively, formed two discrete overall populations based on waveform properties. b, Intracellular in vivo recording of an RS cell in a PV-Cre animal. A 1-ms pulse of blue light at low power evoked an IPSP with a sharp onset. c, The latency to light-activated FS spikes (filled circles) agreed well with the onset latency of the resulting IPSPs (open circles). The IPSP time to peak decreased with increasing power (low power: 46 mW mm-2; high power: 68 mW mm-2). d, Sustained activation of FS inhibitory interneurons eliminated sensory responses in nearby RS neurons. A layer 2/3 FS cell was reliably activated by a 10-ms light pulse ( left panel). An RS cell recorded on the same tetrode responded to vibrissa deflection ( centre panel). Activation of inhibitory activity simultaneously with vibrissa deflection eliminated the RS sensory response (right panel). e, Mean RS vibrissa response decreased significantly in the presence of increased FS cell activity. **P?&?0.01; error bars, mean±s.e.m.
To confirm the activation of inhibitory interneurons and their postsynaptic impact on excitatory neurons, we performed in vivo intracellular recordings of RS cells in barrel cortex of PV-Cre mice (n = 5). We found that a 1-ms light pulse was sufficient to evoke large, fast IPSPs, confirming direct synaptic inhibition of RS cells by light-activated FS cells (Fig. 2b). The latencies of the presynaptic light-evoked FS spikes agreed well with the onset times of the postsynaptic IPSPs, with FS spikes preceding IPSP onset by 0.5 to 0.75?ms (Fig. 2c). Both the time to peak and the peak timing variability of the evoked IPSPs decreased with increasing light pulse power (Fig. 2c). Mean IPSP peak amplitude at membrane potentials of -55 to -60mV was 2.7±1.0mV. The mean reversal potential of the evoked IPSPs (see Supplementary Methods) was -67.6±1.9mV, indicating a GABAA-mediated Cl- conductance characteristic of FS synapses. Consistent with IPSP induction, activation of FS cells blocked vibrissa-evoked responses in neighbouring RS cells (Fig. 2d, n = 6 sites in 5 PV-Cre mice).
FS activation generates gamma oscillations
A strong prediction of the FS-gamma hypothesis is that synchronously active FS cells are sufficient for gamma induction. This hypothesis predicts that light pulses presented at a broad range of frequencies should reveal a selective peak in enhancement of the LFP, a measure of synchronous local network activity25, when FS cells are driven in the gamma range.
To test this hypothesis, we drove cortical FS cell spiking in virus-transduced PV-Cre mice at a range of frequencies (8-200?Hz) with 1-ms light pulses. Light pulses in the gamma range (40?Hz) resulted in reliable action potential output at 25-ms intervals (Fig. 3a). Across the population, FS and RS cells were driven with equally high reliability by light pulses at low frequencies (Fig. 3b). At higher frequencies, spike probability on each light cycle remained high for FS cells but decreased for RS cells.
Figure 3: FS inhibitory interneurons generate gamma oscillations in the local cortical network. a, In response to 40-Hz light pulses (blue bars), this FS cell fired reliably at 25-ms intervals, giving an instantaneous firing frequency of 40Hz (inset). b, Average spike probability per light-pulse cycle in light-activated FS and RS cells in the PV-Cre and αCamKII-Cre mice, respectively (RS, n = 17, FS, n = 22, filled circles). c, Example of the increase in power at ~40Hz in the LFP caused by activation of FS cells by light pulses at 40Hz. d, Mean power ratio in each frequency band in response to light activation of FS (filled circles) and RS (open circles) cells at those frequencies. e, f, Comparison of the effect of activating FS and RS cells at 8 and 40?Hz on relative LFP power in those frequency bands. Black bars, relative power in the baseline LFP; blue bars, relative power in the presence of light pulses. g, Average spike probability of FS cells per light pulse cycle in response to three levels of light intensity. h, Mean power ratios from LFP recordings at the light intensity levels shown in g. i, The trace shows spontaneously occurring gamma activity in the LFP. Brief activation of FS cells (blue asterisk) prolonged the duration of the ongoing gamma cycle and consequently shifted the phase of the following cycles. The duration of the cycle during which the light stimulus was given (Light) was significantly longer than the preceding (Pre) or the following (Post) cycle. **P?&?0.01; error bars, mean±s.e.m.
Driving FS cells at 40?Hz caused a specific increase in the 35-40?Hz frequency band in the LFP (Fig. 3c and Supplementary Figs 5 and 6). We found that activation of FS cells in the 20-80Hz range resulted in significant amplification of LFP power at those frequencies (n = 14 sites in 6 Fig. 3d). However, activation of FS cells at lower frequencies did not affect LFP power, despite robust evoked FS firing on every light cycle. In contrast, 8-24Hz light activation of RS cells in αCamKII-Cre mice induced increased LFP power at these frequencies, but RS activation at higher frequencies did not affect LFP power (n = 13 sites in 5 Fig. 3d and Supplementary Fig. 5). Light stimulation in the untransduced contralateral barrel cortex did not affect LFP power at any frequency (n = 6 PV-Cre and 5 αCamKII-C Supplementary Fig. 6).
This double dissociation of cell-type-specific state induction (gamma by FS and lower frequencies by RS) directly supports the prediction that FS-PV+ interneuron activation is sufficient and specific for induction of gamma oscillations. To highlight this distinction, we compared the effects of stimulating the two cell types at 8 and 40?Hz. Stimulation of FS cells at 8Hz in the PV-Cre mice had no effect on LFP power at 8?Hz, but FS stimulation at 40Hz caused a significant increase in 40-Hz LFP power (paired t- P & 0.001; Fig. 3e). In contrast, stimulation of RS cells at 8Hz in the αCamKII-Cre mice caused a significant increase of LFP power at 8?Hz (P & 0.001), whereas RS stimulation at 40?Hz caused only a small, nonsignificant increase in 40-Hz LFP power (Fig. 3f).
Gamma generation is a resonant circuit property
One possible explanation for these results is that increased FS firing recruits resonant gamma-range activity in the surrounding local network as a function of the synaptic and biophysical properties of the cortical circuit. Alternatively, the increase in gamma activity may result from the specific level of evoked FS spiking, and changing spiking probability would shift the frequency of the enhanced LFP band. To discriminate between these possibilities, we stimulated FS cells at varying levels of light intensity. We found that FS spike probability changed with light intensity such that the spike probability curve shifted laterally (Fig. 3g). Whereas drive affected the amplitude of enhancement, LFP power was selectively amplified within the gamma range regardless of light intensity or spike probability (Fig. 3h), indicating that the gamma oscillations evoked by FS activity are a resonant circuit property. In addition, randomly patterned light stimulation of FS cells with frequencies evenly distributed across a broad range evoked a significant increase in LFP power specific to the gamma range (n = 7 sites in 4 P & 0.05; Supplementary Fig. 7), further indicating that FS-evoked gamma oscillations are an emergent property of the circuit and do not require exclusive drive in the gamma range.
Natural gamma oscillations require FS activity
To test whether intrinsically occurring gamma oscillations show a similar dependence on FS activity, we gave single light pulses during epochs of natural gamma. We found that brief FS activation shifted the phase of both spontaneously occurring gamma oscillations (n = 26 trials, 4 Kruskal–Wallis test with Dunn’s post- P?&?0.01; Fig. 3i) and those evoked by midbrain reticular formation stimulation (n = 18 trials, 2 P & 0.05; Supplementary Fig. 8). Furthermore, light-induced gamma oscillations were largely eliminated by blocking AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid) and NMDA (N-methyl-d-aspartate) receptors, despite high levels of evoked FS firing (n = 4 sites in 4 P & 0.01; Supplementary Fig. 9). These results indicate that induced gamma oscillations depend on rhythmic excitatory synaptic activity, as predicted by computational models of natural gamma oscillations and previous experiments4, 9, 11, 12, 26. In further agreement, spontaneous RS activity was entrained by 40?Hz FS stimulation, resulting in RS firing during the decay phase of the IPSP and preceding subsequent evoked FS spiking (Supplementary Fig. 10).
Evoked gamma phase regulates sensory processing
Gamma oscillations are thought to have a functional impact on cortical information processing by synchronizing the output of excitatory neurons27, 28. This synchrony selects cell assemblies involved in a common task, such as encoding a sensory stimulus, and enhances their impact on downstream targets27. The cyclical FS inhibition underlying gamma oscillations is believed to cause this synchrony by rhythmically gating synaptic inputs27, 29. Synaptic inputs arriving at the peak of inhibition should therefore produce a diminished response, but those arriving at the opposite phase in the gamma cycle should evoke a large response.
To test this hypothesis directly, we stimulated FS cells at 40Hz with light pulses to establish gamma oscillations, and recorded the responses of RS cells to a single vibrissa deflection presented at one of five phases relative to a single gamma cycle (n = 20 cells in 3 Fig. 4a). The timing of vibrissa-induced RS action potentials relative to light-evoked inhibition and the gamma cycle had a significant impact on the amplitude, timing and precision of the sensory-evoked responses of RS cells (Fig. 4b, c). The presence of gamma oscillations significantly decreased the amplitude of the RS sensory response at three phase points, consistent with the enhanced level of overall inhibition in this state (P & 0.05; 1-way ANOVA with Dunnett’s post- Fig. 4d)28. Gamma phase also modulated the overall timing of the sensory response (P & 0.01; Fig. 4e), with spike latency delayed at phases 1-3 and unaffected at phases 4-5 (ref. 28). The precision of sensory-evoked spikes was significantly enhanced in a gamma-phase-dependent manner (P & 0.01; Fig. 4f). Our results indicate that the rhythmic, FS-induced IPSP restricts sensory transmission during its peak, and permits transmission after its decay, leading to a temporal sharpening of cortical sensory responses (Fig. 4g).
Figure 4: Gamma oscillations gate sensory responses of excitatory neurons. a, In each trial, FS-PV+ inhibitory interneurons were activated at 40Hz and a single vibrissa deflection (whisker stimulus, WS) was presented at one of five phases. b, Baseline response of one layer 4 RS cell to single vibrissa deflections, shown in units of spikes per trial. c, Responses of the same cell when the whisker was deflected at each of five temporal phases relative to the induced gamma oscillation. d, Average spikes evoked per trial under each condition. Dotted line indicates baseline responses. e, Timing of the RS spike response, measured as median spike latency. f, Spike precision of the RS responses. g, Schematic model of the gating of sensory responses by gamma oscillations. IPSP and LFP examples are averaged data traces. *P & 0.05, **P?&?0.01; error bars, mean±s.e.m.
Our results provide the first causal demonstration of cortical oscillations induced by cell-type-specific activation. Synchronous FS-PV+ interneuron activity driven by periodic stimulation of light-activated channels generated gamma oscillations in a cortical network, and these gated sensory processing in a temporally specific manner. These findings also demonstrate a unique application of optogenetic engineering in the in vivo brain for the study of discrete neuronal cell types under active network conditions. Future use of these techniques will allow direct testing of the impact of brain states on information processing in the behaving animal30, and potentially the rescue of functional states in models of brain disease31, 32, 33.
Online Methods
All procedures were conducted in accordance with the National Institutes of Health guidelines and with the approval of the Committee on Animal Care at MIT. PV-Cre (n = 21) and CW2 (n = 7) mice were 6-12 weeks old at the time of viral injections. Electrophysiological recordings and immunohistochemical analyses were performed 1-3 weeks after viral injections.
AAV vectors
ChR2 fused to the fluorescent protein mCherry was cloned in antisense direction into pAAV-MCS (Stratagene) to create AAV DIO ChR2-mCherry (Fig. 1a and Supplementary Fig. 1; for vector outline and sequence see http://www.optogenetics.org). ChR2-mCherry was flanked by a pair of canonical loxP sites and a pair of mutated lox2272 sites. A woodchuck hepatatis B virus post-transcriptional element was placed in sense direction 5′ of the poly(A). Adeno-associated viral particles of serotype 2 were produced by the Vector Core Facility at The University of North Carolina at Chapel Hill.
Virus injections
Adult PV-Cre18 or CW2 (ref. 24) mice were anesthetized with an intraperitoneal injection of a mixture of ketamine (1.1 mg kg-1) and xylazine (0.16mg kg-1). A small craniotomy was made 1.5mm posterior to bregma and 3.0?mm lateral to the midline. Virus was delivered through a small durotomy by a glass micropipette attached to a Quintessential Stereotaxic Injector (Stoelting). The glass micropipette was lowered to 0.4mm below the cortical surface. A bolus of 0.5?μl of virus (AAV DIO ChR2-mC 2×1012 viral molecules per ml) was injected into barrel cortex at 0.1?l min-1. The pipette was then retracted to a depth of 250?m below the surface and an additional 0.5?l virus was injected at the same rate. The pipette was held in place for 5min after the injection before being retracted from the brain. The scalp incision was sutured, and post-injection analgesics were given to aid recovery (0.1mg kg-1 Buprenex).
Immunohistochemistry
Mice were transcardially perfused with 100mM PBS followed by 4% formaldehyde in PBS, and brains were post-fixed for 18?h at 4℃ Free-floating sections (30?m) were cut using a vibratome (Leica VT100) and incubated with blocking solution (10% donkey serum in PBS with 0.3% Triton-X 100) for 1h at room temperature (20℃) and then incubated at room temperature overnight with primary antibody diluted in blocking solution. The following primary antibodies were used: NeuN (C 1:1,000), parvalbumin PVG-214 (S 1:2,000), GABA (S 1:4,000) and CamKII (E 1:500). After washing, antibody staining was revealed using species-specific fluorophore-conjugated secondary antibodies ( Cy5 from Jackson Laboratories, Alexa 488 from Molecular Probes). GABA was detected with biotinylated secondary antibodies (Jackson Laboratories) and revealed using a combination of ABC kit (Vector Laboratories) and TSA fluorescent amplification kit (Perkin-Elmer). Sections were mounted on glass slides with Vectashield (Vector Laboratories) and coverslipped.
Quantification
Spread and labelling efficiency were scored by hand by examination of every 30??m coronal section (n = 3 animals per genotype) for the presence of mCherry fluorescence using a Zeiss LSM510 confocal microscope. For quantification of co-labelling of ChR2-mCherry and PV (n = 4 animals per genotype) confocal images were acquired and individual cells were identified independently for each of the two fluorescent channels. Scans from each channel were collected in multi-track mode to avoid cross-talk between channels.
Electrophysiology
Mice were anesthetized with isoflurane and held in place with a head post cemented to the skull. All incisions were infiltrated with lidocaine. A small craniotomy was made over barrel cortex approximately 200μm anterior to the virus injection site. Extracellular single-unit and LFP recordings were made with tetrodes or stereotrodes. Intracellular recordings were conducted by whole-cell in vivo recording in current clamp mode. Stimulus control and data acquisition was performed using software custom-written in LabView (National Instruments) and Matlab (The Mathworks). Further electrophysiology methods and a description of the reversal potential calculation are given in Supplementary Methods.
Light stimulation was generated by a 473nm laser (Shanghai Dream Lasers) controlled by a Grass stimulator (Grass Technologies) or computer. Light pulses were given via a 200-μm diameter, unjacketed optical fibre (Ocean Optics) positioned at the cortical surface 75-200μm from the recording electrodes. For experiments using the broad range of light-stimulation frequencies (8, 16, 24, 32, 40, 48, 80, 100 and 200Hz), we stimulated in bouts of 3s of 1-ms pulses at 46 mW mm-2 at each frequency in a random order. In a subset of these experiments, we stimulated at 31, 46 and 68 mW mm-2.
Vibrissae were stimulated by computer-controlled movements of piezoelectric wafers (Piezo Systems). Vibrissa stimulations were single high-velocity deflections in the dorsal and then in the ventral direction (~6ms duration). In most cases, adjacent vibrissae that yielded indistinguishable amplitude responses during hand mapping were deflected simultaneously. Vibrissa stimulations evoked layer 4 RS spike responses with an onset latency of 9.1±0.08ms. For RS cell response suppression experiments, light pulses were given on randomly interleaved trials. For gamma-phase experiments, we gave a series of trials each consisting of a 1-s series of 1-ms light pulses at 40Hz, with a single whisker deflection after the thirtieth light pulse. The precise timing of the whisker deflection relative to the light pulses was varied across five phase points. Each of the five phase points was included in a random order across a minimum of 250 total trials.
Unit and LFP analysis used software custom-written in Igor Pro (Wavemetrics). For each stimulation frequency, we measured the relative power in an 8-Hz band centred on that frequency. For each recording site, we measured power from 5-10 LFP traces under each condition. Example power spectra are averages of the power spectra from 5-10 traces of unfiltered LFPs from individual experiments. Relative power was calculated by measuring the ratio of power within the band of interest to total power in the power spectrum of the unfiltered LFP. We also measured the power ratio: Plight/Pbaseline, where Plight is the relative power in a frequency band in the presence of light stimulation and Pbaseline is the power in that band in the absence of light stimulation. All numbers are given as mean±s.e.m., except where otherwise noted.
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