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Enhancement of encoding and retrieval functions through theta phase-specific manipulation of hippocampus.

Siegle JH, Wilson MA - Elife (2014)

Bottom Line: Assessing the behavioral relevance of the hippocampal theta rhythm has proven difficult, due to a shortage of experiments that selectively manipulate phase-specific information processing.Using closed-loop stimulation, we triggered inhibition of dorsal CA1 at specific phases of the endogenous theta rhythm in freely behaving mice.Conversely, stimulation in the retrieval segment enhanced performance when inhibition was triggered by the trough of theta.

View Article: PubMed Central - PubMed

Affiliation: Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, United States Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, United States jsiegle@mit.edu.

No MeSH data available.


Direct recruitment of fast-spiking inhibition with light.(A) Expression of ChR2-EYFP throughout the dorsal hippocampus.Note the strong labeling in stratum pyramidale, indicative of dense PV+projections in this layer. Bilateral fiber optic lesions are marked withwhite rectangles, centered at ∼2 mm posterior to bregma and∼1.75 mm lateral to the midline. (B) Projection plot ofpeak heights from a CA1 electrode containing a well-isolated fast-spikingunit (blue) and a well-isolated regular-spiking unit (yellow).(C) Mean waveforms (with SD) for each tetrode channel forthe same units as in panel B. (D) Raw, broadbandtrace for a single trial, aligned to the 10 ms light pulse. Fourlight-evoked spikes from the fast-spiking unit are clearly identifiable.(E) Peri-stimulus time histogram for the fast-spiking unitin B, C, and D, aligned to the startof each light pulse (N = 1106 pulses from onesession). This unit responds with 3–4 spikes per stimulus, thenremains silent for a period of ∼15 ms following light offset.(F) Peri-stimulus time histogram for the regular-spikingunit in B and C, aligned to the start of eachlight pulse (N = 1106 pulses from one session). Thisunit is silenced for ∼25 ms following light onset.DOI:http://dx.doi.org/10.7554/eLife.03061.004
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fig2: Direct recruitment of fast-spiking inhibition with light.(A) Expression of ChR2-EYFP throughout the dorsal hippocampus.Note the strong labeling in stratum pyramidale, indicative of dense PV+projections in this layer. Bilateral fiber optic lesions are marked withwhite rectangles, centered at ∼2 mm posterior to bregma and∼1.75 mm lateral to the midline. (B) Projection plot ofpeak heights from a CA1 electrode containing a well-isolated fast-spikingunit (blue) and a well-isolated regular-spiking unit (yellow).(C) Mean waveforms (with SD) for each tetrode channel forthe same units as in panel B. (D) Raw, broadbandtrace for a single trial, aligned to the 10 ms light pulse. Fourlight-evoked spikes from the fast-spiking unit are clearly identifiable.(E) Peri-stimulus time histogram for the fast-spiking unitin B, C, and D, aligned to the startof each light pulse (N = 1106 pulses from onesession). This unit responds with 3–4 spikes per stimulus, thenremains silent for a period of ∼15 ms following light offset.(F) Peri-stimulus time histogram for the regular-spikingunit in B and C, aligned to the start of eachlight pulse (N = 1106 pulses from one session). Thisunit is silenced for ∼25 ms following light onset.DOI:http://dx.doi.org/10.7554/eLife.03061.004

Mentions: After at least 8 days of training, mice were implanted with a multielectrode arraythat targeted movable tetrodes and stationary fiber optic cables to hippocampusbilaterally. Two fiber optic cables (one per hemisphere) were implanted to a depth of0.9 mm at the time of surgery. In the same procedure, we injected 1.0 µl of anadeno-associated virus carrying the gene for channelrhodopsin-2 (Nagel et al., 2003) into both sides of thebrain, centered on CA1 approximately 1 mm posterior to the septal pole ofhippocampus. Expression spread at least 2 mm along the septotemporal axis, coveringmost of dorsal CA1 as well as overlying cortex (Figure 2A).10.7554/eLife.03061.004Figure 2.Direct recruitment of fast-spiking inhibition with light.


Enhancement of encoding and retrieval functions through theta phase-specific manipulation of hippocampus.

Siegle JH, Wilson MA - Elife (2014)

Direct recruitment of fast-spiking inhibition with light.(A) Expression of ChR2-EYFP throughout the dorsal hippocampus.Note the strong labeling in stratum pyramidale, indicative of dense PV+projections in this layer. Bilateral fiber optic lesions are marked withwhite rectangles, centered at ∼2 mm posterior to bregma and∼1.75 mm lateral to the midline. (B) Projection plot ofpeak heights from a CA1 electrode containing a well-isolated fast-spikingunit (blue) and a well-isolated regular-spiking unit (yellow).(C) Mean waveforms (with SD) for each tetrode channel forthe same units as in panel B. (D) Raw, broadbandtrace for a single trial, aligned to the 10 ms light pulse. Fourlight-evoked spikes from the fast-spiking unit are clearly identifiable.(E) Peri-stimulus time histogram for the fast-spiking unitin B, C, and D, aligned to the startof each light pulse (N = 1106 pulses from onesession). This unit responds with 3–4 spikes per stimulus, thenremains silent for a period of ∼15 ms following light offset.(F) Peri-stimulus time histogram for the regular-spikingunit in B and C, aligned to the start of eachlight pulse (N = 1106 pulses from one session). Thisunit is silenced for ∼25 ms following light onset.DOI:http://dx.doi.org/10.7554/eLife.03061.004
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Related In: Results  -  Collection

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fig2: Direct recruitment of fast-spiking inhibition with light.(A) Expression of ChR2-EYFP throughout the dorsal hippocampus.Note the strong labeling in stratum pyramidale, indicative of dense PV+projections in this layer. Bilateral fiber optic lesions are marked withwhite rectangles, centered at ∼2 mm posterior to bregma and∼1.75 mm lateral to the midline. (B) Projection plot ofpeak heights from a CA1 electrode containing a well-isolated fast-spikingunit (blue) and a well-isolated regular-spiking unit (yellow).(C) Mean waveforms (with SD) for each tetrode channel forthe same units as in panel B. (D) Raw, broadbandtrace for a single trial, aligned to the 10 ms light pulse. Fourlight-evoked spikes from the fast-spiking unit are clearly identifiable.(E) Peri-stimulus time histogram for the fast-spiking unitin B, C, and D, aligned to the startof each light pulse (N = 1106 pulses from onesession). This unit responds with 3–4 spikes per stimulus, thenremains silent for a period of ∼15 ms following light offset.(F) Peri-stimulus time histogram for the regular-spikingunit in B and C, aligned to the start of eachlight pulse (N = 1106 pulses from one session). Thisunit is silenced for ∼25 ms following light onset.DOI:http://dx.doi.org/10.7554/eLife.03061.004
Mentions: After at least 8 days of training, mice were implanted with a multielectrode arraythat targeted movable tetrodes and stationary fiber optic cables to hippocampusbilaterally. Two fiber optic cables (one per hemisphere) were implanted to a depth of0.9 mm at the time of surgery. In the same procedure, we injected 1.0 µl of anadeno-associated virus carrying the gene for channelrhodopsin-2 (Nagel et al., 2003) into both sides of thebrain, centered on CA1 approximately 1 mm posterior to the septal pole ofhippocampus. Expression spread at least 2 mm along the septotemporal axis, coveringmost of dorsal CA1 as well as overlying cortex (Figure 2A).10.7554/eLife.03061.004Figure 2.Direct recruitment of fast-spiking inhibition with light.

Bottom Line: Assessing the behavioral relevance of the hippocampal theta rhythm has proven difficult, due to a shortage of experiments that selectively manipulate phase-specific information processing.Using closed-loop stimulation, we triggered inhibition of dorsal CA1 at specific phases of the endogenous theta rhythm in freely behaving mice.Conversely, stimulation in the retrieval segment enhanced performance when inhibition was triggered by the trough of theta.

View Article: PubMed Central - PubMed

Affiliation: Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, United States Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, United States jsiegle@mit.edu.

No MeSH data available.