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Gating multiple signals through detailed balance of excitation and inhibition in spiking networks.

Vogels TP, Abbott LF - Nat. Neurosci. (2009)

Bottom Line: We illustrate gating through detailed balance in large networks of integrate-and-fire neurons.We show successful gating of multiple signals and study failure modes that produce effects reminiscent of clinically observed pathologies.Provided that the individual signals are detectable, detailed balance has a large capacity for gating multiple signals.

View Article: PubMed Central - PubMed

Affiliation: Center for Neurobiology and Behavior, Department of Physiology and Cellular Biophysics, Columbia University College of Physicians and Surgeons, New York, New York, USA.

ABSTRACT
Recent theoretical work has provided a basic understanding of signal propagation in networks of spiking neurons, but mechanisms for gating and controlling these signals have not been investigated previously. Here we introduce an idea for the gating of multiple signals in cortical networks that combines principles of signal propagation with aspects of balanced networks. Specifically, we studied networks in which incoming excitatory signals are normally cancelled by locally evoked inhibition, leaving the targeted layer unresponsive. Transmission can be gated 'on' by modulating excitatory and inhibitory gains to upset this detailed balance. We illustrate gating through detailed balance in large networks of integrate-and-fire neurons. We show successful gating of multiple signals and study failure modes that produce effects reminiscent of clinically observed pathologies. Provided that the individual signals are detectable, detailed balance has a large capacity for gating multiple signals.

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Related in: MedlinePlus

Gain Propertiesa) Maximum values of the cross-correlations (termed "similarity", see methods) between the sender region and the excitatory and inhibitory receiver cells (red and blue respectively) for different gains. Solid lines show similarity values for symmetric gain reduction, dashed lines show similarity for asymmetric gain reduction, when only the gain of the excitatory synapses onto the inhibitory receiver cells is changed. b) Similarity values between excitatory receiver activity and the signal in the balanced (gated-off) state as a function of increasing the variability (standard deviation σ) of the synaptic strengths of the excitatory (green trace) and inhibitory (blue trace) pathways. The arrows mark the variability limits beyond which the tails of the strength distributions get rectified to zero. c) Effect of reducing the number of inhibitory receiver neurons on the ability to gate signals off. Similarity values in the balanced state for decreasing numbers of inhibitory receiver cells, without and with synapse strength compensation (solid and dotted line, respectively). d) Operation of the gating mechanism with only 20 inhibitory receiver neurons by compensating synapse strength and shortened refractory times to allow for more rapid inhibitory firing. Similarity between the signal and the excitatory (red trace) and inhibitory (blue trace) receiver activity is plotted as a function of change in inhibitory gain.
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Figure 4: Gain Propertiesa) Maximum values of the cross-correlations (termed "similarity", see methods) between the sender region and the excitatory and inhibitory receiver cells (red and blue respectively) for different gains. Solid lines show similarity values for symmetric gain reduction, dashed lines show similarity for asymmetric gain reduction, when only the gain of the excitatory synapses onto the inhibitory receiver cells is changed. b) Similarity values between excitatory receiver activity and the signal in the balanced (gated-off) state as a function of increasing the variability (standard deviation σ) of the synaptic strengths of the excitatory (green trace) and inhibitory (blue trace) pathways. The arrows mark the variability limits beyond which the tails of the strength distributions get rectified to zero. c) Effect of reducing the number of inhibitory receiver neurons on the ability to gate signals off. Similarity values in the balanced state for decreasing numbers of inhibitory receiver cells, without and with synapse strength compensation (solid and dotted line, respectively). d) Operation of the gating mechanism with only 20 inhibitory receiver neurons by compensating synapse strength and shortened refractory times to allow for more rapid inhibitory firing. Similarity between the signal and the excitatory (red trace) and inhibitory (blue trace) receiver activity is plotted as a function of change in inhibitory gain.

Mentions: The gain changes used to gate signals on have been fairly large, so we next examined different degrees and types of gain modulation in the inhibitory receiver neurons. Beginning with no gain change (Δ Gain = 0), we decreased the responsiveness and thus the firing rate of the inhibitory receiver population. This causes the firing rate of the excitatory receiver neurons and its similarity to the sender signal in the gated-on state (Fig. 4a, solid red trace) to increase. At Δ Gain ~80%, the signal similarity of the activity of the inhibitory neurons goes rapidly to zero (Fig. 4a, solid blue trace), and the similarity of the excitatory receiver activity plateaus at ~90%. Alternatively, it is possible to reach this same plateau level with a gain shift of only 30% (Fig. 4a, dotted traces) by modulating the inhibitory population asymmetrically, which means modifying only the responsiveness to excitatory inputs.


Gating multiple signals through detailed balance of excitation and inhibition in spiking networks.

Vogels TP, Abbott LF - Nat. Neurosci. (2009)

Gain Propertiesa) Maximum values of the cross-correlations (termed "similarity", see methods) between the sender region and the excitatory and inhibitory receiver cells (red and blue respectively) for different gains. Solid lines show similarity values for symmetric gain reduction, dashed lines show similarity for asymmetric gain reduction, when only the gain of the excitatory synapses onto the inhibitory receiver cells is changed. b) Similarity values between excitatory receiver activity and the signal in the balanced (gated-off) state as a function of increasing the variability (standard deviation σ) of the synaptic strengths of the excitatory (green trace) and inhibitory (blue trace) pathways. The arrows mark the variability limits beyond which the tails of the strength distributions get rectified to zero. c) Effect of reducing the number of inhibitory receiver neurons on the ability to gate signals off. Similarity values in the balanced state for decreasing numbers of inhibitory receiver cells, without and with synapse strength compensation (solid and dotted line, respectively). d) Operation of the gating mechanism with only 20 inhibitory receiver neurons by compensating synapse strength and shortened refractory times to allow for more rapid inhibitory firing. Similarity between the signal and the excitatory (red trace) and inhibitory (blue trace) receiver activity is plotted as a function of change in inhibitory gain.
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Related In: Results  -  Collection

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Figure 4: Gain Propertiesa) Maximum values of the cross-correlations (termed "similarity", see methods) between the sender region and the excitatory and inhibitory receiver cells (red and blue respectively) for different gains. Solid lines show similarity values for symmetric gain reduction, dashed lines show similarity for asymmetric gain reduction, when only the gain of the excitatory synapses onto the inhibitory receiver cells is changed. b) Similarity values between excitatory receiver activity and the signal in the balanced (gated-off) state as a function of increasing the variability (standard deviation σ) of the synaptic strengths of the excitatory (green trace) and inhibitory (blue trace) pathways. The arrows mark the variability limits beyond which the tails of the strength distributions get rectified to zero. c) Effect of reducing the number of inhibitory receiver neurons on the ability to gate signals off. Similarity values in the balanced state for decreasing numbers of inhibitory receiver cells, without and with synapse strength compensation (solid and dotted line, respectively). d) Operation of the gating mechanism with only 20 inhibitory receiver neurons by compensating synapse strength and shortened refractory times to allow for more rapid inhibitory firing. Similarity between the signal and the excitatory (red trace) and inhibitory (blue trace) receiver activity is plotted as a function of change in inhibitory gain.
Mentions: The gain changes used to gate signals on have been fairly large, so we next examined different degrees and types of gain modulation in the inhibitory receiver neurons. Beginning with no gain change (Δ Gain = 0), we decreased the responsiveness and thus the firing rate of the inhibitory receiver population. This causes the firing rate of the excitatory receiver neurons and its similarity to the sender signal in the gated-on state (Fig. 4a, solid red trace) to increase. At Δ Gain ~80%, the signal similarity of the activity of the inhibitory neurons goes rapidly to zero (Fig. 4a, solid blue trace), and the similarity of the excitatory receiver activity plateaus at ~90%. Alternatively, it is possible to reach this same plateau level with a gain shift of only 30% (Fig. 4a, dotted traces) by modulating the inhibitory population asymmetrically, which means modifying only the responsiveness to excitatory inputs.

Bottom Line: We illustrate gating through detailed balance in large networks of integrate-and-fire neurons.We show successful gating of multiple signals and study failure modes that produce effects reminiscent of clinically observed pathologies.Provided that the individual signals are detectable, detailed balance has a large capacity for gating multiple signals.

View Article: PubMed Central - PubMed

Affiliation: Center for Neurobiology and Behavior, Department of Physiology and Cellular Biophysics, Columbia University College of Physicians and Surgeons, New York, New York, USA.

ABSTRACT
Recent theoretical work has provided a basic understanding of signal propagation in networks of spiking neurons, but mechanisms for gating and controlling these signals have not been investigated previously. Here we introduce an idea for the gating of multiple signals in cortical networks that combines principles of signal propagation with aspects of balanced networks. Specifically, we studied networks in which incoming excitatory signals are normally cancelled by locally evoked inhibition, leaving the targeted layer unresponsive. Transmission can be gated 'on' by modulating excitatory and inhibitory gains to upset this detailed balance. We illustrate gating through detailed balance in large networks of integrate-and-fire neurons. We show successful gating of multiple signals and study failure modes that produce effects reminiscent of clinically observed pathologies. Provided that the individual signals are detectable, detailed balance has a large capacity for gating multiple signals.

Show MeSH
Related in: MedlinePlus