“…This resulted in the average contrast response curve to shift upward (Fig. 2C) [27-30], although some neurons showed a multiplicative increase in responsiveness upon suppression of PV+ interneurons (Fig. S1) [26,31].…”
Background
To ensure that neuronal networks function in a stable fashion, neurons receive balanced inhibitory and excitatory inputs. In various brain regions this balance has been found to change temporarily during plasticity. Whether changes in inhibition have an instructive or permissive role in plasticity remains unclear. Several studies have addressed this question using ocular dominance plasticity in the visual cortex as a model, but so far it remains controversial whether changes in inhibition drive this form of plasticity by directly affecting eye-specific responses or through increasing the plasticity potential of excitatory connections.
Results
We tested how three major classes of interneurons affect eye-specific responses in normally reared or monocularly deprived mice by optogenetically suppressing their activity. We find that in contrast to somatostatin or vasoactive intestinal polypeptide expressing interneurons, parvalbumin (PV)-expressing interneurons strongly inhibit visual responses. In individual neurons of normal mice, inhibition and excitation driven by either eye are balanced and suppressing PV interneurons does not alter ocular preference. Monocular deprivation disrupts the binocular balance of inhibition and excitation in individual neurons, causing suppression of PV interneurons to change their ocular preference. Importantly however, these changes do not consistently favor responses to one of the eyes at the population level.
Conclusion
Monocular deprivation disrupts the binocular balance of inhibition and excitation of individual cells. This disbalance does not affect the overall expression of ocular dominance. Our data therefore support a permissive rather than an instructive role of inhibition in ocular dominance plasticity.
“…This resulted in the average contrast response curve to shift upward (Fig. 2C) [27-30], although some neurons showed a multiplicative increase in responsiveness upon suppression of PV+ interneurons (Fig. S1) [26,31].…”
Background
To ensure that neuronal networks function in a stable fashion, neurons receive balanced inhibitory and excitatory inputs. In various brain regions this balance has been found to change temporarily during plasticity. Whether changes in inhibition have an instructive or permissive role in plasticity remains unclear. Several studies have addressed this question using ocular dominance plasticity in the visual cortex as a model, but so far it remains controversial whether changes in inhibition drive this form of plasticity by directly affecting eye-specific responses or through increasing the plasticity potential of excitatory connections.
Results
We tested how three major classes of interneurons affect eye-specific responses in normally reared or monocularly deprived mice by optogenetically suppressing their activity. We find that in contrast to somatostatin or vasoactive intestinal polypeptide expressing interneurons, parvalbumin (PV)-expressing interneurons strongly inhibit visual responses. In individual neurons of normal mice, inhibition and excitation driven by either eye are balanced and suppressing PV interneurons does not alter ocular preference. Monocular deprivation disrupts the binocular balance of inhibition and excitation in individual neurons, causing suppression of PV interneurons to change their ocular preference. Importantly however, these changes do not consistently favor responses to one of the eyes at the population level.
Conclusion
Monocular deprivation disrupts the binocular balance of inhibition and excitation of individual cells. This disbalance does not affect the overall expression of ocular dominance. Our data therefore support a permissive rather than an instructive role of inhibition in ocular dominance plasticity.
“…Genetically and morphologically distinct groups of interneurons contribute inhibitory inputs to specific layers of neocortex, and perform different roles [30,36]. Although no consensus has been reached about the contribution of specific inhibitory cell types to orientation tuning in mouse V1, multiple papers show that optogenetic excitation of different inhibitory cell types can influence tuning properties of nearby pyramidal neurons [37,38,39,40]. It is plausible that, like excitatory input into the apical dendrites, inhibition located in spatially distinct regions of the pyramidal neuron also contribute to orientation tuning.…”
L5 pyramidal neurons are the only neocortical cell type with dendrites reaching all six layers of cortex, casting them as one of the main integrators in the cortical column. What is the nature and mode of computation performed in mouse primary visual cortex (V1) given the physiology of L5 pyramidal neurons? First, we experimentally establish active properties of the dendrites of L5 pyramidal neurons of mouse V1 using patch-clamp recordings. Using a detailed multi-compartmental model, we show this physiological setup to be well suited for coincidence detection between basal and apical tuft inputs by controlling the frequency of spike output. We further show how direct inhibition of calcium channels in the dendrites modulates such coincidence detection. To establish the singe-cell computation that this biophysics supports, we show that the combination of frequency-modulation of somatic output by tuft input and (simulated) calcium-channel blockage functionally acts as a composite sigmoidal function. Finally, we explore how this computation provides a mechanism whereby dendritic spiking contributes to orientation tuning in pyramidal neurons.
“…With regards to the impact of FS activation on sensory coding, these studies diverged substantially and these differences have been the subject of extensive discussion [73][74][75]. Lee et al (2012) observed that FS activation not only reduced the rate of activity, but also substantially sharpened the width of tuning curves, increasing their apparent precision.…”
Section: Optogenetic Drive Of Fs Interneurons Impacts Sensory Gain Anmentioning
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