Elizabeth M. Quinlan

Scholarly discussions about online research techniques have yet to fully consider their value in light of the growing right-wing authoritarianism and attacks on gender equity. This is particularly true for Participatory Action Research methods that rely on embodied action, collective emotional energy, and interaction. This paper examines the use of Participatory Theatre, a Participatory Action Research methodology that employs applied theatre techniques, to critically research the problem of campus sexual violence while building allyship among anti-violence activists to evoke progressive social transformation. Through the lens of a research project on campus sexual violence, and the application of Randall Collins’s theory of interaction rituals, we reflect on the challenges and opportunities of conducting Participatory Theatre studies online. We conclude that interaction ritual can be coupled with the emancipatory aims of Participatory Theatre to produce knowledge of mutual benefit to both researchers and communities by reaffirming our shared power, strengthen, and capacity for collective resistance in this critical time of political and economic turmoil.

The deletion of matrix metalloproteinase MMP9 is combined here with chronic monocular deprivation (cMD) to identify the contributions of this proteinase to plasticity in the visual system. Calcium imaging of supragranular neurons of the binocular region of primary visual cortex (V1b) of wild-type mice revealed that cMD initiated at eye opening significantly decreased the strength of deprived-eye visual responses to all stimulus contrasts and spatial frequencies. cMD did not change the selectivity of V1b neurons for the spatial frequency, but orientation selectivity was higher in low spatial frequency-tuned neurons, and orientation and direction selectivity were lower in high spatial frequency-tuned neurons. Constitutive deletion of MMP9 did not impact the stimulus selectivity of V1b neurons, including ocular preference and tuning for spatial frequency, orientation, and direction. However, MMP9^−/− mice were completely insensitive to plasticity engaged by cMD, such that the strength of the visual responses evoked by deprived-eye stimulation was maintained across all stimulus contrasts, orientations, directions, and spatial frequencies. Other forms of experience-dependent plasticity, including stimulus selective response potentiation, were normal in MMP9^−/− mice. Thus, MMP9 activity is dispensable for many forms of activity-dependent plasticity in the mouse visual system, but is obligatory for the plasticity engaged by cMD.

The temporal frequency of sensory stimulation is a decisive factor in the plasticity of perceptual detection thresholds. However, surprisingly little is known about how distinct temporal parameters of sensory input differentially recruit activity of neuronal circuits in sensory cortices. Here we demonstrate that brief repetitive visual stimulation induces long-term plasticity of visual responses revealed 24 h after stimulation and that the location and generalization of visual response plasticity is determined by the temporal frequency of the visual stimulation. Brief repetitive low-frequency stimulation (2 Hz) is sufficient to induce a visual response potentiation that is expressed exclusively in visual cortex layer 4 and in response to a familiar stimulus. In contrast, brief, repetitive high-frequency stimulation (HFS, 20 Hz) is sufficient to induce a visual response potentiation that is expressed in all cortical layers and transfers to novel stimuli. HFS induces a long-term suppression of the activity of fast-spiking interneurons and primes ongoing gamma oscillatory rhythms for phase reset by subsequent visual stimulation. This novel form of generalized visual response enhancement induced by HFS is paralleled by an increase in visual acuity, measured as improved performance in a visual detection task.

The temporal frequency of sensory stimulation is a decisive factor in the bidirectional plasticity of perceptual detection thresholds. However, surprisingly little is known about how distinct temporal parameters of sensory input differentially impact neuronal, circuit, and perceptual function. Here we demonstrate that brief repetitive visual stimulation is sufficient to induce long-term plasticity of visual responses, with the temporal frequency of the visual stimulus determining the location and generalization of visual response plasticity. Brief repetitive low frequency stimulation (LFS, 2 Hz) is sufficient to induce a visual response potentiation that is exclusively expressed in layer 4 in response to the familiar stimulus. In contrast, brief, repetitive high frequency stimulation (HFS, 20 Hz) suppresses the activity of fast-spiking interneurons and primes ongoing gamma oscillatory rhythms for visually-evoked phase reset. Accordingly, visual stimulation subsequent to HFS induces non-stimulus specific visual response plasticity that is expressed in all cortical layers. The generalized visual response enhancement induced by HFS is paralleled by an increase in visual acuity measured by improved performance in a visual detection task.

Dark exposure (DE) followed by light reintroduction (LRx) reactivates robust synaptic plasticity in adult mouse primary visual cortex (V1), which allows subsequent recovery from amblyopia. Previously we showed that perisynaptic proteolysis by MMP9 mediates the enhancement of plasticity by LRx in binocular adult mice (Murase et al., 2017). However, it was unknown if a visual system compromised by amblyopia could engage this pathway. Here we show that LRx to adult amblyopic mice induces perisynaptic MMP2/9 activity and extracellular matrix (ECM) degradation in deprived and non-deprived V1. Indeed, LRx restricted to the amblyopic eye is sufficient to induce robust MMP2/9 activity at thalamo-cortical synapses and ECM degradation in deprived V1. Two-photon live imaging demonstrates that the history of visual experience regulates MMP2/9 activity in V1, and that DE lowers the threshold for the proteinase activation. The homeostatic reduction of the MMP2/9 activation threshold by DE enables visual input from the amblyopic pathway to trigger robust perisynaptic proteolysis.

The promotion of structural and functional plasticity by estrogens is a promising approach to enhance central nervous system function in the aged. However, how the sensitivity to estrogens is regulated across brain regions, age and experience is poorly understood. To ask if estradiol treatment impacts structural and functional plasticity in sensory cortices, we examined the acute effect of 17α-Estradiol in adult Long Evans rats following chronic monocular deprivation, a manipulation that reduces the strength and selectivity of deprived eye vision. Chronic monocular deprivation decreased thalamic input from the deprived eye to the binocular visual cortex and accelerated short-term depression of the deprived eye pathway, but did not change the density of excitatory synapses in primary visual cortex. Importantly, we found that the classical estrogen receptors ERα and ERβ were robustly expressed in the adult visual cortex, and that a single dose of 17α-Estradiol reduced the expression of the calcium-binding protein parvalbumin, decreased the integrity of the extracellular matrix and increased the size of excitatory postsynaptic densities. Furthermore, 17α-Estradiol enhanced experience-dependent plasticity in the amblyopic visual cortex, by promoting response potentiation of the pathway served by the non-deprived eye. The promotion of plasticity at synapses serving the non-deprived eye may reflect selectivity for synapses with an initially low probability of neurotransmitter release, and may inform strategies to remap spared inputs around a scotoma or a cortical infarct.

Dark exposure (DE) followed by light reintroduction (LRx) reactivates robust synaptic plasticity in adult mouse V1, which allows recovery from amblyopia. Previously we showed that LRx-induced perisynaptic proteolysis of extracellular substrates by MMP9 mediates the enhanced plasticity in binocular adult mice (Murase et al., 2017). However, it is unknown if a visual system compromised by amblyopia could engage this pathway. Here we show that LRx to adult amblyopic mice induces perisynaptic MMP2/9 activity and degradation of ECM in the deprived and non-deprived V1. LRx restricted to the amblyopic eye induces equally robust MMP2/9 activity at thalamo-cortical synapses and ECM degradation in deprived V1. Two-photon live imaging demonstrates that the history of visual experience regulates MMP2/9 activity in V1, and that DE lowers the threshold for the proteinase activation. This homeostatic reduction of MMP2/9 activation threshold by DE enables the visual input from the amblyopic pathway to trigger robust perisynaptic proteolysis.

Summary: The experience-dependent decrease in stimulus detection thresholds that underly perceptual learning can be induced by repetitive exposure to a visual stimulus. Robust stimulus-selective potentiation of visual responses is induced in the primary mouse visual cortex by repetitive low frequency visual stimulation (LFVS). How the parameters of the repetitive visual stimulus impact the site and specificity of this experience-dependent plasticity is currently a subject of debate. Here we demonstrate that the stimulus selective response potentiation induced by repetitive low frequency (1 Hz) stimulation, which is typically limited to layer 4, shifts to superficial layers following manipulations that enhance plasticity in primary visual cortex. In contrast, repetitive high frequency (10 Hz) visual stimulation induces response potentiation that is expressed in layers 4 and 5/6, and generalizes to novel visual stimuli. Repetitive visual stimulation also induces changes in the magnitude and distribution of oscillatory activity in primary visual cortex, however changes in oscillatory power do not predict the locus or specificity of response potentiation. Instead we find that robust response potentiation is induced by visual stimulation that resets the phase of ongoing gamma oscillations. Furthermore, high frequency, but not low frequency, repetitive visual stimulation entrains oscillatory rhythms with enhanced sensitivity to phase reset, such that familiar and novel visual stimuli induce similar visual response potentiation.

The promotion of structural and functional plasticity by estrogens is a promising therapy to enhance central nervous system function in the aged. However, how the sensitivity to estrogens is regulated across brain regions, age and experience is poorly understood. To ask if estradiol treatment impacts structural and functional plasticity in sensory cortices, we examined the acute effect of 17α Estradiol in adult Long Evans (LE) rats following chronic monocular deprivation, a manipulation that reduces the strength and selectivity of deprived eye vision. Chronic monocular deprivation decreased thalamic input from the deprived eye to the binocular visual cortex and accelerated short-term depression of the deprived eye pathway, without changing the total density of excitatory synapses. Importantly, we found that the classical estrogen receptors ERα and ERβ are robustly expressed in the adult visual cortex, and that a single dose of 17α Estradiol increased the size of excitatory postsynaptic densities, reduced the expression of parvalbumin and decreased the integrity of the extracellular matrix. Furthermore, 17α Estradiol enhanced experience-dependent plasticity in the amblyopic visual cortex, and promoted response potentiation of the pathway served by the non-deprived eye. The promotion of plasticity at synapses serving the non-deprived eye may reflect selectivity for synapses with an initially low probability of neurotransmitter release, and may inform applications to remap spared inputs around a scotoma or a cortical infarct