scholarly journals Perineuronal nets control visual input via thalamic recruitment of cortical PV interneurons

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Giulia Faini ◽  
Andrea Aguirre ◽  
Silvia Landi ◽  
Didi Lamers ◽  
Tommaso Pizzorusso ◽  
...  

In the neocortex, critical periods (CPs) of plasticity are closed following the accumulation of perineuronal nets (PNNs) around parvalbumin (PV)-positive inhibitory interneurons. However, how PNNs tune cortical function and plasticity is unknown. We found that PNNs modulated the gain of visual responses and γ-oscillations in the adult mouse visual cortex in vivo, consistent with increased interneuron function. Removal of PNNs in adult V1 did not affect GABAergic neurotransmission from PV cells, nor neuronal excitability in layer 4. Importantly, PNN degradation coupled to sensory input potentiated glutamatergic thalamic synapses selectively onto PV cells. In the absence of PNNs, increased thalamic PV-cell recruitment modulated feed-forward inhibition differently on PV cells and pyramidal neurons. These effects depended on visual input, as they were strongly attenuated by monocular deprivation in PNN-depleted adult mice. Thus, PNNs control visual processing and plasticity by selectively setting the strength of thalamic recruitment of PV cells.

2018 ◽  
Author(s):  
Giulia Faini ◽  
Andrea Aguirre ◽  
Silvia Landi ◽  
Tommaso Pizzorusso ◽  
Gian Michele Ratto ◽  
...  

SummaryIn the neocortex, the closure of critical periods (CPs) of plasticity is paralleled by the accumulation of perineuronal nets (PNNs) around parvalbumin (PV)-positive inhibitory interneurons. Accordingly, PNN degradation in adult mammals re-opens cortical plasticity. However, how PNNs tune cortical function and plasticity is unknown. We found that PNNs modulated the gain of visual responses in the adult mouse visual cortex in vivo. Removal of PNNs in adult V1 strongly increased thalamic neurotransmission selectively on layer 4 PV cells. This produced a differential gating of feed-forward inhibition on principal neurons and other PV cells, with no alterations of unitary inhibitory synaptic transmission and neuronal excitability. These effects depended on visual input, as they were strongly attenuated by monocular deprivation in PNN-depleted adult mice. Thus, PNNs control visual processing and plasticity by selectively setting the strength of thalamic recruitment of PV cells. We conclude that PNN accumulation during circuit maturation likely prevents excessive thalamic excitation of PV cells at the expense of cortical plasticity.


2018 ◽  
Author(s):  
Carey Y. L. Huh ◽  
Karim Abdelaal ◽  
Kirstie J. Salinas ◽  
Diyue Gu ◽  
Jack Zeitoun ◽  
...  

ABSTRACTMonocular deprivation (MD) during the juvenile critical period leads to long-lasting impairments in binocular function and visual acuity. The site of these changes has been widely considered to be cortical. However, recent evidence indicates that binocular integration may first occur in the dorsolateral geniculate nucleus of the thalamus (dLGN), raising the question of whether MD during the critical period may produce long-lasting deficits in dLGN binocular integration. Using in vivo two-photon Ca2+ imaging of dLGN afferents and excitatory neurons in superficial layers of primary visual cortex (V1), we demonstrate that critical-period MD leads to a persistent and selective loss of binocular dLGN inputs, while leaving spatial acuity in the thalamocortical pathway intact. Despite being few in number, binocular dLGN boutons display remarkably robust visual responses, on average twice stronger than monocular boutons, and their responses are exquisitely well-matched between the eyes. To our surprise, we found that MD leads to a profound binocular mismatch of response amplitude, spatial frequency and orientation tuning detected at the level of single thalamocortical synapses. In comparison, V1 neurons display deficits in both binocular integration and spatial acuity following MD. Our data provide the most compelling evidence to date demonstrating that following critical-period MD, binocular deficits observed at the level of V1 may at least in part originate from dLGN binocular dysfunction, while spatial acuity deficits arise from cortical circuits. These findings highlight a hitherto unknown role of the thalamus as a site for developmental refinement of binocular vision.


2016 ◽  
Author(s):  
Nathaniel C. Wright ◽  
Ralf Wessel

A primary goal of systems neuroscience is to understand cortical function, which typically involves studying spontaneous and sensory-evoked cortical activity. Mounting evidence suggests a strong and complex relationship between the ongoing and evoked state. To date, most work in this area has been based on spiking in populations of neurons. While advantageous in many respects, this approach is limited in scope; it records the activities of a minority of neurons, and gives no direct indication of the underlying subthreshold dynamics. Membrane potential recordings can fill these gaps in our understanding, but are difficult to obtain in vivo. Here, we record subthreshold cortical visual responses in the ex vivo turtle eye-attached whole-brain preparation, which is ideally-suited to such a study. In the absence of visual stimulation, the network is “synchronous”; neurons display network-mediated transitions between low- and high-conductance membrane potential states. The prevalence of these slow-wave transitions varies across turtles and recording sessions. Visual stimulation evokes similar high-conductance states, which are on average larger and less reliable when the ongoing state is more synchronous. Responses are muted when immediately preceded by large, spontaneous high-conductance events. Evoked spiking is sparse, highly variable across trials, and mediated by concerted synaptic inputs that are in general only very weakly correlated with inputs to nearby neurons. Together, these results highlight the multiplexed influence of the cortical network on the spontaneous and sensory-evoked activity of individual cortical neurons.


2018 ◽  
Author(s):  
Anna Steinzeig ◽  
Cecilia Cannarozzo ◽  
Eero Castren

Heightened neuronal plasticity expressed during early postnatal life has been thought to permanently decline once critical periods have ended. For example, monocular deprivation is able to shift ocular dominance in the mouse visual cortex during the first months of life, but this effect is lost later in life. However, various treatments such as the antidepressant fluoxetine can reactivate a critical period-like plasticity in the adult brain. When monocular deprivation is supplemented with chronic fluoxetine administration, a major shift in ocular dominance is produced after the critical period has ended. In the current study, we characterized the temporal patterns of fluoxetine-induced plasticity in the adult mouse visual cortex, using in vivo optical imaging. We found that artificially-induced plasticity in ocular dominance extended beyond the duration of the naturally occurring critical period, and continued as long as fluoxetine was administered. However, this fluoxetine-induced plasticity period ended as soon as the drug was not given. Taken together, our data highlights how a combination of pharmacological treatment and environmental change could be used to improve strategies in antidepressant therapy in humans.


2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Clémence Bernard ◽  
Alain Prochiantz

The ability of the environment to shape cortical function is at its highest during critical periods of postnatal development. In the visual cortex, critical period onset is triggered by the maturation of parvalbumin inhibitory interneurons, which gradually become surrounded by a specialized glycosaminoglycan-rich extracellular matrix: the perineuronal nets. Among the identified factors regulating cortical plasticity in the visual cortex, extracortical homeoprotein Otx2 is transferred specifically into parvalbumin interneurons and this transfer regulates both the onset and the closure of the critical period of plasticity for binocular vision. Here, we review the interaction between the complex sugars of the perineuronal nets and homeoprotein Otx2 and how this interaction regulates cortical plasticity during critical period and in adulthood.


2016 ◽  
Vol 37 (5) ◽  
pp. 1820-1828 ◽  
Author(s):  
Krzysztof Kucharz ◽  
Ida Søndergaard Rasmussen ◽  
Anders Bach ◽  
Kristian Strømgaard ◽  
Martin Lauritzen

Cortical spreading depression is associated with activation of NMDA receptors, which interact with the postsynaptic density protein 95 (PSD-95) that binds to nitric oxide synthase (nNOS). Here, we tested whether inhibition of the nNOS/PSD-95/NMDA receptor complex formation by anti-ischemic compound, UCCB01-144 (Tat- N-dimer) ameliorates the persistent effects of cortical spreading depression on cortical function. Using in vivo two-photon microscopy in somatosensory cortex in mice, we show that fluorescently labelled Tat- N-dimer readily crosses blood-brain barrier and accumulates in nerve cells during the first hour after i.v. injection. The Tat- N-dimer suppressed stimulation-evoked synaptic activity by 2–20%, while cortical blood flow and cerebral oxygen metabolic (CMRO2) responses were preserved. During cortical spreading depression, the Tat- N-dimer reduced the average amplitude of the negative shift in direct current potential by 33% (4.1 mV). Furthermore, the compound diminished the average depression of spontaneous electrocorticographic activity by 11% during first 40 min of post-cortical spreading depression recovery, but did not mitigate the suppressing effect of cortical spreading depression on cortical blood flow and CMRO2. We suggest that uncoupling of PSD-95 from NMDA receptors reduces overall neuronal excitability and the amplitude of the spreading depolarization wave. These findings may be of interest for understanding the neuroprotective effects of the nNOS/PSD-95 uncoupling in stroke.


Author(s):  
Antonio Wlisses da Silva ◽  
Maria Kueirislene A. Ferreira ◽  
Lucas Ramos Pereira ◽  
Emanuela L. Rebouças ◽  
Marnielle Rodrigues Coutinho ◽  
...  

2008 ◽  
Vol 31 (2) ◽  
pp. 210-212 ◽  
Author(s):  
J. Patrick Mayo ◽  
Marc A. Sommer

AbstractSaccades divide visual input into rapid, discontinuous periods of stimulation on the retina. The response of single neurons to such sequential stimuli is neuronal adaptation; a robust first response followed by an interval-dependent diminished second response. Adaptation is pervasive in both early and late stages of visual processing. Given its inherent coding of brief time intervals, neuronal adaptation may play a fundamental role in compensating for visual delays.


2018 ◽  
Vol 32 (01) ◽  
pp. 1750274 ◽  
Author(s):  
Ying-Mei Qin ◽  
Cong Men ◽  
Jia Zhao ◽  
Chun-Xiao Han ◽  
Yan-Qiu Che

We focus on the role of heterogeneity on the propagation of firing patterns in feedforward network (FFN). Effects of heterogeneities both in parameters of neuronal excitability and synaptic delays are investigated systematically. Neuronal heterogeneity is found to modulate firing rates and spiking regularity by changing the excitability of the network. Synaptic delays are strongly related with desynchronized and synchronized firing patterns of the FFN, which indicate that synaptic delays may play a significant role in bridging rate coding and temporal coding. Furthermore, quasi-coherence resonance (quasi-CR) phenomenon is observed in the parameter domain of connection probability and delay-heterogeneity. All these phenomena above enable a detailed characterization of neuronal heterogeneity in FFN, which may play an indispensable role in reproducing the important properties of in vivo experiments.


2021 ◽  
Author(s):  
Natalia Ladyka-Wojcik ◽  
Zhong-Xu Liu ◽  
Jennifer D. Ryan

Scene construction is a key component of memory recall, navigation, and future imagining, and relies on the medial temporal lobes (MTL). A parallel body of work suggests that eye movements may enable the imagination and construction of scenes, even in the absence of external visual input. There are vast structural and functional connections between regions of the MTL and those of the oculomotor system. However, the directionality of connections between the MTL and oculomotor control regions, and how it relates to scene construction, has not been studied directly in human neuroimaging. In the current study, we used dynamic causal modeling (DCM) to investigate this relationship at a mechanistic level using a scene construction task in which participants' eye movements were either restricted (fixed-viewing) or unrestricted (free-viewing). By omitting external visual input, and by contrasting free- versus fixed- viewing, the directionality of neural connectivity during scene construction could be determined. As opposed to when eye movements were restricted, allowing free viewing during construction of scenes strengthened top-down connections from the MTL to the frontal eye fields, and to lower-level cortical visual processing regions, suppressed bottom-up connections along the visual stream, and enhanced vividness of the constructed scenes. Taken together, these findings provide novel, non-invasive evidence for the causal architecture between the MTL memory system and oculomotor system associated with constructing vivid mental representations of scenes.


Sign in / Sign up

Export Citation Format

Share Document