Differential alterations in the morphology and electrophysiology of layer II pyramidal cells in the primary visual cortex of a mouse model prenatally exposed to LPS

2015 ◽  
Vol 591 ◽  
pp. 138-143 ◽  
Author(s):  
Ying Gao ◽  
Lixiong Liu ◽  
Qiqin Li ◽  
Yun Wang
Keyword(s):  
Visual Cortex ◽  
Mouse Model ◽  
Primary Visual Cortex ◽  
Pyramidal Cells ◽  
Prenatally Exposed

scholarly journals Functional selectivity and specific connectivity of inhibitory neurons in primary visual cortex

2018 ◽  
Author(s):  
Petr Znamenskiy ◽  
Mean-Hwan Kim ◽  
Dylan R. Muir ◽  
Maria Florencia Iacaruso ◽  
Sonja B. Hofer ◽  
...  
Keyword(s):  
Visual Cortex ◽  
Primary Visual Cortex ◽  
Pyramidal Cells ◽  
Fine Tuning ◽  
Inhibitory Neurons ◽  
Local Network ◽  
Cortical Circuits ◽  
Sensory Stimuli ◽  
Excitatory Neurons ◽  
Strong Excitation

In the cerebral cortex, the interaction of excitatory and inhibitory synaptic inputs shapes the responses of neurons to sensory stimuli, stabilizes network dynamics1 and improves the efficiency and robustness of the neural code2–4. Excitatory neurons receive inhibitory inputs that track excitation5–8. However, how this co-tuning of excitation and inhibition is achieved by cortical circuits is unclear, since inhibitory interneurons are thought to pool the inputs of nearby excitatory cells and provide them with non-specific inhibition proportional to the activity of the local network9–13. Here we show that although parvalbumin-expressing (PV) inhibitory cells in mouse primary visual cortex make connections with the majority of nearby pyramidal cells, the strength of their synaptic connections is structured according to the similarity of the cells’ responses. Individual PV cells strongly inhibit those pyramidal cells that provide them with strong excitation and share their visual selectivity. This fine-tuning of synaptic weights supports co-tuning of inhibitory and excitatory inputs onto individual pyramidal cells despite dense connectivity between inhibitory and excitatory neurons. Our results indicate that individual PV cells are preferentially integrated into subnetworks of inter-connected, co-tuned pyramidal cells, stabilising their recurrent dynamics. Conversely, weak but dense inhibitory connectivity between subnetworks is sufficient to support competition between them, de-correlating their output. We suggest that the history and structure of correlated firing adjusts the weights of both inhibitory and excitatory connections, supporting stable amplification and selective recruitment of cortical subnetworks.

scholarly journals A biological blueprint for the axons of superficial layer pyramidal cells in cat primary visual cortex

2017 ◽  
Vol 222 (8) ◽  
pp. 3407-3430 ◽  
Author(s):  
Kevan A. C. Martin ◽  
Stephan Roth ◽  
Elisha S. Rusch
Keyword(s):  
Visual Cortex ◽  
Primary Visual Cortex ◽  
Pyramidal Cells ◽  
Superficial Layer

Expression of GABAAReceptor Subunit mRNAs by Layer V Pyramidal Cells of the Rat Primary Visual Cortex

1997 ◽  
Vol 9 (4) ◽  
pp. 857-862 ◽  
Author(s):  
Diego Ruano ◽  
David Perrais ◽  
Jean Rosier ◽  
Nicole Ropert
Keyword(s):  
Visual Cortex ◽  
Primary Visual Cortex ◽  
Pyramidal Cells ◽  
Layer V

scholarly journals Opposing forms of adaptation in mouse visual cortex are controlled by distinct inhibitory microcircuits and gated by locomotion

2020 ◽  
Author(s):  
Tristan G. Heintz ◽  
Antonio J. Hinojosa ◽  
Leon Lagnado
Keyword(s):  
Visual Cortex ◽  
Primary Visual Cortex ◽  
Internal State ◽  
Pyramidal Cells ◽  
External World ◽  
Neural Circuitry ◽  
Cortical Processing ◽  
Locomotor Behaviour ◽  
Different Types ◽  
Mouse Visual Cortex

SummaryCortical processing of sensory signals adjusts to changes in both the external world and the internal state of the animal. We investigated the neural circuitry by which these processes interact in the primary visual cortex of mice. An increase in contrast caused as many pyramidal cells (PCs) to sensitize as depress, reflecting the dynamics of adaptation in different types of interneuron (PV, SST and VIP). Optogenetic manipulations demonstrate that the net effect within PCs reflects the balance of PV inputs, driving depression, and a subset of SST interneurons, driving sensitization. Locomotor behaviour increased the gain of PC responses by disinhibition through both the VIP->SST and SST->PV pathways, thereby maintaining the balance between opposing forms of plasticity. These experiments reveal how inhibitory microcircuits interact to purpose different subsets of PCs for the signalling of increases or decreases in contrast while also allowing for behavioural control of gain across the population.

scholarly journals Paroxetine can improve primary visual cortex activity in a high-risk mouse model of schizophrenia

2020 ◽  
Vol 34 (1) ◽  
pp. 1299-1303
Author(s):  
Xinying Chen ◽  
Ziyao Cai ◽  
Feng Ji ◽  
Xiaodong Lin ◽  
Deguo Jiang ◽  
...  
Keyword(s):  
Visual Cortex ◽  
High Risk ◽  
Mouse Model ◽  
Primary Visual Cortex

scholarly journals Abnormal dendrite and spine morphology in primary visual cortex in the CGG knock-in mouse model of the fragile X premutation

Epilepsia ◽  
2012 ◽  
Vol 53 ◽  
pp. 150-160 ◽  
Author(s):  
Robert F. Berman ◽  
Karl D. Murray ◽  
Gloria Arque ◽  
Michael R. Hunsaker ◽  
H. Jürgen Wenzel
Keyword(s):  
Visual Cortex ◽  
Mouse Model ◽  
Primary Visual Cortex ◽  
Fragile X ◽  
Spine Morphology ◽  
Fragile X Premutation

scholarly journals Closing the Critical Period Is Required for the Maturation of Binocular Integration in Mouse Primary Visual Cortex

2021 ◽  
Vol 15 ◽  
Author(s):  
Jiangping Chan ◽  
Xiangwen Hao ◽  
Qiong Liu ◽  
Jianhua Cang ◽  
Yu Gu
Keyword(s):  
Visual Cortex ◽  
Mouse Model ◽  
Primary Visual Cortex ◽  
Depth Perception ◽  
Critical Period ◽  
Visual Experience ◽  
Extracellular Recording ◽  
Molecular Assay ◽  
Binocular Matching

Binocular matching of orientation preference between the two eyes is a common form of binocular integration that is regarded as the basis for stereopsis. How critical period plasticity enables binocular matching under the guidance of normal visual experience has not been fully demonstrated. To investigate how critical period closure affects the binocular matching, a critical period prolonged mouse model was constructed through the administration of bumetanide, an NKCC1 transporter antagonist. Using acute in vivo extracellular recording and molecular assay, we revealed that binocular matching was transiently disrupted due to heightened plasticity after the normal critical period, together with an increase in the density of spines and synapses, and the upregulation of GluA1 expression. Diazepam (DZ)/[(R, S)-3-(2-carboxypiperazin-4-yl) propyl-1-phosphonic acid (CPP)] could reclose the extended critical period, and rescue the deficits in binocular matching. Furthermore, the extended critical period, alone, with normal visual experience is sufficient for the completion of binocular matching in amblyopic mice. Similarly, prolonging the critical period into adulthood by knocking out Nogo-66 receptor can prevent the normal maturation of binocular matching and depth perception. These results suggest that maintaining an optimal plasticity level during adolescence is most beneficial for the systemic maturation. Extending the critical period provides new clues for the maturation of binocular vision and may have critical implications for the treatment of amblyopia.

scholarly journals Deficits in higher visual area representations in a mouse model of Angelman syndrome

2020 ◽  
Vol 12 (1) ◽  
Author(s):  
Leah B. Townsend ◽  
Kelly A. Jones ◽  
Christopher R. Dorsett ◽  
Benjamin D. Philpot ◽  
Spencer L. Smith
Keyword(s):  
Visual Cortex ◽  
Mouse Model ◽  
Primary Visual Cortex ◽  
Angelman Syndrome ◽  
Calcium Imaging ◽  
Neurodevelopmental Disorders ◽  
Synaptic Function ◽  
Strong Response ◽  
Intrinsic Signal ◽  
Two Photon

Abstract Background Sensory processing deficits are common in individuals with neurodevelopmental disorders. One hypothesis is that deficits may be more detectable in downstream, “higher” sensory areas. A mouse model of Angelman syndrome (AS), which lacks expression of the maternally inherited Ube3a allele, has deficits in synaptic function and experience-dependent plasticity in the primary visual cortex. Thus, we hypothesized that AS model mice have deficits in visually driven neuronal responsiveness in downstream higher visual areas (HVAs). Methods Here, we used intrinsic signal optical imaging and two-photon calcium imaging to map visually evoked neuronal activity in the primary visual cortex and HVAs in response to an array of stimuli. Results We found a highly specific deficit in HVAs. Drifting gratings that changed speed caused a strong response in HVAs in wildtype mice, but this was not observed in littermate AS model mice. Further investigation with two-photon calcium imaging revealed the effect to be largely driven by aberrant responses of inhibitory interneurons, suggesting a cellular basis for higher level, stimulus-selective cortical dysfunction in AS. Conclusion Assaying downstream, or “higher” circuitry may provide a more sensitive measure for circuit dysfunction in mouse models of neurodevelopmental disorders. Trial registration Not applicable.

scholarly journals Irreversible Primary Visual Cortex Impairment in a Mouse Model of High-Risk Schizophrenia

2021 ◽  
Vol Volume 17 ◽  
pp. 277-282
Author(s):  
Xinying Chen ◽  
Ce Chen ◽  
Feng Ji ◽  
Yong Xu ◽  
Wenqiang Wang ◽  
...  
Keyword(s):  
Visual Cortex ◽  
High Risk ◽  
Mouse Model ◽  
Primary Visual Cortex
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