Circuit Mechanisms Underlying Epileptogenesis in a Mouse Model of Focal Cortical Malformation

Yang, Weiguo; Williams, Anthony; Sun, Qian‐Quan

doi:10.1016/j.cub.2020.10.029

Cited by 10 publications

(11 citation statements)

References 73 publications

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“…Yang et al set out to better understand circuit aberrations resulting in epileptogenesis using a neonatal freeze lesion (FL) model of focal cortical malformations in mouse. 6 Lesions in this model result in a 4-layered cortex similar to that seen in PMG in patients, 7,8 as opposed to the normal 6-layered architecture; however, a general supragranular, granular, and infragranular organization is maintained. 8 Lesions in this model also cause spike-wave discharges and spontaneous seizures similar to patients with PMG and other focal cortical malformations.…”

Section: Commentarymentioning

confidence: 80%

Seizing After Freezing: Layer-, Site-, and Cell-Type-Specific Rewiring Mediates Epileptogenesis Following Cortical Freeze Lesion in Mouse

Buchanan¹

2021

Epilepsy Curr

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Section: Commentarymentioning

confidence: 80%

Seizing After Freezing: Layer-, Site-, and Cell-Type-Specific Rewiring Mediates Epileptogenesis Following Cortical Freeze Lesion in Mouse

Buchanan¹

2021

Epilepsy Curr

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“…This suggests an interaction between layer-specific myelination and excitation/inhibition modulation that could be investigated in-vivo with the methodology introduced here. Losing myelin progressively can result in epilepsy-like brain activity, as inhibition of slow brain waves decreases 64 , and epileptogenic hyperexcitability and lesions often present layer-specific 64,65,66 . A multimodal layer-specific investigation could help lesion detection and uncover underlying mechanisms.…”

Section: Discussionmentioning

confidence: 99%

“…Quaerosys, http://www.quaerosys.com, see Fig. 1) 64,65,66 . Individually-adjusted vibrotactile stimulation was applied at a frequency of 16 Hz 77 using 16 pin combinations per second 64,65,66 , raising 2 pins at a time.…”

Section: Human Fmri Tasksmentioning

confidence: 99%

Cortical sensory aging is layer-specific

Liu,

Doehler,

Henschke

et al. 2023

Preprint

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The segregation of processes into cortical layers is a convergent feature in animal evolution. However, it remains unclear how changes in the cortical layer architecture affect sensory system function and dysfunction. To address this, we conducted layer-specific in-vivo 7T-MRI of the primary somatosensory cortex in younger and older adults and in an adult with congenital arm loss. Input layer IV was enlarged and more myelinated in older adults, which drove extended sensory input signals, whereas with congenital arm loss, input layer IV contralateral to the missing limb had shrunk. Age-related cortical thinning was driven by deep layers, and accompanied by altered functional modulation and behavioral readouts. Neuronal calcium imaging and histology across aging mice revealed altered excitatory/inhibitory balance, with deep-layer cell loss and overall increased parvalbumin cell density as potential neural underpinnings. We here uncover the segregation of processes into cortical layers and its unique age-related profile.

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“…All procedures were approved by the Institutional Animal Care and Use Committee (IACUC) and the Biosafety Committee of the University of Wyoming 53, 54 . Immune-competent mice of both sexes (age range p60–p300) were used in the experiments described here.…”

Section: Methodsmentioning

confidence: 99%

“…Mice were anesthetized with 3% isoflurane (v/v) and maintained with 0.4 LPM oxygenated 2% isoflurane (vol/vol) throughout the surgery 53, 54 . The animals were mounted on a stereotaxic device (NARISHIGE SG-4N) and maintained at 37°C using a heat pad (K&H no.1060).…”

Section: Methodsmentioning

confidence: 99%

Learning induced neuronal identity switch in the superficial layers of the primary somatosensory cortex

Dai,

Sun

2023

Preprint

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During learning, multi-dimensional inputs are integrated within the sensory cortices. However, the strategies by which the sensory cortex employs to achieve learning remains poorly understood. We studied the sensory cortical neuronal coding of trace eyeblink conditioning (TEC) in head-fixed, freely running mice, where whisker deflection was used as a conditioned stimulus (CS) and an air puff to the cornea delivered after an interval was used as unconditioned stimulus (US). After training, mice learned the task with a set of stereotypical behavioral changes, most prominent ones include prolonged closure of eyelids, and increased reverse running between CS and US onset. The local blockade of the primary somatosensory cortex (S1) activities with muscimol abolished the behavior learning suggesting that S1 is required for the TEC. In naive animals, based on the response properties to the CS and US, identities of the small proportion (~20%) of responsive primary neurons (PNs) were divided into two subtypes: CR (i.e. CS-responsive) and UR neurons (i.e. US-responsive). After animals learned the task, identity of CR and UR neurons changed: while the CR neurons are less responsive to CS, UR neurons gain responsiveness to CS, a new phenomenon we defined as 'learning induced neuronal identity switch (LINIS)'. To explore the potential mechanisms underlying LINIS, we found that systemic and local (i.e. in S1) administration of the nicotinic receptor antagonist during TEC training blocked the LINIS, and concomitantly disrupted the behavior learning. Additionally, we monitored responses of two types of cortical interneurons (INs) and observed that the responses of the somatostatin-expressing (SST), but not parvalbumin-expressing (PV) INs are negatively correlated with the learning performance, suggesting that SST-INs contribute to the LINIS. Thus, we conclude that L2/3 PNs in S1 encode perceptual learning by LINIS like mechanisms, and cholinergic pathways and cortical SST interneurons are involved in the formation of LINIS.

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Circuit Mechanisms Underlying Epileptogenesis in a Mouse Model of Focal Cortical Malformation

Cited by 10 publications

References 73 publications

Seizing After Freezing: Layer-, Site-, and Cell-Type-Specific Rewiring Mediates Epileptogenesis Following Cortical Freeze Lesion in Mouse

Seizing After Freezing: Layer-, Site-, and Cell-Type-Specific Rewiring Mediates Epileptogenesis Following Cortical Freeze Lesion in Mouse

Cortical sensory aging is layer-specific

Learning induced neuronal identity switch in the superficial layers of the primary somatosensory cortex

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