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Article ; Online: Barrel cortex development lacks a key stage of hyperconnectivity from deep to superficial layers in a rat model of Absence Epilepsy.

Plutino, Simona / Laghouati, Emel / Jarre, Guillaume / Depaulis, Antoine / Guillemain, Isabelle / Bureau, Ingrid

2024 Volume 234, Page(s) 102564

Abstract: During development of the sensory cortex, the ascending innervation from deep to upper layers provides a temporary scaffold for the construction of other circuits that remain at adulthood. Whether an alteration in this sequence leads to brain dysfunction ...

Abstract	During development of the sensory cortex, the ascending innervation from deep to upper layers provides a temporary scaffold for the construction of other circuits that remain at adulthood. Whether an alteration in this sequence leads to brain dysfunction in neuro-developmental diseases remains unknown. Using functional approaches in a genetic model of Absence Epilepsy (GAERS), we investigated in barrel cortex, the site of seizure initiation, the maturation of excitatory and inhibitory innervations onto layer 2/3 pyramidal neurons and cell organization into neuronal assemblies. We found that cortical development in GAERS lacks the early surge of connections originating from deep layers observed at the end of the second postnatal week in normal rats and the concomitant structuring into multiple assemblies. Later on, at seizure onset (1 month old), excitatory neurons are hyper-excitable in GAERS when compared to Wistar rats. These findings suggest that early defects in the development of connectivity could promote this typical epileptic feature and/or its comorbidities.
MeSH term(s)	Rats ; Animals ; Epilepsy, Absence/genetics ; Rats, Wistar ; Neurons/physiology ; Cerebral Cortex ; Seizures
Language	English
Publishing date	2024-01-19
Publishing country	England
Document type	Journal Article
ZDB-ID	185535-9
ISSN	1873-5118 ; 0301-0082
ISSN (online)	1873-5118
ISSN	0301-0082
DOI	10.1016/j.pneurobio.2023.102564
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Article ; Online: The development of cortical columns: role of Fragile X mental retardation protein.

Bureau, Ingrid

The Journal of physiology

2009 Volume 587, Issue Pt 9, Page(s) 1897–1901

Abstract: Neuronal circuits in the brain are complex and precise. Here, I review aspects of the development of cortical columns in the rodent barrel cortex, focusing on the anatomical and functional data describing the maturation of ascending glutamatergic ... ...

Abstract	Neuronal circuits in the brain are complex and precise. Here, I review aspects of the development of cortical columns in the rodent barrel cortex, focusing on the anatomical and functional data describing the maturation of ascending glutamatergic circuits. Projections from layer 4 to layer 3 develop into cortical columns with little macroscopic refinement. Depriving animals of normal sensory experience induces long-term synaptic depression but does not perturb this pattern of development. Mouse models of mental retardation can help us understand the mechanisms of development of cortical columns. Fmr1 knock-out (ko) mice, a model for Fragile X syndrome, lack Fragile X mental retardation protein (FMRP), a suppressor of translation present in synapses. Because FMRP expression is stimulated by neuronal activity, Fmr1-ko mice provide a model to survey the role of sensory input in brain development. Layer 4 to layer 3 projections are altered in multiple ways in the young mutant mice: connection rate is low and layer 4 cell axons are spatially diffuse. Sensory deprivation rescues the connection rate phenotype. The interaction of FMRP and neuronal activity in the development of cortical circuits is discussed.
MeSH term(s)	Cerebral Cortex/embryology ; Cerebral Cortex/physiology ; Fragile X Mental Retardation Protein/metabolism ; Humans ; Models, Neurological ; Nerve Net/physiology ; Neuronal Plasticity/physiology ; Neurons/physiology
Chemical Substances	Fragile X Mental Retardation Protein (139135-51-6)
Language	English
Publishing date	2009-01-12
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	3115-x
ISSN	1469-7793 ; 0022-3751
ISSN (online)	1469-7793
ISSN	0022-3751
DOI	10.1113/jphysiol.2008.167155
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Article ; Online: Grey matter heterotopia subtypes show specific morpho-electric signatures and network dynamics.

Vermoyal, Jean-Christophe / Hardy, Delphine / Goirand-Lopez, Lucas / Vinck, Antonin / Silvagnoli, Lucas / Fortoul, Aurélien / Francis, Fiona / Cappello, Silvia / Bureau, Ingrid / Represa, Alfonso / Cardoso, Carlos / Watrin, Françoise / Marissal, Thomas / Manent, Jean-Bernard

Brain : a journal of neurology

2023 Volume 147, Issue 3, Page(s) 996–1010

Abstract: Grey matter heterotopia (GMH) are neurodevelopmental disorders associated with abnormal cortical function and epilepsy. Subcortical band heterotopia (SBH) and periventricular nodular heterotopia (PVNH) are two well-recognized GMH subtypes in which ... ...

Abstract	Grey matter heterotopia (GMH) are neurodevelopmental disorders associated with abnormal cortical function and epilepsy. Subcortical band heterotopia (SBH) and periventricular nodular heterotopia (PVNH) are two well-recognized GMH subtypes in which neurons are misplaced, either forming nodules lining the ventricles in PVNH, or forming bands in the white matter in SBH. Although both PVNH and SBH are commonly associated with epilepsy, it is unclear whether these two GMH subtypes differ in terms of pathological consequences or, on the contrary, share common altered mechanisms. Here, we studied two robust preclinical models of SBH and PVNH, and performed a systematic comparative assessment of the physiological and morphological diversity of heterotopia neurons, as well as the dynamics of epileptiform activity and input connectivity. We uncovered a complex set of altered properties, including both common and distinct physiological and morphological features across heterotopia subtypes, and associated with specific dynamics of epileptiform activity. Taken together, these results suggest that pro-epileptic circuits in GMH are, at least in part, composed of neurons with distinct, subtype-specific, physiological and morphological properties depending on the heterotopia subtype. Our work supports the notion that GMH represent a complex set of disorders, associating both shared and diverging pathological consequences, and contributing to forming epileptogenic networks with specific properties. A deeper understanding of these properties may help to refine current GMH classification schemes by identifying morpho-electric signatures of GMH subtypes, to potentially inform new treatment strategies.
MeSH term(s)	Humans ; Gray Matter ; Cerebellar Vermis ; Neurodevelopmental Disorders ; Neurons ; Epilepsy
Language	English
Publishing date	2023-09-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80072-7
ISSN	1460-2156 ; 0006-8950
ISSN (online)	1460-2156
ISSN	0006-8950
DOI	10.1093/brain/awad318
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Article ; Online: The Functional Organization of Neocortical Networks Investigated in Slices with Local Field Recordings and Laser Scanning Photostimulation.

Erlandson, Melissa A / Manzoni, Olivier J / Bureau, Ingrid

PloS one

2015 Volume 10, Issue 7, Page(s) e0132008

Abstract: The organization of cortical networks can be investigated functionally in brain slices. Laser scanning photostimulation (LSPS) with glutamate-uncaging allows for a rapid survey of all connections impinging on single cells recorded in patch-clamp. We ... ...

Abstract	The organization of cortical networks can be investigated functionally in brain slices. Laser scanning photostimulation (LSPS) with glutamate-uncaging allows for a rapid survey of all connections impinging on single cells recorded in patch-clamp. We sought to develop a variant of the method that would allow for a more exhaustive mapping of neuronal networks at every experiment. We found that the extracellular field recordings could be used to detect synaptic responses evoked by LSPS. One to two electrodes were placed in all six cortical layers of barrel cortex successively and maps were computed from the size of synaptic negative local field potentials. The field maps displayed a laminar organization similar to the one observed in maps computed from excitatory postsynaptic currents recorded in patch-clamp mode. Thus, LSPS combined with field recording is an interesting alternative to obtain for every animal tested a comprehensive map of the excitatory intracortical network.
MeSH term(s)	Animals ; Male ; Mice ; Mice, Inbred C57BL ; Neocortex/physiology ; Nerve Net/physiology ; Patch-Clamp Techniques ; Photic Stimulation ; Synapses/physiology
Language	English
Publishing date	2015
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0132008
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Article ; Online: The Functional Organization of Neocortical Networks Investigated in Slices with Local Field Recordings and Laser Scanning Photostimulation.

Melissa A Erlandson / Olivier J Manzoni / Ingrid Bureau

PLoS ONE, Vol 10, Iss 7, p e

2015 Volume 0132008

Abstract	The organization of cortical networks can be investigated functionally in brain slices. Laser scanning photostimulation (LSPS) with glutamate-uncaging allows for a rapid survey of all connections impinging on single cells recorded in patch-clamp. We sought to develop a variant of the method that would allow for a more exhaustive mapping of neuronal networks at every experiment. We found that the extracellular field recordings could be used to detect synaptic responses evoked by LSPS. One to two electrodes were placed in all six cortical layers of barrel cortex successively and maps were computed from the size of synaptic negative local field potentials. The field maps displayed a laminar organization similar to the one observed in maps computed from excitatory postsynaptic currents recorded in patch-clamp mode. Thus, LSPS combined with field recording is an interesting alternative to obtain for every animal tested a comprehensive map of the excitatory intracortical network.
Keywords	Medicine ; R ; Science ; Q
Language	English
Publishing date	2015-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
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Article ; Online: The Timing of Sensory-Guided Behavioral Response is Represented in the Mouse Primary Somatosensory Cortex.

Camon, Jérémy / Hugues, Sandrine / Erlandson, Melissa A / Robbe, David / Lagoun, Sabria / Marouane, Emna / Bureau, Ingrid

Cerebral cortex (New York, N.Y. : 1991)

2018 Volume 29, Issue 7, Page(s) 3034–3047

Abstract: Whisker-guided decision making in mice is thought to critically depend on information processing occurring in the primary somatosensory cortex. However, it is not clear if neuronal activity in this "early" sensory region contains information about the ... ...

Abstract	Whisker-guided decision making in mice is thought to critically depend on information processing occurring in the primary somatosensory cortex. However, it is not clear if neuronal activity in this "early" sensory region contains information about the timing and speed of motor response. To address this question we designed a new task in which freely moving mice learned to associate a whisker stimulus to reward delivery. The task was tailored in such a way that a wide range of delays between whisker stimulation and reward collection were observed due to differences of motivation and perception. After training, mice were anesthetized and neuronal responses evoked by stimulating trained and untrained whiskers were recorded across several cortical columns of barrel cortex. We found a strong correlation between the delay of the mouse behavioral response and the timing of multiunit activity evoked by the trained whisker, outside its principal cortical column, in layers 4 and 5A but not in layer 2/3. Circuit mapping ex vivo revealed this effect was associated with a weakening of layer 4 to layer 2/3 projection. We conclude that the processes controlling the propagation of key sensory inputs to naive cortical columns and the timing of sensory-guided action are linked.
MeSH term(s)	Afferent Pathways/physiology ; Animals ; Decision Making/physiology ; Male ; Mice ; Mice, Inbred C57BL ; Psychomotor Performance/physiology ; Reward ; Somatosensory Cortex/physiology ; Time Factors ; Vibrissae
Language	English
Publishing date	2018-07-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1077450-6
ISSN	1460-2199 ; 1047-3211
ISSN (online)	1460-2199
ISSN	1047-3211
DOI	10.1093/cercor/bhy169
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Article ; Online: Direct and Collateral Alterations of Functional Cortical Circuits in a Rat Model of Subcortical Band Heterotopia.

Plantier, Vanessa / Watrin, Françoise / Buhler, Emmanuelle / Martineau, Fanny Sandrine / Sahu, Surajit / Manent, Jean-Bernard / Bureau, Ingrid / Represa, Alfonso

Cerebral cortex (New York, N.Y. : 1991)

2018 Volume 29, Issue 10, Page(s) 4253–4262

Abstract: Subcortical band heterotopia (SBH), also known as double-cortex syndrome, is a neuronal migration disorder characterized by an accumulation of neurons in a heterotopic band below the normotopic cortex. The majority of patients with SBH have mild to ... ...

Abstract	Subcortical band heterotopia (SBH), also known as double-cortex syndrome, is a neuronal migration disorder characterized by an accumulation of neurons in a heterotopic band below the normotopic cortex. The majority of patients with SBH have mild to moderate intellectual disability and intractable epilepsy. However, it is still not clear how cortical networks are organized in SBH patients and how this abnormal organization contributes to improper brain function. In this study, cortical networks were investigated in the barrel cortex in an animal model of SBH induced by in utero knockdown of Dcx, main causative gene of this condition in human patients. When the SBH was localized below the Barrel Field (BF), layer (L) four projection to correctly positioned L2/3 pyramidal cells was weakened due to lower connectivity. Conversely, when the SBH was below an adjacent cortical region, the excitatory L4 to L2/3 projection was stronger due to increased L4 neuron excitability, synaptic strength and excitation/inhibition ratio of L4 to L2/3 connection. We propose that these developmental alterations contribute to the spectrum of clinical dysfunctions reported in patients with SBH.
MeSH term(s)	Animals ; Classical Lissencephalies and Subcortical Band Heterotopias/physiopathology ; Disease Models, Animal ; Gene Knockdown Techniques ; Membrane Potentials ; Microtubule-Associated Proteins/genetics ; Neurons/physiology ; Neuropeptides/genetics ; Rats, Wistar ; Somatosensory Cortex/pathology ; Somatosensory Cortex/physiopathology ; Synapses/physiology
Chemical Substances	Microtubule-Associated Proteins ; Neuropeptides ; doublecortin protein
Language	English
Publishing date	2018-12-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1077450-6
ISSN	1460-2199 ; 1047-3211
ISSN (online)	1460-2199
ISSN	1047-3211
DOI	10.1093/cercor/bhy307
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Article ; Online: Associative learning changes the organization of functional excitatory circuits targeting the supragranular layers of mouse barrel cortex.

Rosselet, Céline / Fieschi, Maxime / Hugues, Sandrine / Bureau, Ingrid

Frontiers in neural circuits

2011 Volume 4, Page(s) 126

Abstract: In primary sensory cortices, neuronal circuits change throughout life as a function of learning. During associative learning a neutral sensory stimulus acquires the emotional valence of an aversive event or a reward after repetitive contingent pairing. ... ...

Abstract	In primary sensory cortices, neuronal circuits change throughout life as a function of learning. During associative learning a neutral sensory stimulus acquires the emotional valence of an aversive event or a reward after repetitive contingent pairing. One important consequence is the enlargement of the representational area of the conditioned stimulus in the cortical map of its sensory modality. The details of this phenomenon at the circuit level are still largely unknown. Here, mice were trained in a differential conditioning paradigm where the deflections of one whisker row were paired with tail shocks and the deflections of two others were not. Changes occurring in excitatory circuits of barrel cortex were then examined in brain slices with laser scanning photostimulation mapping. We found that learning affected the projections targeting the supragranular layers in the columns of unpaired whiskers: Pyramidal cells located in layer (L) 3 received enhanced inputs from L5A cells located in their home column and new inputs from L2/3 and L4 cells located in the neighboring column of the paired whisker. In contrast, the excitatory projections impinging onto L2/3 cells in the column of the paired whisker were not altered. Together, these data reveal that associative learning alters the canonical columnar organization of functional ascending L4 projections and strengthens transcolumnar excitatory projections in barrel cortex. These phenomena could participate to the transformation of the whisker somatotopic map induced by associative learning.
Language	English
Publishing date	2011-01-14
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452968-0
ISSN	1662-5110 ; 1662-5110
ISSN (online)	1662-5110
ISSN	1662-5110
DOI	10.3389/fncir.2010.00126
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Article ; Online: Diverse thalamocortical short-term plasticity elicited by ongoing stimulation.

Díaz-Quesada, Marta / Martini, Francisco J / Ferrati, Giovanni / Bureau, Ingrid / Maravall, Miguel

The Journal of neuroscience : the official journal of the Society for Neuroscience

2014 Volume 34, Issue 2, Page(s) 515–526

Abstract: To produce sensation, neuronal pathways must transmit and process stimulus patterns that unfold over time. This behavior is determined by short-term synaptic plasticity (STP), which shapes the temporal filtering properties of synapses in a pathway. We ... ...

Abstract	To produce sensation, neuronal pathways must transmit and process stimulus patterns that unfold over time. This behavior is determined by short-term synaptic plasticity (STP), which shapes the temporal filtering properties of synapses in a pathway. We explored STP variability across thalamocortical (TC) synapses, measuring whole-cell responses to stimulation of TC fibers in layer 4 neurons of mouse barrel cortex in vitro. As expected, STP during stimulation from rest was dominated by depression. However, STP during ongoing stimulation was strikingly diverse across TC connections. Diversity took the form of variable tuning to the latest interstimulus interval: some connections responded weakly to shorter intervals, while other connections were facilitated. These behaviors did not cluster into categories but formed a continuum. Diverse tuning did not require disynaptic inhibition. Hence, monosynaptic excitatory lemniscal TC connections onto layer 4 do not behave uniformly during ongoing stimulation. Each connection responds differentially to particular stimulation intervals, enriching the ability of the pathway to convey complex, temporally fluctuating information.
MeSH term(s)	Animals ; Electric Stimulation ; Mice ; Neural Pathways/physiology ; Neuronal Plasticity ; Patch-Clamp Techniques ; Somatosensory Cortex/physiology ; Thalamus/physiology
Language	English
Publishing date	2014-01-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604637-x
ISSN	1529-2401 ; 0270-6474
ISSN (online)	1529-2401
ISSN	0270-6474
DOI	10.1523/JNEUROSCI.2441-13.2014
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Article ; Online: Circuit and plasticity defects in the developing somatosensory cortex of FMR1 knock-out mice.

Bureau, Ingrid / Shepherd, Gordon M G / Svoboda, Karel

The Journal of neuroscience : the official journal of the Society for Neuroscience

2008 Volume 28, Issue 20, Page(s) 5178–5188

Abstract: Silencing of the Fmr1 gene causes fragile X syndrome. Although defects in synaptic plasticity in the cerebral cortex have been linked to cognitive impairments in Fmr1 knock-out (ko) mice, the specific cortical circuits affected in the syndrome are ... ...

Abstract	Silencing of the Fmr1 gene causes fragile X syndrome. Although defects in synaptic plasticity in the cerebral cortex have been linked to cognitive impairments in Fmr1 knock-out (ko) mice, the specific cortical circuits affected in the syndrome are unknown. Here, we investigated the development of excitatory projections in the barrel cortex of Fmr1 ko mice. In 2-week-old Fmr1 ko mice, a major ascending projection connecting layer 4 (L4) to L3 (L4-->L3), was defective in multiple and independent ways: its strength was reduced, caused by a lower connection probability; the axonal arbors of L4 cells were spatially diffuse in L2/3; the L4-->L3 projection did not show experience-dependent plasticity. By 3 weeks, the strength of the L4-->L3 projection was similar to that of wild type. Our data indicate that Fmr1 shapes sensory cortical circuits during a developmental critical period.
MeSH term(s)	Animals ; Disease Models, Animal ; Excitatory Postsynaptic Potentials/genetics ; Fragile X Mental Retardation Protein/genetics ; Fragile X Syndrome/genetics ; Fragile X Syndrome/metabolism ; Fragile X Syndrome/physiopathology ; Gene Expression Regulation, Developmental/genetics ; Genetic Predisposition to Disease/genetics ; Growth Cones/metabolism ; Growth Cones/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Nervous System Malformations/genetics ; Nervous System Malformations/metabolism ; Nervous System Malformations/physiopathology ; Neural Pathways/abnormalities ; Neural Pathways/metabolism ; Neural Pathways/physiopathology ; Neuronal Plasticity/genetics ; Organ Culture Techniques ; Sensation/genetics ; Somatosensory Cortex/abnormalities ; Somatosensory Cortex/metabolism ; Somatosensory Cortex/physiopathology ; Synaptic Transmission/genetics
Chemical Substances	Fmr1 protein, mouse ; Fragile X Mental Retardation Protein (139135-51-6)
Language	English
Publishing date	2008-05-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604637-x
ISSN	1529-2401 ; 0270-6474
ISSN (online)	1529-2401
ISSN	0270-6474
DOI	10.1523/JNEUROSCI.1076-08.2008
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