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Development of GABA innervation in the cerebral and cerebellar cortices
In many areas of the vertebrate brain, such as the cerebral and cerebellar cortices, neural circuits rely on inhibition mediated by GABA (γ-aminobutyric acid) to shape the spatiotemporal patterns of
Subcellular domain-restricted GABAergic innervation in primary visual cortex in the absence of sensory and thalamic inputs
TLDR
It is shown that the distributions of two major classes of GABAergic synapses along the perisomatic and dendritic domains of pyramidal neurons were indistinguishable between primary visual cortex in vivo and cortical organotypic cultures, indicating that subcellular synapse targeting is independent of thalamic input.
Requirement of ERK Activation for Visual Cortical Plasticity
TLDR
It is demonstrated that two different inhibitors of the ERK pathway suppress the induction of two forms of long-term potentiation (LTP) in rat cortical slices and that their intracortical administration to monocularly deprived rats prevents the shift in ocular dominance towards the nondeprived eye.
Activity-dependent PSA expression regulates inhibitory maturation and onset of critical period plasticity
TLDR
It is shown that polysialic acid (PSA), presented by the neural cell adhesion molecule, has a role in the maturation of GABAergic innervation and ocular dominance plasticity.
GABAergic Circuit Dysfunctions in Neurodevelopmental Disorders
TLDR
Recent studies suggesting a role for alterations of GABA transmission in the pathophysiology of two neurodevelopmental diseases, schizophrenia, and autism are highlighted and how manipulations of GABA signaling may be used for novel therapeutic interventions are discussed.
Development of cortical GABAergic circuits and its implications for neurodevelopmental disorders
TLDR
This review summarizes recent findings on the mechanisms underlying the construction of GABAergic circuits in the cortex, with a particular focus on potential implications for brain diseases with neurodevelopmental origin.
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