introduction: (s)- 3,5-dihydroxyphenylglycine (dhpg) is an agonist for group i metabotropic glutamate receptors. dhpg-induced synaptic depression of excitatory synapses on hippocampal pyramidal neurons is well known model for synaptic plasticity studies. the aim of the present study was to examine the effects of dhpg superfusion on excitatory synapses on pyramidal and fast-spiking gabaergic cel...

Midbrain- and hindbrain-derived GABAergic interneurons are critical for regulation of sleep, respiratory, sensory-motor and motivational processes, and they are implicated in human neurological disorders. However, the precise mechanisms that underlie generation of GABAergic neuron diversity in the midbrain-hindbrain region are poorly understood. Here, we show unique and overlapping requirements...

Diverse mechanisms regulate development of GABAergic neurons in different regions of the central nervous system. We have addressed the roles of a proneural gene, Ascl1, and a postmitotic selector gene, Gata2, in the differentiation of GABAergic neuron subpopulations in three diencephalic prosomeres: prethalamus (P3), thalamus (P2) and pretectum (P1). Although the different proliferative progeni...

Neural circuits are composed of mainly glutamatergic and GABAergic neurons, which communicate through synaptic connections. Many factors instruct the formation and function of these synapses; however, it is difficult to dissect the contribution of intrinsic cell programs from that of extrinsic environmental effects in an intact network. Here, we perform paired recordings from two-neuron microcu...

GABAergic neurons and oligodendrocytes originate from progenitors within the ventral telencephalon. However, the molecular mechanisms that control neuron-glial cell-fate segregation, especially how extrinsic factors regulate cell-fate changes, are poorly understood. We have discovered that the Wnt receptor Ryk promotes GABAergic neuron production while repressing oligodendrocyte formation in th...

Midbrain GABAergic neurons control several aspects of behavior, but regulation of their development and diversity is poorly understood. Here, we further refine the midbrain regions active in GABAergic neurogenesis and show their correlation with the expression of the transcription factor Gata2. Using tissue-specific inactivation and ectopic expression, we show that Gata2 regulates GABAergic neu...

BACKGROUND Acidosis impairs cognitions and behaviors presumably by acidification-induced changes in neuronal metabolism. Cortical GABAergic neurons are vulnerable to pathological factors and their injury leads to brain dysfunction. How acidosis induces GABAergic neuron injury remains elusive. As the glia cells and neurons interact each other, we intend to examine the role of the astrocytes in a...

and ectopic expression, we demonstrated that Gata2 regulates GABAergic neuron development in the midbrain, but not in the rhombomere1. Without Gata2, all the precursors in the embryonic midbrain fail to activate GABAergic neuron-specific gene expression and switch to a glutamatergic phenotype instead. Surprisingly, this fate switch is also observed throughout the neonatal midbrain, except for t...

GABAergic neuronal cell grafting has promise for treating a multitude of neurological disorders including epilepsy, age-related memory dysfunction, Alzheimer's disease and schizophrenia. However, identification of an unlimited source of GABAergic cells is critical for advancing such therapies. Our previous study implied that reprogramming of bone marrow-derived mesenchymal stem cells (BMSCs) th...

and ectopic expression, we demonstrated that Gata2 regulates GABAergic neuron development in the midbrain, but not in the rhombomere1. Without Gata2, all the precursors in the embryonic midbrain fail to activate GABAergic neuron-specific gene expression and switch to a glutamatergic phenotype instead. Surprisingly, this fate switch is also observed throughout the neonatal midbrain, except for t...