Glutamic Acid Decarboxylase- and γ-Aminobutyric Acid-Like Immunoreactivities in Corticotropin-Releasing Factor-Containing Parvocellular Neurons of the Hypothalamic Paraventricular Nucleus

1988 ◽  
Vol 48 (5) ◽  
pp. 516-526 ◽  
Author(s):  
Björn Meister ◽  
Tomas Hökfelt ◽  
Michel Geffard ◽  
Wolfgang Oertel
Keyword(s):  
Glutamic Acid ◽  
Paraventricular Nucleus ◽  
Glutamic Acid Decarboxylase ◽  
Corticotropin Releasing Factor ◽  
Hypothalamic Paraventricular Nucleus ◽  
Aminobutyric Acid ◽  
Acid Decarboxylase ◽  
Parvocellular Neurons

Ectopic expression of the Dlx genes induces glutamic acid decarboxylase and Dlx expression

Development ◽  
2002 ◽  
Vol 129 (1) ◽  
pp. 245-252 ◽  
Author(s):  
Thorsten Stühmer ◽  
Stewart A. Anderson ◽  
Marc Ekker ◽  
John L. R. Rubenstein
Keyword(s):  
Cerebral Cortex ◽  
Glutamic Acid ◽  
Glutamic Acid Decarboxylase ◽  
Family Members ◽  
Ectopic Expression ◽  
Gabaergic Neurons ◽  
Aminobutyric Acid ◽  
Acid Decarboxylase ◽  
Reporter Construct ◽  
Dlx Genes

The expression of the Dlx homeobox genes is closely associated with neurons that express γ-aminobutyric acid (GABA) in the embryonic rostral forebrain. To test whether the Dlx genes are sufficient to induce some aspects of the phenotype of GABAergic neurons, we adapted the electroporation method to ectopically express DLX proteins in slice cultures of the mouse embryonic cerebral cortex. This approach showed that ectopic expression of Dlx2 and Dlx5 induced the expression of glutamic acid decarboxylases (GADs), the enzymes that synthesize GABA. We also used this method to show cross-regulation between different Dlx family members. We find that Dlx2 can induce Dlx5 expression, and that Dlx1, Dlx2 and Dlx5 can induce expression from a Dlx5/6-lacZ enhancer/”reporter construct.

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