Progesterone Suppression of Glutamic Acid Decarboxylase (GAD67) mRNA Levels in the Preoptic Area: Correlation to the Luteinizing Hormone Surge

1995 ◽  
Vol 62 (6) ◽  
pp. 562-570 ◽  
Author(s):  
Richard Unda ◽  
Darrell W. Brann ◽  
Virendra B. Mahesh
Keyword(s):  
Luteinizing Hormone ◽  
Glutamic Acid ◽  
Glutamic Acid Decarboxylase ◽  
Preoptic Area ◽  
Acid Decarboxylase ◽  
Mrna Levels ◽  
Luteinizing Hormone Surge

Estrogen modulation of mRNA levels for the two forms of glutamic acid decarboxylase (GAD) in female rat brain

1995 ◽  
Vol 360 (4) ◽  
pp. 685-697 ◽  
Author(s):  
M. M. McCarthy ◽  
L. C. Kaufman ◽  
P. J. Brooks ◽  
D. W. Pfaff ◽  
S. Schwartz-Giblin
Keyword(s):  
Glutamic Acid ◽  
Rat Brain ◽  
Glutamic Acid Decarboxylase ◽  
Acid Decarboxylase ◽  
Mrna Levels ◽  
Female Rat

Glutamic Acid Decarboxylase-Containing Axons Synapse on LHRH Neurons in the Rat Medial Preoptic Area

1985 ◽  
Vol 40 (6) ◽  
pp. 536-539 ◽  
Author(s):  
Csaba Leranth ◽  
Neil J. MacLusky ◽  
Hideki Sakamoto ◽  
Marya Shanabrough ◽  
Frederick Naftolin
Keyword(s):  
Glutamic Acid ◽  
Glutamic Acid Decarboxylase ◽  
Preoptic Area ◽  
Medial Preoptic Area ◽  
Acid Decarboxylase

scholarly journals Estradiol Alters Only GAD67 mRNA Levels in Ischemic Rat Brain with No Consequent Effects on GABA

2005 ◽  
Vol 26 (4) ◽  
pp. 518-526 ◽  
Author(s):  
Hung-Dong Joh ◽  
Robin V Searles ◽  
Michael Selmanoff ◽  
Nabil J Alkayed ◽  
Raymond C Koehler ◽  
...  
Keyword(s):  
Glutamic Acid ◽  
Rat Brain ◽  
Glutamic Acid Decarboxylase ◽  
Brain Regions ◽  
Artery Occlusion ◽  
Acid Decarboxylase ◽  
Ribonuclease Protection Assay ◽  
Mrna Levels ◽  
Gaba Transporters ◽  
Ribonuclease Protection

The present study tested the hypothesis that estradiol reduces tissue infarction after middle cerebral artery occlusion (MCAO) in estradiol-deficient females by augmenting glutamic acid decarboxylase (GAD) expression and thus activity, leading to increases in γ-amino-butyric acid (GABA) tissue levels. Glutamic acid decarboxylase is the principal enzyme for GABA synthesis and has two isoforms, GAD65 and GAD67, which differ in size and cellular distribution. Rats were ovariectomized 7 to 8 days before receiving no hormone, placebo, or 25 μg estradiol via subcutaneous implant 7 to 10 days before harvesting tissue in either ischemic cohorts after 2 h of MCAO (end-ischemia) or in nonischemic cohorts. Selected cortical and striatal regions were microdissected from harvested brains. GAD65/67 mRNA levels were determined by microlysate ribonuclease protection assay. End-ischemic GABA concentrations were determined by HPLC. Steroid treatment selectively decreased ischemic cortical GAD67 mRNA levels. In most brain regions evaluated, regional GABA concentrations increased with ischemia regardless of treatment. Estradiol blocked MCAO-induced increases in GABA concentration only in dorsomedial cortex. These data suggest that estradiol repletion in ischemic rat brain selectively decreases GAD67 mRNA levels but does not alter steady-state GABA concentrations. It may be that estradiol under ischemic conditions is attenuating GABA metabolism rather than enhancing synthesis or is augmenting other aspects of GABAergic transmission such as GABA transporters and receptors.

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