High impact information on GAD2

• Both the GAD67 and the GAD65 antisense D-oligos induced a large and prompt increase in LHRH release, whereas the scrambled D-oligos did not induce any significant effect [1].
• No significant change in GAD65 concentration was detected in the microdissected dentate gyrus despite the induction of GAD65-LI [2].
• Regional distribution of glutamic acid decarboxylase (GAD65 and GAD67) mRNA in the hypothalamus of male rhesus macaques before and after puberty [3].

Anatomical context of GAD2

• First, both GAD67 and GAD65 mRNAs were detectable by reverse transcription-PCR analysis in the preoptic area, medio-basal hypothalamus, posterior hypothalamic area, and hippocampus of the monkey brain [1].
• The gamma-aminobutyric acid (GABAergic) system of the hippocampal formation of Macaca fascicularis monkeys was studied immunohistochemically with a monoclonal antibody to GABA and with nonisotopic in situ hybridization with cRNA probes for glutamic acid decarboxylase 65 (GAD65) and GAD67 [4].
• In MPTP-treated monkeys that received L-DOPA, a significant increase in both GAD67 and GAD65 mRNA levels was measured in the putamen when compared to control or MPTP-treated monkeys [5].

Other interactions of GAD2

• The GAD67 or GAD65 antisense D-oligos or scrambled D-oligos were infused directly into the stalk-median eminence [1].

Analytical, diagnostic and therapeutic context of GAD2

• Bilateral orchidectomy produced a significant increase in GnRH mRNA levels that was restricted to the mediobasal hypothalamus and that was associated with a significant decrease in POMC, GAD65 and GAD67 mRNA levels in this region of the hypothalamus [6].

References