Regional distribution of glutamic acid decarboxylase (GAD 65 and GAD 67) mRNA in the hypothalamus of male rhesus macaques before and after puberty

• Published in: Brain research. Molecular brain research. 1998-06, Vol.57 (1), p.86-91
• Main Authors: Urbanski, Henryk F, Rodrigues, Sarina M, Garyfallou, Vasilios T, Kohama, Steven G
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Development. Senescence. Regeneration. Transplantation; Fundamental and applied biological sciences. Psychology; gamma-Aminobutyric Acid - physiology; Gene Expression Regulation, Developmental - physiology; Glutamate Decarboxylase - genetics; Gonadotropin-releasing hormone; Gonadotropin-Releasing Hormone - physiology; Hypothalamus - cytology; Hypothalamus - enzymology; Hypothalamus - growth & development; In Situ Hybridization; Macaca mulatta - growth & development; Male; Neurons - chemistry; Neurons - enzymology; RNA, Messenger - analysis; Sexual Maturation - physiology; Vertebrates: nervous system and sense organs; γ-Aminobutyric acid
• ISSN: 0169-328X; 1872-6941
• DOI: 10.1016/S0169-328X(98)00070-9

Glutamic acid decarboxylase (GAD) is the rate-limiting enzyme in the γ-aminobutyric acid (GABA) biosynthetic pathway, and is coded for by two mRNAs, GAD 65 and GAD 67. Using in situ hybridization, we examine the distribution pattern of both GAD mRNAs in the hypothalamus and thalamus of prepubertal and adult male rhesus macaques. Qualitatively, GAD 65 and GAD 67 mRNAs showed a similar wide, but highly specific distribution pattern, supporting the view that GABAergic neurons play an important role in modulating neuroendocrine function. However, no quantitative difference in the intensity of hybridization signal was detected between prepubertal and adult animals in any of the hypothalamic or thalamic nuclei. Therefore, although GABAergic neurons are anatomically well-placed to control the secretion of gonadotropin-releasing hormone (GnRH) in primates, it is unlikely that the onset of puberty and the associated increase in GnRH secretion is triggered by a change in GAD gene transcription.