Action of the sexual hormones on the endogenous norepinephrine of the central nervous system (author's transl)]

The effects of ovariectomy and the injection of sexual hormones on the norepinephrine (NE) content in different areas of the central nervous system were studied in the Wistar female rat. The ovariectomy increased the NE in the hypothalamus, cerebellum and the medulla oblongata. The estradiol benzoate did not modify the NE levels in the ovariectomized rats. Progesterone decreased the NE in the hypothalamus and testosterone dipropionate increased it in the brain hemispheres. It seems possible that the hypersecretion of FSH would increase the synthesis of NE in castrated animals through the potentation of the tyroxine-hydroxylase activity. Increase in testosterone synthesis was probably responsible for the raise in NE levels. The progesterone moderated the effects of the ovariectomy, probably through feed-back mechanisms involving the hypothalamic-hypophyseal tract.     

Oxygen-sensing neurons in the central nervous system.

This mini-review summarizes the present knowledge regarding central oxygen-chemosensitive sites with special emphasis on their function in regulating changes in cardiovascular and respiratory responses. These oxygen-chemosensitive sites are distributed throughout the brain stem from the thalamus to the medulla and may form an oxygen-chemosensitive network. The ultimate effect on respiratory or sympathetic activity presumably depends on the specific neural projections from each of these brain stem oxygen-sensitive regions as well as on the developmental age of the animal. Little is known regarding the cellular mechanisms involved in the chemotransduction process of the central oxygen sensors. The limited information available suggests some conservation of mechanisms used by other oxygen-sensing systems, e.g., carotid body glomus cells and pulmonary vascular smooth muscle cells. However, major gaps exist in our understanding of the specific ion channels and oxygen sensors required for transducing central hypoxia by these central oxygen-sensitive neurons. Adaptation of these central oxygen-sensitive neurons during chronic or intermittent hypoxia likely contributes to responses in both physiological conditions (ascent to high altitude, hypoxic conditioning) and clinical conditions (heart failure, chronic obstructive pulmonary disease, obstructive sleep apnea syndrome, hypoventilation syndromes). This review underscores the lack of knowledge about central oxygen chemosensors and highlights real opportunities for future research.