Abstract
A sugar acid, 2-B4O has been found to increase from 3.5 to 13 in rat serum μM at 36 h after food deprivation. Injections of 2-B4O (2.5 μM) into rat III cerebral ventricle suppress food intake and single neuronal activity in the lateral hypothalamic area (LHA, feeding center) . 2-B4O hyperpolarizes glucose-sensitive neurons in the LHA via Na-K pump activation, while depolarizes the glucoreceptor neurons in the ventromedial nucleus, satiety center, via closure of ATP-sensitive K channels. The plasma levels of glucose, corticosterone, and catecholamines, and firing rate in both parvocellular neurons in the paraventricular nucleus and sympathetic efferent nerves all increase 2-B4O intravenous injection, indicating activation of the hypothalamo-pituitary-adrenal axis. A 2-B4O (iv) facilitates emotional and spatial learning and memory, and pretreatment of anti-acidic fibroblast growth factor (aFGF) antibody icv eliminates these effects. aFGF is released from ependymal cells in the III ventricle in response to the glucose increase in CSF induced by 2-B4O (iv). 2-B4O suppresses the clinical symptoms of experimental allergic encephalomyelitis (EAE) in Lewis rats ,a model for human multiple sclerosis. These results indicate that 2-B4O is not only a powerful satiety substance, but also effective as an activator of the hypothalamo-pituitary-adrenal axis and sympathetic efferent outflow, and as a memory facilitation and a suppressant of autoimmune function. [Jpn J Physiol 54 Suppl:S188 (2004)]
