Abstract
G A A b st ra ct s plasma ghrelin levels at 2 h after ICV UCN. UCN induces c-fos mRNA and Fos protein expression in the supraoptic nucleus, paraventricular nucleus of hypothalamus (PVN), locus coeruleus, solitary tract nucleus (NTS), and ventrolateral nucleus of medulla oblongata (VLM), known to influence sympathetic outflow. Fos expression in NTS was markedly suppressed by coadministration of RKT (control 84 ± 28, UCN 352 ± 130, UCN + RKT 48 ± 15; P , 0.05). UCN-induced Fos expression in VLM was also suppressed by RKT (control 35 ± 10, UCN 289 ± 94, UCN + RKT 133 ± 27), but not significant (P=0.08). RKT also suppressed UCN-induced c-fos expression in PVN. In contrast, the dorsal motor nucleus involved in vagal outflow did not show any changes in Fos and fos expression by RKT. Conclusions: These data indicate that a) RKT inhibits the activity of the neuron of NTS suggesting that RKT inhibits vagal input from the periphery to central nerves. b) As the result of inhibiton of vagal input, activity of hypothalamic satiety center, PVN is suppressed resulting in the inhibition of the sympathetic outflow from the central nerve to the periphery. RKT may restore disturbed appetite and ghrelin secretion through the restoration of balance of central autonomic nervous system.
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