SHIODA Seiji Showa University School of Medicine, Assistant Professor, 医学部, 講師 (80102375)
OCHIAI Hidehiko Showa University School of Medicine, Assistant Professor, 医学部, 講師 (40053954)
NAITO Nobuko Showa University School of Medicine, Assistant Professor, 医学部, 講師 (30053903)
|Budget Amount *help
¥2,400,000 (Direct Cost : ¥2,400,000)
Fiscal Year 1991 : ¥700,000 (Direct Cost : ¥700,000)
Fiscal Year 1990 : ¥1,700,000 (Direct Cost : ¥1,700,000)
Synaptic inputs of noradrenaline- and brain natriuretic peptide-containing terminals to arginine-vasopressin producing cells(AVP cells)were observed, respectively, in the supraoptic and paraventricular nuclei(SON, PVN)of the rat hypothalamus using double immunostaining. In addition, axon terminals orginated from the neurons in the Al/Cl cell group in the medulla oblongata have been found to make synapses with AVP cells in the PVN and the SON using a double labeling technique combining WGA-HRP anterograde tracing with AVP immunocytochemistry at electron microscopic level.
Using in situ hybridization and immunocytochemistry, we ekamined neuronal influence on vasopressin(AVP)-gene expression in rat hypothalamus after unilateral electrolytic lesion of the ventrolateral medulla, containing catecholaminergic neurons forming the Al cell group. Because Al neurons are throught to be the source of noradrenergic terminals upon the magnocellular neurons that release AVP dominantly.
In the normal con
trol rat, there was no difference in AVP-MRNA levels in magnocellular neurons between, the PVN and SON nuclei. However, unilateral Allesion caused AVP-MRNA levels between the normal and the lesioned rats. Furthermore, stimulation of water-deprivation in the lesioned rat increased in AVP-mRNA levels significantly not only in the SON but also in the PVN. I these experiments, there was no significant difference in rat plasma osmolarity and electrolytes(Na^+, K^+, Ca^<++>)(p<0.05).
These results indicate that the AVP-gene expression in rat magnocellular neurons in differentially influenced between the PVN and SON by the neuronal regulation through the ventrolateral medulla, and at least in part, some pathways may through Al area to contribute to increase in levels in the PVN. Moreover, it is clarified that Al lesion does not inhibit the response of waterdeprivation in magnocellular neurons in both nuclei, suggesting deprovation in magnocellular neurosecretory neurons in both nuclei, suggesting different pathways and different mechanisms concerning to the AVP-gene expression. Less