$23 THE EFFECTS OF SUBSTANCE P ON THE NEURAL ACTIVITY OF PREOPTIC THERMOSENSITIVE NEURONS MASAAKI SHIBATA*, TETSURO HORI, TOSHIKAZU KIYOHARA, ~ R I YAMASAKI*, TANEMICHI CHIBA#, and HITOSHI KAWANO*#, Department of Physiology and Anatomy#, Saga Medical College, Nabeshima, Saga 840-01, Japan. Systemic i n j e c t i o n of capsaicin, the pungent algesic substance of the red pepper, produces a dose dependent hypothermia in mammals, probably by i t s action on warm sensors. Capsaicin s e l e c t i v e l y releases and subsequently depletes the substance P (SP) in the primary sensory neurons subserving the nociception. The hypothermia is also induced by microinjection of capsaicin into the preoptic area (POA), where thermosensitive neurons e x i s t , andSP-containing terminals and c e l l bodies are immunohistochemically found. The present work is concerned to see whether central capsaicin influences thermoregulation by the release of SP at POA. Single-unit a c t i v i t y of POA neurons was recorded in urethane-anesthetized rats (1.2 g/Kg, i . p . ) with a 7-barrelled microelectrode and the effects of SP and capsaicin applied e l e c t r o p h o r e t i c a l l y to the neurons were observed. In a t o t a l of 34 POA thermosensitive neurons (21 warm units, 13 cold u n i t s ) , 27 units (80%) were not affected, and only 7 units (20%) responded to SP. In cont r a s t , 23 (40%) of 57 thermally i n s e n s i t i v e neurons responded to SP. Of 31 thermosensitive neurons tested by both SP and capsaicin, the responses of 3 units (10%) were in the same direction and those of 4 units (13%) in the opposite direction. The majority of the neurons (17 u n i t s , 55%) responded to only one of e i t h e r substance. While d r a s t i c a l l y reduced immunohistochemical SP was in the dorsal horn of capsaicin-treated r a t s , there was no change in immunohistochemical SP in POA even a f t e r local i n j e c t i o n of capsaicin. The present results suggest that the hypothalamic SP does not p a r t i c i p a t e in hypothermic e f f e c t of capsaicin observed a f t e r POA i n j e c t i o n . THE E F F E C T OF C E N T R A L N E R V O U S M E T A B O L I S M IN RAT LIVER.
SYSTEM(CNS)
LESION
ON LIPID
SHUNICHI MURANO*, KOHJI SHIRAI*, YASUSHI SAITO* and SHO Y O S H I D A The S e c o n d D e p a r t m e n t of Internal Medicine, School of Medicine, C h i b a University, 1-8-1, Inohana, Chiba, Chiba, 280, Japan. In order to e l u c i d a t e the role of CNS on lipid m e t a b o l i s m in p e r i p h e r a l tissue, t r i g l y c e r i d e m e t a b o l i s m in the liver of CNSl e s i o n e d obese rats, m o n o s o d i u m g l u t a m a t e ( M S G ) - i n d u c e d obese rats and high fat d i e t - f e d rats was investigated. CNS lesions i n v o l v i n g the v e n t r o m e d i a l h y p o t h a l a m u s were made by e l e c t r i c a l d e s t r u c t i o n at 2-months old. These rats were used for the e x p e r i m e n t after six months' feeding. There was a c l o s e r e l a t i o n s h i p b e t w e e n adipose tissue w e i g h t a n d t r i g l y c e r i d e c o n t e n t in liver in c o n t r o l rats, M S G - i n d u c e d obese rats and h i g h fat d i e t - f e d rats. This result showed that o b e s i t y itself i n d u c e d fatty liver. However, a group of CNSl e s i o n e d obese rats s h o w e d a five times higher t r i g l y c e r i d e c o n t e n t in liver than that e x p e c t e d by its a d i p o s e tissue weight. This group of rats had more m a s s i v e CNS lesion than the other C N S - l e s i o n e d obese rats h a v i n g no such severe fatty livers. There was no s i g n i f i c a n t d i f f e r e n c e in the enzyme a c t i v i t i e s of t r i g l y c e r i d e s y n t h e s i s in the liver b e t w e e n these two groups of C N S - l e s i o n e d o b e s e rats. S e r u m V L D L - t r i g l y c e r i d e was rather lower in the e x c e s s i v e fatty liver group. F r o m those results, it was s u g g e s t e d that an i n c r e a s e in t r i g l y c e r i d e in the liver m i g h t be c a u s e d by d i s o r d e r s in V L D L f o r m a t i o n o r / a n d VLDL s e c r e t i o n from liver, a n d that CNS was r e g u l a t i n g the t r i g l y c e r i d e m e t a b o l i s m in liver at this site.