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Central cardiovascular regulation of tachykinin peptides: The sympathetic nervous system and vasopressin release
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28. Neuropeptides CHANGES IN SYNTHESES OF PEPTIDES IN RAT FACIAL MOTONEURONS AFTER FACIAL NERVE CRUSHING AND TRANSECTION. TAKANORI SAIKA 1 , EHIKO SENBA2 , KOICttI NOGUCHI2 AND HASAYA TOttYAMA2 , D e p a r t m e n t o f l O t o l a r y n g o l o g y and 2 A n a t o m y I I , O s a k a U n i v . Medical School. 1-1-50, Fukushima, Fukushtma-ku, Osaka 553, Japan. We h a v e e x a m i n e d t h e c h a n g e s of mRNAs c o d i n g f o r n e r v e g r o w t h f a c t o r r e c e p t o r (NGF-R), a a n d B - c a l c i t o n i n gene-related peptide (a a n d B-CGRP), c h o l e e y s t o k i n i n (CCK) and g a l a n i n in the facial motoneurons following nerve crushing and transection by u s i n g i n s i t u h y b r i d i z a t i o n histoehemistry. The l e v e l s o f mRNA f o r NGF-R, a-CGRP, CCK a n d g a l a n i n w e r e i n c r e a s e d w h i l e t h e B-CGRP mRNA l e v e l was decreased after axotomy. The l e v e l s o£ mRNAs f o r t h e s e s u b s t a n c e s returned to t h e c o n t r o l v a l u e s 2 - 4 weeks a f t e r n e r v e c r u s h i n g , whereas nerve transection had prolonged effects on t h e e x p r e s s i o n o f t h e s e mRNAs. Nerve transection h a d more prominent effects on B-CGRP, CCK, g a l a n i n mRNAs, w h i l e NGF-R mRNA was more profoundly
influenced
by nerve
crushing.
THE EFFECT OF MORPHINE ON CALCIUM DYNAMICS IN RAT HIPPOCAMPAL PREPARATIONS. TETSUO OHNISHIl , KIHACHI SAITOz AND REIZO INOKI2, IThe Second Department of Oral and M a x i l l o f a c i a t Surgery and 2Department of Pharmacology, Faculty of Dentistry, ~-s-aka U n i v e r s i t y , I - 8 Yamadaoka, Suita 565, Japan. The e f f e c t of morphine on calcium dynamics was studied in r a t hippocampal preparations. Rats were k i l l e d by decapitation and brains were quickly removed and p a r a s a g i t t a l s l i c e s containing the hippocampus were cut at a thickness of 300 ~m. In these hippocampal s l i c e s , morphine enhanced the amplitude of the f i e l d p o t e n t i a l s evoked in CAt pyramidal c e l l s . This e f f e c t of morphine was antagonized by calcium. GTPyS reduced the e f f e c t of morphine, whereas the e f f e c t of GDPBS was s i m i l a r to that of morphine. The conversion of 3H-nitrendipine binding to a low a f f i n i t y state was observed in membrane f r a c t i o n s prepared from s l i c e s treated with morphine. I t was also observed that GTPyS antagonized the e f f e c t of morphine, while the e f f e c t of GDPBS was s i m i l a r to that of morphine. These r e s u l t s suggest that morphine changes th~ a f f i n i t y of calcium channels to Caz• through GTP-binding proteins and reduces CaL÷ i n f l u x .
C E N T R A L C A R D I O V A S C U L A R R E G U L A T I O N O F T A C H Y K I N I N PEPTIDES: T H E SYMPATI-fl~TIC NERVOUS SYSTEM AND VASOPRESSIN P,ELEASE. YUKIO TAKANO, TETSUYA I4_AGIO*, YASUHISA NAKAYAMA*, RYO SAITO* T AKIRA NAGASHIMA* AND HIRO-O KAMIYA, Department of Pharmacology) Faculty of Pharmaceutical Sciences) Fukuoka University, Fukuoka 814-01, Japan. W e h a v e e x a m i n e d t h e m e c h a n i s m s o f c e n t r a l c a r d i o v a s c u l a r r e g u l a t i o n of t a c h y k i n i n peptides. Intracerebroventricular injections (i.c.v.) of tachykinin peptides caused dosed e p e n d e n t i n c r e a s e s in b l o o d p r e s s u r e a n d h e a r t rate in a n e s t h e t i z e d rats. T h e p r e s s o r r e s p o n s e s to s u b s t a n c e P (10lag, i.c.v.), n e u r o k i n i n A (10lag, i.c.v.) and n e u r o p e p t i d e y (l~tg, i.c.v.) w e r e b l o c k e d by p e r i p h e r a l a d m i n i s t r a t i o n o f p e n t o l i n i u m a n d p h e n t o l a m i n e . T h e p r e s s o r r e s p o n s e to the s e l e c t i v e n e u r o k i n i n B r e c e p t o r l i g a n d , s e n k t i d e (10~g, i.c.v.), was i n h i b i t e d b y p r e t r e a t m e n t with v a s o p r e s s i n V1 r e c e p t o r a n t a g o n i s t , a n d s e n k t i d e c a u s e d a n i n c r e a s e in p l a s m a v a s o p r e s s i n l e v e l . T h e s e r e s u l t s s u g g e s t t h a t c e n t r a l s u b s t a n c e P, n e u r o k i n i n A a n d n e u r o p e p t i d e 7, d e r i v e d f r o m the p r e p r o t a c h y k i n i n A g e n e , i n c r e a s e the blood p r e s s u r e and h e a r t rate v i a s y m p a t h e t i c n e r v e a c t i v i t y , w h e r e a s c e n t r a l n e u r o k i n i n B , derived f r o m the p r e p r o t a c h y k i n i n B gene, i n c r e a s e s the b l o o d p r e s s u r e m a i n l y via release o f v a s o p r e s s i n f r o m the pituitary.
28. Neuropeptides CHANGES IN SYNTHESES OF PEPTIDES IN RAT FACIAL MOTONEURONS AFTER FACIAL NERVE CRUSHING AND TRANSECTION. TAKANORI SAIKA 1 , EHIKO SENBA2 , KOICttI NOGUCHI2 AND HASAYA TOttYAMA2 , D e p a r t m e n t o f l O t o l a r y n g o l o g y and 2 A n a t o m y I I , O s a k a U n i v . Medical School. 1-1-50, Fukushima, Fukushtma-ku, Osaka 553, Japan. We h a v e e x a m i n e d t h e c h a n g e s of mRNAs c o d i n g f o r n e r v e g r o w t h f a c t o r r e c e p t o r (NGF-R), a a n d B - c a l c i t o n i n gene-related peptide (a a n d B-CGRP), c h o l e e y s t o k i n i n (CCK) and g a l a n i n in the facial motoneurons following nerve crushing and transection by u s i n g i n s i t u h y b r i d i z a t i o n histoehemistry. The l e v e l s o f mRNA f o r NGF-R, a-CGRP, CCK a n d g a l a n i n w e r e i n c r e a s e d w h i l e t h e B-CGRP mRNA l e v e l was decreased after axotomy. The l e v e l s o£ mRNAs f o r t h e s e s u b s t a n c e s returned to t h e c o n t r o l v a l u e s 2 - 4 weeks a f t e r n e r v e c r u s h i n g , whereas nerve transection had prolonged effects on t h e e x p r e s s i o n o f t h e s e mRNAs. Nerve transection h a d more prominent effects on B-CGRP, CCK, g a l a n i n mRNAs, w h i l e NGF-R mRNA was more profoundly
influenced
by nerve
crushing.
THE EFFECT OF MORPHINE ON CALCIUM DYNAMICS IN RAT HIPPOCAMPAL PREPARATIONS. TETSUO OHNISHIl , KIHACHI SAITOz AND REIZO INOKI2, IThe Second Department of Oral and M a x i l l o f a c i a t Surgery and 2Department of Pharmacology, Faculty of Dentistry, ~-s-aka U n i v e r s i t y , I - 8 Yamadaoka, Suita 565, Japan. The e f f e c t of morphine on calcium dynamics was studied in r a t hippocampal preparations. Rats were k i l l e d by decapitation and brains were quickly removed and p a r a s a g i t t a l s l i c e s containing the hippocampus were cut at a thickness of 300 ~m. In these hippocampal s l i c e s , morphine enhanced the amplitude of the f i e l d p o t e n t i a l s evoked in CAt pyramidal c e l l s . This e f f e c t of morphine was antagonized by calcium. GTPyS reduced the e f f e c t of morphine, whereas the e f f e c t of GDPBS was s i m i l a r to that of morphine. The conversion of 3H-nitrendipine binding to a low a f f i n i t y state was observed in membrane f r a c t i o n s prepared from s l i c e s treated with morphine. I t was also observed that GTPyS antagonized the e f f e c t of morphine, while the e f f e c t of GDPBS was s i m i l a r to that of morphine. These r e s u l t s suggest that morphine changes th~ a f f i n i t y of calcium channels to Caz• through GTP-binding proteins and reduces CaL÷ i n f l u x .
C E N T R A L C A R D I O V A S C U L A R R E G U L A T I O N O F T A C H Y K I N I N PEPTIDES: T H E SYMPATI-fl~TIC NERVOUS SYSTEM AND VASOPRESSIN P,ELEASE. YUKIO TAKANO, TETSUYA I4_AGIO*, YASUHISA NAKAYAMA*, RYO SAITO* T AKIRA NAGASHIMA* AND HIRO-O KAMIYA, Department of Pharmacology) Faculty of Pharmaceutical Sciences) Fukuoka University, Fukuoka 814-01, Japan. W e h a v e e x a m i n e d t h e m e c h a n i s m s o f c e n t r a l c a r d i o v a s c u l a r r e g u l a t i o n of t a c h y k i n i n peptides. Intracerebroventricular injections (i.c.v.) of tachykinin peptides caused dosed e p e n d e n t i n c r e a s e s in b l o o d p r e s s u r e a n d h e a r t rate in a n e s t h e t i z e d rats. T h e p r e s s o r r e s p o n s e s to s u b s t a n c e P (10lag, i.c.v.), n e u r o k i n i n A (10lag, i.c.v.) and n e u r o p e p t i d e y (l~tg, i.c.v.) w e r e b l o c k e d by p e r i p h e r a l a d m i n i s t r a t i o n o f p e n t o l i n i u m a n d p h e n t o l a m i n e . T h e p r e s s o r r e s p o n s e to the s e l e c t i v e n e u r o k i n i n B r e c e p t o r l i g a n d , s e n k t i d e (10~g, i.c.v.), was i n h i b i t e d b y p r e t r e a t m e n t with v a s o p r e s s i n V1 r e c e p t o r a n t a g o n i s t , a n d s e n k t i d e c a u s e d a n i n c r e a s e in p l a s m a v a s o p r e s s i n l e v e l . T h e s e r e s u l t s s u g g e s t t h a t c e n t r a l s u b s t a n c e P, n e u r o k i n i n A a n d n e u r o p e p t i d e 7, d e r i v e d f r o m the p r e p r o t a c h y k i n i n A g e n e , i n c r e a s e the blood p r e s s u r e and h e a r t rate v i a s y m p a t h e t i c n e r v e a c t i v i t y , w h e r e a s c e n t r a l n e u r o k i n i n B , derived f r o m the p r e p r o t a c h y k i n i n B gene, i n c r e a s e s the b l o o d p r e s s u r e m a i n l y via release o f v a s o p r e s s i n f r o m the pituitary.