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Difference between D1 and D2 receptors for regulating dopamine release in the cadate-putamen
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IN VIVO VOLTAMMETRIC STUDY OF KAINATE-INDUCED NEURONAL DEGRADATION IN T I l E RAT STRIATUM. TAIZO NAKAZATO l AND AKITANE AKIYAMA .2, 1Department of Physiology, Juntendo Uuiversity School of Medicine, 2-1-1 Honso, Bunkyo-ku, Tokyo 113 and 2Department of Electronic Chemistry, Graduate School at Nagatsuta, Tokyo Institute of Technolosy, Yokohama 227, Japan. This study was designed to investigate the mechanism of neuronal degradation induced by kainate using microcomputer-controlled in vivo voltammetry. Carbon fiber electrodes (IITA-7, 7tLm in diameter) were implanted bilaterally in the rat striatum, and a stainless-steel cannula was inserted into the unilateral striatum for ]esioni~g by kainate. Kainate (2pg,/pl, 30 ,nin) was injected intrastriatally to freely moving rats. Dopamine (DA) and 5-hydroxytryptamine were released 1 hr after the start of the injection. The releases reached a macimum after 4-5 hr, and continued for about a month. When L-DOPA (]00mg/kg, i.p.) was administered to the kainate-treated rat 45 days after the kainate injection, the conversion of L-DOPA to DA was equal to that in the pretreated rat adnfinistered at 7 days (7 days before the kainate injection). These results suggested that the function of the L-DOPA conversion was not impaired, although a large amount of DA was released for a long time by the kainate injection.
D I F F E R E N C E B E T W E E N Dx A N D D2 R E C E P T O R S FOR R E G U L A T I N G D O P A M I N E R E L E A S E IN THE C A D A T E - P U T A M E N . KOUICHI KURATA, R Y O K O SHIBATA AND M A S A Y O S H I KURACHI', D e p a r t m e n t of Neuropsychiatry, Faculty of Medicine, Toyama Medical and P h a r m a c e u t i c a l University, 2630 S u g i t a n i , T o y a m a 930-01, Japan. First, the effects of three kind of d o p a m i n e ( D A ) agonists, a p o m o r p h i n e ( A P 0 ) , SKF-38393 and quinpirole(QPL), on D A release w e r e e x a m i n e d in the c a u d a t e - p u t a m e n (CPu) of free m o v i n g rats by m i c r o d i a l y s i s d u r i n g local a d m i n i s t r a t i o n of these chemicals. Infusion of 10-4M of A P 0 and 10-SM of SKF-38393 induced a brief increase in DA release followed by a m a r k e d decrease. These p h e n o m e n o n w e r e sensitive to tetrodotoxin. QPL reduced D A release w i t h o u t s h o w i n g a t r a n s i e n t increase. Next, effects of DI and D= antagonists, SCH-23390 and sulpiride, on the transient increase of DA release induced by both 10-4M of A F O and 10-SM of SKF-38393 were investigated. Infusion of 10-SM and 10-6M of SCH-23390 s u p p r e s s e d the brief increase in DA release. On the o t h e r hand, 10-SM and 10-6M of s u l p i r i d e e x e r t e d a little or no effect. These results indicated that Dx and DR have opposite effects on DA release in the CPu, and that the transient increase by D A agonists is related to Dx receptors.
INFLUENCE OF ANESTHETICS ON RAT STRIATAL ACETYLCHOLINE OUTPUT IN VIVO. HIROSHI WATANABE, S e c t i o n of Pharmacology, R e s e a r c h Institute for W a k a n - Y a k u (Oriental Medicine), Toyama Medical and Pharmaceutical University, Toyama, 930-01, Japan. We have shown that striatal a c e t y l c h o l i n e (ACh) o u t p u t correlates well w i t h the level of spontaneous m o t o r activity in freely moving rats as studied by brain dialysis. The present study c o m p a r e d the effects of anesthetics (chloral hydrate, pentobarbital, urethane and halothane) on rat striatal ACh output, and the effect of a p o m o r p h i n e in a n e s t h e t i z e d and freely m o v i n g rats. The basal level of ACh in the striatal dialysates d i f f e r e d among the four anesthetics. The b a s a l level was the lowest under halothane anesthesia. Apomorphine (0.i - 3.0 mg/kg, i.p.) d e c r e a s e d the striatal ACh output d o s e - d e p e n d e n t l y under urethane a n e s t h e s i a (1.3 g/kg, i.p.) and the effect was b l o c k e d by h a l o p e r i d o l (2.5 mg/kg, i.p.). In freely moving rats, apomorphine (3 mg/kg, i.p.) caused a slight increase followed by a slight decrease in the A C h output. These results indicate that the effect of the anesthetics on the rat striatal ACh output is quite different among them and the effect of apomorphine is m a s k e d by its b e h a v i o r a l effect.
IN VIVO VOLTAMMETRIC STUDY OF KAINATE-INDUCED NEURONAL DEGRADATION IN T I l E RAT STRIATUM. TAIZO NAKAZATO l AND AKITANE AKIYAMA .2, 1Department of Physiology, Juntendo Uuiversity School of Medicine, 2-1-1 Honso, Bunkyo-ku, Tokyo 113 and 2Department of Electronic Chemistry, Graduate School at Nagatsuta, Tokyo Institute of Technolosy, Yokohama 227, Japan. This study was designed to investigate the mechanism of neuronal degradation induced by kainate using microcomputer-controlled in vivo voltammetry. Carbon fiber electrodes (IITA-7, 7tLm in diameter) were implanted bilaterally in the rat striatum, and a stainless-steel cannula was inserted into the unilateral striatum for ]esioni~g by kainate. Kainate (2pg,/pl, 30 ,nin) was injected intrastriatally to freely moving rats. Dopamine (DA) and 5-hydroxytryptamine were released 1 hr after the start of the injection. The releases reached a macimum after 4-5 hr, and continued for about a month. When L-DOPA (]00mg/kg, i.p.) was administered to the kainate-treated rat 45 days after the kainate injection, the conversion of L-DOPA to DA was equal to that in the pretreated rat adnfinistered at 7 days (7 days before the kainate injection). These results suggested that the function of the L-DOPA conversion was not impaired, although a large amount of DA was released for a long time by the kainate injection.
D I F F E R E N C E B E T W E E N Dx A N D D2 R E C E P T O R S FOR R E G U L A T I N G D O P A M I N E R E L E A S E IN THE C A D A T E - P U T A M E N . KOUICHI KURATA, R Y O K O SHIBATA AND M A S A Y O S H I KURACHI', D e p a r t m e n t of Neuropsychiatry, Faculty of Medicine, Toyama Medical and P h a r m a c e u t i c a l University, 2630 S u g i t a n i , T o y a m a 930-01, Japan. First, the effects of three kind of d o p a m i n e ( D A ) agonists, a p o m o r p h i n e ( A P 0 ) , SKF-38393 and quinpirole(QPL), on D A release w e r e e x a m i n e d in the c a u d a t e - p u t a m e n (CPu) of free m o v i n g rats by m i c r o d i a l y s i s d u r i n g local a d m i n i s t r a t i o n of these chemicals. Infusion of 10-4M of A P 0 and 10-SM of SKF-38393 induced a brief increase in DA release followed by a m a r k e d decrease. These p h e n o m e n o n w e r e sensitive to tetrodotoxin. QPL reduced D A release w i t h o u t s h o w i n g a t r a n s i e n t increase. Next, effects of DI and D= antagonists, SCH-23390 and sulpiride, on the transient increase of DA release induced by both 10-4M of A F O and 10-SM of SKF-38393 were investigated. Infusion of 10-SM and 10-6M of SCH-23390 s u p p r e s s e d the brief increase in DA release. On the o t h e r hand, 10-SM and 10-6M of s u l p i r i d e e x e r t e d a little or no effect. These results indicated that Dx and DR have opposite effects on DA release in the CPu, and that the transient increase by D A agonists is related to Dx receptors.
INFLUENCE OF ANESTHETICS ON RAT STRIATAL ACETYLCHOLINE OUTPUT IN VIVO. HIROSHI WATANABE, S e c t i o n of Pharmacology, R e s e a r c h Institute for W a k a n - Y a k u (Oriental Medicine), Toyama Medical and Pharmaceutical University, Toyama, 930-01, Japan. We have shown that striatal a c e t y l c h o l i n e (ACh) o u t p u t correlates well w i t h the level of spontaneous m o t o r activity in freely moving rats as studied by brain dialysis. The present study c o m p a r e d the effects of anesthetics (chloral hydrate, pentobarbital, urethane and halothane) on rat striatal ACh output, and the effect of a p o m o r p h i n e in a n e s t h e t i z e d and freely m o v i n g rats. The basal level of ACh in the striatal dialysates d i f f e r e d among the four anesthetics. The b a s a l level was the lowest under halothane anesthesia. Apomorphine (0.i - 3.0 mg/kg, i.p.) d e c r e a s e d the striatal ACh output d o s e - d e p e n d e n t l y under urethane a n e s t h e s i a (1.3 g/kg, i.p.) and the effect was b l o c k e d by h a l o p e r i d o l (2.5 mg/kg, i.p.). In freely moving rats, apomorphine (3 mg/kg, i.p.) caused a slight increase followed by a slight decrease in the A C h output. These results indicate that the effect of the anesthetics on the rat striatal ACh output is quite different among them and the effect of apomorphine is m a s k e d by its b e h a v i o r a l effect.