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Stimulation of nucleus basalis of Meynert increases cerebral cortical blood flow in rats
$36 STIMULATION OF NUCLEUS BASALIS OF MEYNERT INCREASES CEREBRAL CORTICAL BLOOD FLOW IN RATS. DIETMAR BIESOLD, OSAMU I N A N A M I , A K I n SATO AND Y U K O SATO, Department __°f P h y s i o l o g y ~ Tokyo Metropolitan Institute o.,ff G e r o n t o l o g y , 35-2 Sakaecho, Itabashiku, T o k y o 173, Japan The magnocellular nucleus of the basal forebrain (nucleus b a s a l is of Meynert; NBM) consists mainly of cholinergic neurons projecting their axons to the cortex, Recently, small blood vessels in r a t c e r e b r a l cortex have been reported to receive innervations of the cholinergic fibers from the NBM. We examined whether the CBF of the cortex is r e g u l a t e d by the cholinergic neurons f r o m NBM, The CBF o f p a r i e t a l c o r t e x was m e a s u r e d by laser Doppler flowmetry in u r e t h a n e - a n e s t h e t i z e d rat. Focal electrical stimulation o f t h e NBM or a microinjection of L-glutamate ( 5 0 n m o l ) i n t o t h e NBM i n c r e a s e d CBF in the parietal cortex, Vasodilative responses were observed only in cortex ipsi lateral to the site of stimulation. Furthermore, the vasodilative responses were almost abolished by i n t r a v e n o u s administrations of muscarinic and nicotinic cholinergic blocking agents (atropine O . 5 m g / k g and mecamylamine 2mg/k @). This suggests that the eholinergic projeotons to the parietal cortex f r o m t h e NBM c o n t r i b u t e to vasodilation of the cortex by a c t i v a t i n g muscarinic and n i c o t i n i c cholinergic receptors.
GLUCOSE RESPONSIVE NEURONS WITHIN RAT AREA POSTREMA . AKIRA ADACHI', NORIHIRO MIYOSHI'' AND TOMOKO T O G I Y A M A 'I , * D e p a r t m e n t of Physiology and 'The First Department of O r a l a n d M a x i l l o f a c i a l Surgery, Okayama University Dental School, 2-5-i S h i k a t a - c h o , O k a y a m a 700, Japan. Electrophysiological analysis has revealed three types of che~mosensitive neurons within area postrema: i) glucose responsive neurons, 2) sodium (osmotic pressure) responsive neurons, 3) e m e t i c d r u g r e s p o n s i v e neurons. The present study delineates characteristic features of the glucose responsive neurons in this structure. Two types of glucose responsive neuron were identified: one decreases the d i s c h a r g e r a t e in r e s p o n s e to g l u c o s e (glucose s e n s i t i v e type) a n d the o t h e r b e h a v e s in the o p p o s i t e w a y ( g l u c o r e c e p t o r type). M a n n o s e h a d no e f f e c t o n e i t h e r t y p e of neuron, so t h e s e r e s p o n s e s a r e g l u c o s e specific. In g e n e r a l , the g l u c o s e s e n s i t i v e t y p e n e u r o n s a r e s i m i l a r to t h o s e in the l a t e r a l h y p o t h a l a m i c a r e a a n d the g l u c o r e c e p t o r t y p e o n e s a r e s i m i l a r to those in the ventromedial nucleus. These neurons may play a part in the r e g u l a t i o n of b l o o d g l u c o s e h o m e o s t a s i s .
INSlHITION OF RENAL SYMPATHETIC nERVE ACTIVITY B~ INTRACEREBROVENTRICULAR ADMINISTRATION OF ANGIOTENSIN II IN RATS. HIROSHI KANNAN~ JI XIU JIN AND HIROSHI YAMASHITA a Dept. Physiol. I Univ. of 0ccup. Environ. Health, Seh. Med,, Kitak~ushu 807j Japan ---Angiotensin II (All) produces centrally mediated pressor response. The mechanism of this response consists of at least two components mediated by activation of sympathetic nerve activiy and by r e l e a s e of v a s o p r e s s i n f r o m the n e u r o h y p o p h y s i s . However, the e f f e c t s of intracerebroventricular (i.e.v.) administration of AII on the sympathetic nervous system bj direct recording of nerve activity are controversial. We reexamined the effects of i.c.v. AII on renal sympathetic nerve activity (RSNA), arterial pressure, and heart rate in unanesthetized rats.Administration of AII (lOng) through chronically implanted cannula evoked decreases in RSNA (45.1 + 5.9X) and heart rate (24.5 ! 5.3 beats/mln) and an increase in arterial pressure (22.1 + 2.5 mm-Hg). M a x i m u m changes in these responses were I-2 min after i.c.v, administration of AIIU These changes returned to control levels approximately 30 min after the administration. Prior i.c.v, administration of AII antagonist, saralasin (200 ng), greatly attenuated the responses induced by i.c.v. AII (10 rig). To examine the possibility that the inhibitory response in RSNA is due to barorsceptor activation, baroreceptor-denervated (SAD) rats anesthetized with a mixture of urethane (700 mg/Kg) and~-chloralose (70 mg/Kg) i.p. were used. In the SAD rats, the decrease in RSNA persisted in the same magnitude as in the intact anesthetized rats. These results suggest that central AII directly inhibits RSNA via AII specific receptors. This finding does not support the hypothesis that a generalized sympathetic activation contributes to the central AII-induced pressor response.
GLUCOSE RESPONSIVE NEURONS WITHIN RAT AREA POSTREMA . AKIRA ADACHI', NORIHIRO MIYOSHI'' AND TOMOKO T O G I Y A M A 'I , * D e p a r t m e n t of Physiology and 'The First Department of O r a l a n d M a x i l l o f a c i a l Surgery, Okayama University Dental School, 2-5-i S h i k a t a - c h o , O k a y a m a 700, Japan. Electrophysiological analysis has revealed three types of che~mosensitive neurons within area postrema: i) glucose responsive neurons, 2) sodium (osmotic pressure) responsive neurons, 3) e m e t i c d r u g r e s p o n s i v e neurons. The present study delineates characteristic features of the glucose responsive neurons in this structure. Two types of glucose responsive neuron were identified: one decreases the d i s c h a r g e r a t e in r e s p o n s e to g l u c o s e (glucose s e n s i t i v e type) a n d the o t h e r b e h a v e s in the o p p o s i t e w a y ( g l u c o r e c e p t o r type). M a n n o s e h a d no e f f e c t o n e i t h e r t y p e of neuron, so t h e s e r e s p o n s e s a r e g l u c o s e specific. In g e n e r a l , the g l u c o s e s e n s i t i v e t y p e n e u r o n s a r e s i m i l a r to t h o s e in the l a t e r a l h y p o t h a l a m i c a r e a a n d the g l u c o r e c e p t o r t y p e o n e s a r e s i m i l a r to those in the ventromedial nucleus. These neurons may play a part in the r e g u l a t i o n of b l o o d g l u c o s e h o m e o s t a s i s .
INSlHITION OF RENAL SYMPATHETIC nERVE ACTIVITY B~ INTRACEREBROVENTRICULAR ADMINISTRATION OF ANGIOTENSIN II IN RATS. HIROSHI KANNAN~ JI XIU JIN AND HIROSHI YAMASHITA a Dept. Physiol. I Univ. of 0ccup. Environ. Health, Seh. Med,, Kitak~ushu 807j Japan ---Angiotensin II (All) produces centrally mediated pressor response. The mechanism of this response consists of at least two components mediated by activation of sympathetic nerve activiy and by r e l e a s e of v a s o p r e s s i n f r o m the n e u r o h y p o p h y s i s . However, the e f f e c t s of intracerebroventricular (i.e.v.) administration of AII on the sympathetic nervous system bj direct recording of nerve activity are controversial. We reexamined the effects of i.c.v. AII on renal sympathetic nerve activity (RSNA), arterial pressure, and heart rate in unanesthetized rats.Administration of AII (lOng) through chronically implanted cannula evoked decreases in RSNA (45.1 + 5.9X) and heart rate (24.5 ! 5.3 beats/mln) and an increase in arterial pressure (22.1 + 2.5 mm-Hg). M a x i m u m changes in these responses were I-2 min after i.c.v, administration of AIIU These changes returned to control levels approximately 30 min after the administration. Prior i.c.v, administration of AII antagonist, saralasin (200 ng), greatly attenuated the responses induced by i.c.v. AII (10 rig). To examine the possibility that the inhibitory response in RSNA is due to barorsceptor activation, baroreceptor-denervated (SAD) rats anesthetized with a mixture of urethane (700 mg/Kg) and~-chloralose (70 mg/Kg) i.p. were used. In the SAD rats, the decrease in RSNA persisted in the same magnitude as in the intact anesthetized rats. These results suggest that central AII directly inhibits RSNA via AII specific receptors. This finding does not support the hypothesis that a generalized sympathetic activation contributes to the central AII-induced pressor response.