$39 SYMPATHETIC NERVE RHYTHMS DURING MORPHINE-INDUCED PHRENIC NERVE QUIESCENCE. NAOFUMI KIMURA, KAZUO TAKANO~ FUSAO KATO, YOKO FUJIWARA t AND TAKEHIKO :FUKUHARA I Department o f Pharmacology II, The Jikei University School of Medicine~ 3-25-8 Nishi-Shinbashi, Minato-ku~ Tokyo i05~ Japan. The sympathetic nerve rhythms during the phrenic nerve quiescence induced by morphine (6-14 mg/kg, i.v.) were studied using spectral analyses. Vagotomized rabbits were anesthetized with urethane (0.9-1.0 g/kg, i.p.), immobilized, and artificially ventilated. Efferent discharges of the renal and phrenic nerves were recorded. Carotid sinus nerves were intact and depressor nerves were cut. Cardiac-related rhythm (3-6 Hz) synchronized with the pulse wave and slower sympathetic rhythms (0.5-2 Hz) around the phrenic respiratory cycle were observed in the renal sympathetic nerve discharge (SND). Before the administration of morphine, a major component of the slow sympathetic rhythms was locked in a i:i relation to the phrenic cycle and a minor component was related to the blood pressure fluctuation (0.75 Hz) induced by artificial ventilation (pump-related rhythm). When the phrenic respiratory discharge was stopped by morphine, the slow sympathetic rhythm synchronized with a phrenic respiratory cycle disappeared and the cardiac-related and pump-related components in SND increased in the animals showing slight changes in arterial pressure. In animals with noticeable hypotension after morphine, the cardiac-related and pump-related rhythms were abolished and slow sympathetic rhythms (0.5-2 Hz) which were uncorrelated with the above rhythms were observed in SND. The slow sympathetic rhythm with a phrenic cycle reappeared after naloxone (0.1-4 mg/kg). These results suggest that the central neural mechanisms responsible for SND are capable of generating inherent rhythms and synchronizing with the major periodic inputs from the baroreceptors and/or respiratory oscillator.
ACETYLCHOLINE(ACh) RELEASE IN C E R E B R A L C O R T E X I N C R E A S E S IN R E S P O N S E TO FOCAL S T I M U L A T I O N OF N U C L E U S B A S A L I S OF M E Y N E R T (NBM) A N D S O M A T I C S E N S O R Y S T I M U L A T I O N . MIEKO KUROSAWA, A K I O SATO, Y U K O SATO, D e p a r t m e n t of P h y s i o l o g y , Tokyo Metrop o l i t a n I n s t i t u t e of G e r o n t o l o g y , 35-2 S a k a e c h o , I t a b a s h i k u , T o k y o 173, Japan. C e r e b r a l c o r t i c a l b l o o d f l o w r e p o r t e d l y i n c r e a s e s f o l l o w i n g focal s t i m u l a t i o n of the NBM, and the i n c r e a s e d response is m a r k e d l y attenuated following administration of c h o l i n e r g i c b l o c k i n g a g e n t s in rats (i). Furthermore, somatic s e n s o r y s t i m u l a t i o n e x c i t e s n e u r o n a l a c t i v i t y of the NBM. These results suggest that t h e s e s t i m u l a t i o n s m a y i n c r e a s e r e l e a s e of A C h in the cortex. Our present experiments examined the e f f e c t s of t h e s e s t i m u l a t i o n s on extracellular ACh release in c e r e b r a l c o r t e x in rats a n e s t h e t i z e d w i t h h a l o t h a n e . ACh in the c o r t e x was m e a s u r e d by a m i c r o d i a l y s i s . A C h r e l e a s e in c e r e b r a l p a r i e t a l c o r t e x under resting conditions was approximately 0.5-1.0 pmol/20~l-10min. ACh release was increased by e l e c t r i c a l or c h e m i c a l s t i m u l a t i o n of NBM (2), and also by cutaneous p i n c h i n g or b r u s h i n g s t i m u l a t i o n of a h i n d l i m b . The i n c r e a s e in A C h r e l e a s e in the c o r t e x a f t e r s t i m u l a t i o n of the N B M or of s o m a t i c a f f e r e n t s seems to result from increased release of A C h from the cortical terminals of cholinergic nerve fibers originating in the NBM. References:(1) B i e s o l d , D., Inanami, 0., Sato, A. a n d Sato, Y., N e u r o s c i . Lett., 98, 39-44, 1989. (2) K u r o s a w a , M., Sato, A. a n d Sato, Y., Neurosci. Lett., 98, 45-50, 1989.
NEURONAL ACTIVITY OF THE NUCLEUS BASALIS OF MEYNERT ( N B M ) IS I N C R E A S E D BY N O C I C E P T I V E S T I M U L A T I O N OF P A W S IN A N E S T H E T I Z E D RATS. T A K A O A K A I S H I .I . A K I O SATO2o 1 D e p t . of P h y s i o l . , Niiqata Univ. School of M e d i c i n e ° Niiaata 951. 2 D e n t . of Physiol., Tokyo Metropolitan Inst. of G e r o n t o l , . I t a b a s h i k u ° T o k y o 173. A s e r i e s of o u r s t u d i e s h a s s h o w n t h a t t h e c h o l i n e r g i c neuronal mechanism o r i g i n a t i n g f r o m the N B M is i n v o l v e d in i n c r e a s e s in c e r e b r a l c o r t i c a l b l o o d f l o w following mechanical nociceptive stimulation of the skin. T h e p r e s e n t s t u d y w a s undertaken to d e t e r m i n e whether neuronal activity of t h e N B M is i n f l u e n c e d by m e c h a n i c a l s t i m u l a t i o n of skin. T h e e x p e r i m e n t s were performed using 9 male Wistar rats anesthetized with urethane (1.1 g / k g B.W., i.p.). E l e c t r i c a l activity of a single neuron in t h e N B M w a s r e c o r d e d extracellularly using a glass microe l e c t r o d e i n s e r t e d into the N B M s t e r e o t a x i c a l l y . T h e n e u r o n in the N B M p r o j e c t i n g its a x o n to the p a r i e t a l c o r t e x w a s i d e n t i f i e d by a n t i d r o m i c a l l y stimulating the axon using bipolar stimulating e l e c t r o d e s p l a c e d in the p a r i e t a l cortex. B r u s h i n g stimulation to s k i n of f a c e , f o r e l i m b , back or hindlimb did not produce any s i g n i f i c a n t c h a n g e in n e u r o n a l activity. In c o n t r a s t , p i n c h i n g s t i m u l a t i o n to s k i n of f o r e p a w or h i n d p a w induced a significant (p<0.01, p a i r e d t - t e s t ) i n c r e a s e in a c t i v i t y . P i n c h i n g of the face or b a c k s k i n w a s not e f f e c t i v e .