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Contribution of intracellular Ca release to the spike after-hyperpolarization in rat superior cervical ganglion
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16. EEG and evoked potentials C O N T R I B U T I O N O F I N T R A C E L L U L A R Ca R E L E A S E TO T H E S P I K E , A F T E R - H Y P E R P O L A R I Z A T I O ~ I IN R A T S U P E R I O R C E R V I C A L G A N G L I O N . T O M O Y U K I K A W A I AND M I N O R U W A T A N A B E , D e p a r t m e n t of Chemical Ph~rma¢olow. Faculty of Pharmaceutical Sciences. Nagoya Citv University. 3-1 Tanabed0hri, Mizuho-ku, 467 Nagoya. Jaoan. The characteristics of-the after-hyperpolarization (AH) following an action potential in rat superior cervical ganglion were examined by intracellular recording to determine the source of increasing intraceUular free Ca. The A H was maximally but not completely depressed by 1)aM ryanodine, and was augmented by 2mM caffeine but was not affected by caffeine in the presence of ryanodine. The Ca-spike in the presence of TTX and T E A was not inhibited by ryanodine. The ryanodine-sensitive component of the A H was depressed in a frequency-dependent m a n n e r when action potentials were evoked at frequencies between 0.1 and 2Hz. Half maximal depression was caused at 0.5Hz. The time-course of the depression at 1Hz roughly fitted an exponential curve with a time constant of 3s. Half recovery from the depression induced by stimulation at 2Hz was observed ca. 10s after the last stimulation. The spontaneously occurring rhythmic hyperpolarizations (SH) observed in some cells were facilitated by caffeine and abolished by ryanodine. During continuous stimulation at 0.1Hz, the A H was depressed after an event of the SH and thereafter gradually recovered before the next SH. After conditioning stimuli at 2Hz, the time to generate first SH was similar to the full recovery time of the A H from the depression. These results suggest that the mechanism of Ca release from store sites contributes to increase the intracellular free Ca concentration during A H in rat sympathetic neurons. The depletion of stored Ca during repetitive stimulation may frequency-dependently depress the AH.
D I P O L E - T R A C I N G OF A B N O R M A L SLOW BRAIN POTENTIAL A F T E R CEREBRAL STROKE. SABURO HOMMA, YOSHIO NAKAJIMA, T O S H I M I T S U M U S H A *I, and Y O S H I O W OKAMOTO *I, Department of Physiology, School of Medicine, Chiba University, 1-8-1 Inohana, Chiba 280 and iDepartment of A p p l i e d Electronics, Tokyo Institute of Technoloqy, 4259 Nagatsuta-cho, Midori-ku, Yokohama 227, Japan. We estimated the location of an electric source generator (e.g. a current dipole) in human brain, using a new c o m p u t e r - a i d e d method. A c t i v i t y of a neuronal structure in the brain was r e p r e s e n t e d as one equivalent dipole. This method, called the d i p o l e - t r a c i n g (DT), enabled us to estimate the location and vector moment of the dipole. In the present study, abnormal, big and slow potentials were recorded from a patient with cerebral infarction under resting condition and byperventilation. H y p e r v e n t i l a t i o n enhanced the abnormal activity. The abnormal electrical activity under these conditions was c a l c u l a t e d by DT and the e s t i m a t e d locations were compared with abnormal regions revealed by MRI and PET (oxygen c o n s u m p t i o n rate). DT analysis showed that the dipole of the slow wave is located at the fronto-orbital a s s o c i a t i o n cortex n e i g h b o r i n g the affected region, and indicated high oxygen consumption rate. The enhanced potential by h y p e r v e n t i l a t i o n was located a p p r o x i m a t e l y 30 mm above the region obtained with resting condition.
EFFECT OF CLOSINGEYELIDS ON q}IE NEONATALDEVELOP~NTOF VISION; EVALUATEDBY PRIMARYAND SECONDARYEVOKEDPOTENTIAL TARO OKAHOTO'. (SflIFID/[ITAK~SHI(7~.~ DeDartaent of Physiolosy~ School of Medicine~ ShowaUniversity, I ~-~ gatanodai~
$bina~awa-kn, Tokyo 142. Japan, Development of vision obviously depends not only on development of the visual cortex but also on the perception process of vision. Whenvisual evoked potentiaIs (YEP) are used as indications of visual sensation) the primary and secondary evoked potentials are those of the visual cortex and whole cortex, respectively. We examined the neonatal development of visual sensation by recording both primary and secondary evoked potentials.
YEP were recorded by cranial surface plate electrodes bipolarly between Pz and Inion corresponding regions using the ten-twenty recording methods for electroencephalogram. Flash light was applied from a hole on top of a box in which animals were unanesthetized and unrestricted. Secondary VEP was classified from primary YEP by latency of VEP with around lOOmsec. Development of neuronal activities in the visual cortex is reportedly profoundly influenced by eyelid closure during the critical period, a few days at the beginning of the fourth week after birth. In the present experiaents: 1) Eyelids were closed at 2 weeks after birth for 2 weeks, 2) at 4 weeks after birth for 3 or 7 weeks, or 3) at 2 weeks after birth for 4 weeks. Primary VEP appeared 2. 5 weeks after birth, developed gradually, reached maximumat 5 weeks after birth and then remained stable. Secondary YEP appeared 3 weeks after birth and was unstable, depending on the state of the animals during experimental periods up to 12 weeks. Development of primaryVEP was transiently depressed during eyelid closure, but it was evoked and developed gradually to control level after eyelids were opened. On the other hand, secondary YEP was not induced during eyelid closure. In eyelid closures 1) and 2), the reappearanceof secondary VEP after eyelids were opened was very slow, but it did recover to control level 50-120 days later. However,in eyelid closure 3), secondary VEP never recovered. The perception process seems to be more influenced by eyelid closure than the process of visual cortex.
16. EEG and evoked potentials C O N T R I B U T I O N O F I N T R A C E L L U L A R Ca R E L E A S E TO T H E S P I K E , A F T E R - H Y P E R P O L A R I Z A T I O ~ I IN R A T S U P E R I O R C E R V I C A L G A N G L I O N . T O M O Y U K I K A W A I AND M I N O R U W A T A N A B E , D e p a r t m e n t of Chemical Ph~rma¢olow. Faculty of Pharmaceutical Sciences. Nagoya Citv University. 3-1 Tanabed0hri, Mizuho-ku, 467 Nagoya. Jaoan. The characteristics of-the after-hyperpolarization (AH) following an action potential in rat superior cervical ganglion were examined by intracellular recording to determine the source of increasing intraceUular free Ca. The A H was maximally but not completely depressed by 1)aM ryanodine, and was augmented by 2mM caffeine but was not affected by caffeine in the presence of ryanodine. The Ca-spike in the presence of TTX and T E A was not inhibited by ryanodine. The ryanodine-sensitive component of the A H was depressed in a frequency-dependent m a n n e r when action potentials were evoked at frequencies between 0.1 and 2Hz. Half maximal depression was caused at 0.5Hz. The time-course of the depression at 1Hz roughly fitted an exponential curve with a time constant of 3s. Half recovery from the depression induced by stimulation at 2Hz was observed ca. 10s after the last stimulation. The spontaneously occurring rhythmic hyperpolarizations (SH) observed in some cells were facilitated by caffeine and abolished by ryanodine. During continuous stimulation at 0.1Hz, the A H was depressed after an event of the SH and thereafter gradually recovered before the next SH. After conditioning stimuli at 2Hz, the time to generate first SH was similar to the full recovery time of the A H from the depression. These results suggest that the mechanism of Ca release from store sites contributes to increase the intracellular free Ca concentration during A H in rat sympathetic neurons. The depletion of stored Ca during repetitive stimulation may frequency-dependently depress the AH.
D I P O L E - T R A C I N G OF A B N O R M A L SLOW BRAIN POTENTIAL A F T E R CEREBRAL STROKE. SABURO HOMMA, YOSHIO NAKAJIMA, T O S H I M I T S U M U S H A *I, and Y O S H I O W OKAMOTO *I, Department of Physiology, School of Medicine, Chiba University, 1-8-1 Inohana, Chiba 280 and iDepartment of A p p l i e d Electronics, Tokyo Institute of Technoloqy, 4259 Nagatsuta-cho, Midori-ku, Yokohama 227, Japan. We estimated the location of an electric source generator (e.g. a current dipole) in human brain, using a new c o m p u t e r - a i d e d method. A c t i v i t y of a neuronal structure in the brain was r e p r e s e n t e d as one equivalent dipole. This method, called the d i p o l e - t r a c i n g (DT), enabled us to estimate the location and vector moment of the dipole. In the present study, abnormal, big and slow potentials were recorded from a patient with cerebral infarction under resting condition and byperventilation. H y p e r v e n t i l a t i o n enhanced the abnormal activity. The abnormal electrical activity under these conditions was c a l c u l a t e d by DT and the e s t i m a t e d locations were compared with abnormal regions revealed by MRI and PET (oxygen c o n s u m p t i o n rate). DT analysis showed that the dipole of the slow wave is located at the fronto-orbital a s s o c i a t i o n cortex n e i g h b o r i n g the affected region, and indicated high oxygen consumption rate. The enhanced potential by h y p e r v e n t i l a t i o n was located a p p r o x i m a t e l y 30 mm above the region obtained with resting condition.
EFFECT OF CLOSINGEYELIDS ON q}IE NEONATALDEVELOP~NTOF VISION; EVALUATEDBY PRIMARYAND SECONDARYEVOKEDPOTENTIAL TARO OKAHOTO'. (SflIFID/[ITAK~SHI(7~.~ DeDartaent of Physiolosy~ School of Medicine~ ShowaUniversity, I ~-~ gatanodai~
$bina~awa-kn, Tokyo 142. Japan, Development of vision obviously depends not only on development of the visual cortex but also on the perception process of vision. Whenvisual evoked potentiaIs (YEP) are used as indications of visual sensation) the primary and secondary evoked potentials are those of the visual cortex and whole cortex, respectively. We examined the neonatal development of visual sensation by recording both primary and secondary evoked potentials.
YEP were recorded by cranial surface plate electrodes bipolarly between Pz and Inion corresponding regions using the ten-twenty recording methods for electroencephalogram. Flash light was applied from a hole on top of a box in which animals were unanesthetized and unrestricted. Secondary VEP was classified from primary YEP by latency of VEP with around lOOmsec. Development of neuronal activities in the visual cortex is reportedly profoundly influenced by eyelid closure during the critical period, a few days at the beginning of the fourth week after birth. In the present experiaents: 1) Eyelids were closed at 2 weeks after birth for 2 weeks, 2) at 4 weeks after birth for 3 or 7 weeks, or 3) at 2 weeks after birth for 4 weeks. Primary VEP appeared 2. 5 weeks after birth, developed gradually, reached maximumat 5 weeks after birth and then remained stable. Secondary YEP appeared 3 weeks after birth and was unstable, depending on the state of the animals during experimental periods up to 12 weeks. Development of primaryVEP was transiently depressed during eyelid closure, but it was evoked and developed gradually to control level after eyelids were opened. On the other hand, secondary YEP was not induced during eyelid closure. In eyelid closures 1) and 2), the reappearanceof secondary VEP after eyelids were opened was very slow, but it did recover to control level 50-120 days later. However,in eyelid closure 3), secondary VEP never recovered. The perception process seems to be more influenced by eyelid closure than the process of visual cortex.