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1424 Pentobarbital anesthesia facilitates induction of long-term synaptic potentiation(LTP) in the hippocampus
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1423
MATURATION OF THE ADENOSINE RECEPTOR AND ITS ROLE IN SYNAPTIC PLASTICITY IN THE RAT HIPPOCAMPUS. YUKO SEKINO1, YOSHIKO SAITOH1, R1TSUKO OHTANI-KANEKOZ, H1ROYASU NAKATA,, YOICHIRO KURODA', ,Dept. of Mol. & Cell. Neurobiol., Tokyo Metropolitan Institute for Nenroscience, Fuchu-shi, Tokyo 183 and 2Dept. of Anatomy, St. Marianna Univ. School of Medicine, Miyamae-ku, Kawasaki 216, Japan.
Long-term potentiation (LTP) and post-tetanic depression (PTD) in hippocampus have been proposed as impotant processes underlying memory. Memory processes are generally thought to change during maturation, therefore, cellular mechanisms that influence LTP and PTD might also change during development. We previously reported that endogenous adenosine released with neurotransmitter plays an essential role in the induction of LTP and FTD in rat hippocampal slices. In order to evaluate developmental changes in the cellular mechanisms underlying memory processes, our study has focused on the adenosine rcceptor and its role in the induction of LTP and PTD. We measured the adenosine binding activity of hippocarnpal membrane prepared from immature and mature rat brain. The activity of AI adenosine receptor increased gradually during the first 2 postnatal weeks and appeared to reach saturation by the third week. Application of the A1 antagonist, 8-cyclopentyltheophylline, increased the synaptic responses of neurons within the CA1 region of slices taken from adult rats. However, the same treatment failed to increase responses and inhibiled the induction of LTP in immature hippocampal slices. Such age-dependent electrophysiological responses may, therefore, depend on the maturation of adenosine receptors. We speculate that the age related changes in adenosine receptors may play a role in the maturation of synaptic plasticity in the hippocampus, and this underlie some of the developmental changes in memory processes.
1424
PENTOBARBITAL ANESTHESIA FACILITATES INDUCTION OF L O N G - T E R M SYNAPTIC POTENTIATION(LTP) IN THE HIPPOCAMPUS. YASUO FUKAI, HISAYUKI OHATA AND EIICHI MARU, D e n a r t m e n t of P h v s i o l o q v , N i p p o n M e d i c a l School, I-1-5 Sendaai, Bunkvo-ku, Tokyo, I ~ J~p~n, Field potentials were recorded from the h i p p o c a m p a l dentate area in o r d e r to compare the characteristics of LTP in u n a n e s t h e t i z e d and pentobarbital (PB:45mg/Kg, i.p.)-ffnesthetized rats. Tetanic stimulations of the p e r f o r a n t p a t h in unanesthetized, freely moving rats enhanced the amplitude of population spikes, while that of p o p u l a t i o n EPSPs r e m a i n e d unchanged. In contrast, both p o p u l a t i o n spikes and EPSPs were s i g n i f i c a n t l y p o t e n t i a t e d by t e t a n i c s t i m u l a t i o n s in PBa n e s t h e t i z e d rats. These p o t e n t i a t i o n s lasted for at least 30 min. The r e c t a l temperature of P B - a n e s t h e t i z e d rats was kept between 36.5° and 37.5°C by m e a n s of heating pads through the experiment. Synaptic LTP was induced under an a n e s t h e t i z e d condition in the animals which had shown no s y n a p t i c LTP u n d e r an unanesthetized condition. These results indicate that synaptic LTP is difficult to be i n d u c e d in u n a n e s t h e t i z e d animals, and that P B - a n e s t h e s i a o v e r c o m e s t h i s difficulty.
1425
RELATION BETWEEN LEARNING IMPAIRMENT, HIPPOCAMPAL PYRAMIDAL CELL LOSS AND OTHER CELLUAR CHANGES IN THE RATS AFTER SEIZURE INDUCED BY KAINIC ACID AND PILOCARPINE. KUNIHIKO OBATA, Lab. of Neurochem., Natl. Inst. for Physiol. Sci., Myodaiii, Okazaki 444, Japan
It is well known that seizure or ischemia results in degeneration of pyramidal cells in the different area of the rodent hippocampus. However, a great deal remains to be clarified on the extent of the cell loss, susceptible age of the animals and changes in animal behavior. Furthermore, reactive or plastic changes in the surviving cells and target-deprived axons will be a matter of great interest. In order to investigate these questions, I induced status epilepticus in 5-week-old Wistar rats by systemic administration of kainic acid or pilocarpine. Autonomic effects were blocked by methyl scopolamine. One to 12 weeks after the treatment, the rats were subjected to Morris water maze test and histological/immunohistochemical examination. Maze learning was impaired in all rats 1-3 weeks after the seizure. Thereafter, the learning disability was maintained in some kainate-treated and all pilocarpine-treated rats and their hippocatnpus atrophied with massive degeneration of CA1 pyramidal cells. The remaining kainate-treated animals, although their seizure was similarly severe, recovered the learning ability and their cell loss was trivial.
1423
MATURATION OF THE ADENOSINE RECEPTOR AND ITS ROLE IN SYNAPTIC PLASTICITY IN THE RAT HIPPOCAMPUS. YUKO SEKINO1, YOSHIKO SAITOH1, R1TSUKO OHTANI-KANEKOZ, H1ROYASU NAKATA,, YOICHIRO KURODA', ,Dept. of Mol. & Cell. Neurobiol., Tokyo Metropolitan Institute for Nenroscience, Fuchu-shi, Tokyo 183 and 2Dept. of Anatomy, St. Marianna Univ. School of Medicine, Miyamae-ku, Kawasaki 216, Japan.
Long-term potentiation (LTP) and post-tetanic depression (PTD) in hippocampus have been proposed as impotant processes underlying memory. Memory processes are generally thought to change during maturation, therefore, cellular mechanisms that influence LTP and PTD might also change during development. We previously reported that endogenous adenosine released with neurotransmitter plays an essential role in the induction of LTP and FTD in rat hippocampal slices. In order to evaluate developmental changes in the cellular mechanisms underlying memory processes, our study has focused on the adenosine rcceptor and its role in the induction of LTP and PTD. We measured the adenosine binding activity of hippocarnpal membrane prepared from immature and mature rat brain. The activity of AI adenosine receptor increased gradually during the first 2 postnatal weeks and appeared to reach saturation by the third week. Application of the A1 antagonist, 8-cyclopentyltheophylline, increased the synaptic responses of neurons within the CA1 region of slices taken from adult rats. However, the same treatment failed to increase responses and inhibiled the induction of LTP in immature hippocampal slices. Such age-dependent electrophysiological responses may, therefore, depend on the maturation of adenosine receptors. We speculate that the age related changes in adenosine receptors may play a role in the maturation of synaptic plasticity in the hippocampus, and this underlie some of the developmental changes in memory processes.
1424
PENTOBARBITAL ANESTHESIA FACILITATES INDUCTION OF L O N G - T E R M SYNAPTIC POTENTIATION(LTP) IN THE HIPPOCAMPUS. YASUO FUKAI, HISAYUKI OHATA AND EIICHI MARU, D e n a r t m e n t of P h v s i o l o q v , N i p p o n M e d i c a l School, I-1-5 Sendaai, Bunkvo-ku, Tokyo, I ~ J~p~n, Field potentials were recorded from the h i p p o c a m p a l dentate area in o r d e r to compare the characteristics of LTP in u n a n e s t h e t i z e d and pentobarbital (PB:45mg/Kg, i.p.)-ffnesthetized rats. Tetanic stimulations of the p e r f o r a n t p a t h in unanesthetized, freely moving rats enhanced the amplitude of population spikes, while that of p o p u l a t i o n EPSPs r e m a i n e d unchanged. In contrast, both p o p u l a t i o n spikes and EPSPs were s i g n i f i c a n t l y p o t e n t i a t e d by t e t a n i c s t i m u l a t i o n s in PBa n e s t h e t i z e d rats. These p o t e n t i a t i o n s lasted for at least 30 min. The r e c t a l temperature of P B - a n e s t h e t i z e d rats was kept between 36.5° and 37.5°C by m e a n s of heating pads through the experiment. Synaptic LTP was induced under an a n e s t h e t i z e d condition in the animals which had shown no s y n a p t i c LTP u n d e r an unanesthetized condition. These results indicate that synaptic LTP is difficult to be i n d u c e d in u n a n e s t h e t i z e d animals, and that P B - a n e s t h e s i a o v e r c o m e s t h i s difficulty.
1425
RELATION BETWEEN LEARNING IMPAIRMENT, HIPPOCAMPAL PYRAMIDAL CELL LOSS AND OTHER CELLUAR CHANGES IN THE RATS AFTER SEIZURE INDUCED BY KAINIC ACID AND PILOCARPINE. KUNIHIKO OBATA, Lab. of Neurochem., Natl. Inst. for Physiol. Sci., Myodaiii, Okazaki 444, Japan
It is well known that seizure or ischemia results in degeneration of pyramidal cells in the different area of the rodent hippocampus. However, a great deal remains to be clarified on the extent of the cell loss, susceptible age of the animals and changes in animal behavior. Furthermore, reactive or plastic changes in the surviving cells and target-deprived axons will be a matter of great interest. In order to investigate these questions, I induced status epilepticus in 5-week-old Wistar rats by systemic administration of kainic acid or pilocarpine. Autonomic effects were blocked by methyl scopolamine. One to 12 weeks after the treatment, the rats were subjected to Morris water maze test and histological/immunohistochemical examination. Maze learning was impaired in all rats 1-3 weeks after the seizure. Thereafter, the learning disability was maintained in some kainate-treated and all pilocarpine-treated rats and their hippocatnpus atrophied with massive degeneration of CA1 pyramidal cells. The remaining kainate-treated animals, although their seizure was similarly severe, recovered the learning ability and their cell loss was trivial.