All issues
Volume 109 (1997)
- Issue 6 Pages 247-
- Issue 5 Pages 213-
- Issue 4 Pages 165-
- Issue 3 Pages 101-
- Issue 2 Pages 61-
- Issue 1 Pages 1-
Volume 109, Issue 3
Displaying 1-7 of 7 articles from this issue
- |<
- <
- 1
- >
- >|
-
[in Japanese]1997 Volume 109 Issue 3 Pages 101-102
Published: 1997
Released on J-STAGE: January 30, 2007
JOURNAL FREE ACCESSDownload PDF (1022K) -
Yoshiyuki HORIO, Yoshihisa KURACHI1997 Volume 109 Issue 3 Pages 103-110
Published: 1997
Released on J-STAGE: January 30, 2007
JOURNAL FREE ACCESSK+ channels play pivotal roles in maintenance of the resting membrane potential, in the regulation of the action potential duration, repolarization of the membrane potential, inhibition of the cellular excitability and transport of K+ across the cell membrane. Various kinds of K+ channels have been cloned. Mammalian K+ channels can be classified into three families according to their number of putative membrane-spanning regions; i.e., six-transmembrane type, four-transmembrane type and two-transmembrane type. Each family consists of many members. These K+ channels are differentially expressed in a variety of cells. The membranes of glial cells are mainly permeable to K+. This is because glial cells express an abundant number of K+ channels. Their main function has been supposed to be aspiration and transportation of extracellular K+, which is liberated from neurons by their excitation. This regulatory function of glial cells is proposed as a spatial buffering mechanism of K+. Recently, molecular level studies on K+ channels of glial cells have been initiated. In this review, we will overview the current understanding of the features and function of K+ channels in glial cells.View full abstractDownload PDF (7509K) -
Yoshihisa KUDO1997 Volume 109 Issue 3 Pages 111-117
Published: 1997
Released on J-STAGE: January 30, 2007
JOURNAL FREE ACCESSBecause glial cells have been characterized by electrophysiological studies as being silent and inactive, neuroscientists have overlooked the roles of these cells in the dynamic function of the central nervous system. Recent measurements of intracellular Ca2+ concentration, however, revealed the dynamic and active features of the glial cells. Some populations of these cells gave rise to increase in intracellular Ca2+ concentration by stimulation with neurotransmitters such as glutamate, acetylcholine, serotonin, noradrenaline and histamine through the activation of specific neurotransmitter receptors distributed on the glial cells. Although the roles of the increased intracellular Ca2+ concentration in glial cells have not been elucidated, these properties suggested the functional participation of glial cells in synaptic modulation and plasticity.View full abstractDownload PDF (5949K) -
Yasuo WATANABE, Ichie HARA, Jing LI, Teruhiko MATSUMIYA1997 Volume 109 Issue 3 Pages 119-128
Published: 1997
Released on J-STAGE: January 30, 2007
JOURNAL FREE ACCESSIn the recent decade of brain research, one of the most interesting findings is the significance of the active neuronal-glial interaction. It is no exaggeration to say that astrocytes in the central nervous system have an important role, participating in the regulation of neuronal functions. For instance, the fate of brain neurotransmitters, especially amino acids, following their release by neurons, is to be mainly inactivated by uptake via specific high-affinity transport systems into not only neuronal cells but also astrocytes, rather than by extracellular enzymatic degradation. These uptake mechanisms in astrocytes are very important for maintaining brain neuronal function under the low energy condition. In our research using the in vitro brain ischemia model, it was demonstrated that the neuronal death induced by excessive amounts of glutamate (Glu) under low energy conditions (hypoglycemia, hypoxia, particularly acidosis) is caused by dysfunctions of astrocyte Glu uptake and glutamine (Gln) output systems, and neural death can be modulated by the number of surrounding astrocytes in the cultured brain cells. Moreover, the neuronal dysfunction induced by excessive amounts of Glu was enhanced by a blocker of Glu uptake into astrocytes rather than an antagonist of Gln synthetase, which mainly exists in the astrocytes. During dysfunctions of astrocytes induced by acidosis, sustained increases of NO metabolites, ammonia and cytokines were produced. These biological substances may regulate the functions of neuronal cells and astrocytes. Thus, the balance of astrocyte-neuronal cells can maintain the brain neuronal homeostasis.View full abstractDownload PDF (8544K) -
Hiroshi HAMA, Masafumi UESUGI, Yoshitoshi KASUYA, Katsutoshi GOTO1997 Volume 109 Issue 3 Pages 129-143
Published: 1997
Released on J-STAGE: January 30, 2007
JOURNAL FREE ACCESSEndothelins and their receptor of type B (ETBR) that couples with G-protein are widely distributed in the mammalian central nervous system (CNS). ETBR mainly exists on astrocytes, and endothelins exert mitogenic action on astrocytes through stimulation of the receptor. The intracellular signaling of ETBR in astrocytes is converged in the activation of mitogen-activated protein kinase through a protein kinase C-dependent pathway and a pertussis toxin-sensitive G-protein-mediated pathway. We demonstrated that cultured astrocytes, when differentiated and growth-arrested by treatment with dibutyryl cyclic AMP, abundantly expressed ETBR and these cells immediately entered into a proliferative state in response to endothelin-1 at the plasma level. This has the following physiological implication in vivo: plasma-derived endothelin-1 intrudes into parenchyme upon CNS damage, and it initiates astrogliosis through activation of ETBR. We used two models of CNS injury in rats. The first is a brain edema model induced by cold-injury, and the second is a spinal cord injury model, both of which allow plasma to exude into the injured tissues and subsequently trigger sequential proliferative responses of astrocytes after the injury. Anti-endothelin monoclonal antibody and SB209670, an endothelin receptor antagonist, specifically and potently inhibited astrocytic proliferation 24 hr after the injury. It is concluded that endothelin-1 plays a key role for initiation of astrocytic proliferation in the acute phase of CNS damage.View full abstractDownload PDF (13113K) -
Masaya TOHYAMA, Satoshi OGAWA1997 Volume 109 Issue 3 Pages 145-151
Published: 1997
Released on J-STAGE: January 30, 2007
JOURNAL FREE ACCESSAs the most abundant cell type in the central nervous system (CNS), astrocytes play a major role in the host defense mechanism even in situations associated with ischemic cerebrovascular diseases. Cultured rat astrocytes exposed to hypoxia (pO2=8-10 torr) expressed a set of stress proteins whose Mrs are 28, 33, 78, 94, and 150 kDa. Northern/western blot analysis indicated that these stress proteins are identical to heme oxygenase-1 (33 kDa), 78-kDa glucose regulated protein (GRP78) and GRP94 (94 kDa), respectively. The amino acid sequence analysis of the 150kDa protein revealed that it (ORP 150: oxygen regulated protein) is a novel stress protein belonging to the heat shock protein family. The induction of this stress protein was seen in the endoplasmic reticulum (ER) and mainly regulated by the decline of atmospheric oxygen tension, not by other chemical stimuli. The abundant expression of these ER-localized stress proteins (ORP150, GRP94 and GRP78) suggest that the stress response of these astrocytes to hypoxia may focus on the restoration of ER function. The unique expression of these stress proteins may provide a clue to understand the role of this cell type in ischemic cerebrovascular accidens.View full abstractDownload PDF (6678K) -
Toshio MATSUDA, Yutaka KOYAMA1997 Volume 109 Issue 3 Pages 153-159
Published: 1997
Released on J-STAGE: January 30, 2007
JOURNAL FREE ACCESS1-6 Yamada-oka, Suita, Osaka 565, Japan). Folia Pharmacol. Jpn. 109, 153 ?? 159 (1997)
The mechanism of induction of reactive astrocytes (activation of astrocytes) that is observed in brain pathological conditions is not fully elucidated, and there is little information on the cell death of astrocytes. This mini-review summarizes our studies on the activation and cell death of astrocytes. Microinjection of endothelin-3 or the endothelinB -receptor agonist ala1, 3, 11, 15-endothelin-1 enhanced the injury-induced increase in glial fibrillary acidic protein staining in rat neostriatum. Under these conditions, the receptor agonist did not affect the number of microglia/ macrophage. The findings suggest that the signal cascade via endothelinB receptors in astrocytes is involved in induction of reactive astrocytes. We also found that Ca2+ depletion followed by reperfusion with Ca2+-containing medium caused cell death in cultured astrocytes (Ca2+ paradox-like injury). The study, carried out by the use of a specific antisense oligomer, provides direct evidence that Ca2+ paradox-like injury is mediated by the Na+-Ca2+ exchanger in the reverse mode. The injury was prevented by inhibitors of the Na+-Ca2+ exchanger and heat shock protein. Heat shock protein may affect processes downstream of the increase in intracellular Ca2+ concentration. Further studies on activation and cell injury of astrocytes will contribute to the development of new drugs that modulate the function of astrocytes.View full abstractDownload PDF (5782K)
- |<
- <
- 1
- >
- >|