Post-ischemic synaptic plasticity in the rat hippocampus after long-term survival: Histochemical and autoradiographic study

Oda, Hiroshi; Aoki, Hiromitsu; Yae, Tetsuji; Kogure, Kyuya

doi:10.1016/0306-4522(90)90379-i

Cited by 43 publications

(15 citation statements)

References 33 publications

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“…The neuronal injury associated with ischemia is accompanied by changing the cholinergic system (Hou et al 2008;Sakuma et al 2008). One-hundred days after ischemia, depletion of CA1 pyramidal cells and marked shrinkage of the CA1 subfield were noted and high density bands of AChE activity in the stratum pyramidale of the CA1 were found to be broadened (Onodera et al 1990). The increase of AChE activity in the hippocampal areas caused by VaD could lead to a reduction of cholinergic neurotransmission efficiency such as the decrease in ACh level in the synaptic cleft, thus contributing to progressive cognitive impairment and other neurological dysfunctions seen in the patients and rats with VaD.…”

Section: Discussionmentioning

confidence: 97%

Correlations Between Cholinesterase Activity and Cognitive Scores in Post-Ischemic Rats and Patients with Vascular Dementia

Xiao

Guan

et al. 2011

Cell Mol Neurobiol

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The biochemical changes such as the activities of acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) were investigated in rats with global cerebral ischemia and in vascular dementia (VaD) subjects in this study. The AChE activity showed a significant decrease in plasma and a significant increase in the hippocampus but not in the cerebral cortices in the post-ischemic rats as compared to the controls. The learning abilities and spatial memory were impaired in the post-ischemic rats as compared to controls. Furthermore, the AChE activity in plasma was significantly reduced in VaD subjects as compared to normal control subjects. The BuChE activity did not show any change in both post-ischemic rats and VaD patients. Interestingly, the decreased AChE activity in plasma from the post-ischemic rats and the VaD subjects showed a significant correlation with the declined learning and memory ability, and the Mini-Mental State Examination score, respectively. These data suggest that the AChE activity is involved in the cognitive recovery after ischemia, and the plasma level of AChE might be a reliable supplementary peripheral biomarker to evaluate the cognitive recovery degree of VaD patients.

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Section: Discussionmentioning

confidence: 97%

Correlations Between Cholinesterase Activity and Cognitive Scores in Post-Ischemic Rats and Patients with Vascular Dementia

Xiao

Guan

et al. 2011

Cell Mol Neurobiol

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“…Thus mossy fiber sprouting has been demonstrated in the kainic acid and pilocarpine models of epilepsy (Nadler 1981;Represa et al 1990;Turski 1989), after kindling (Elmer et al 1996;GarciaCairasco et al 1996;Represa et al 1989Represa et al , 1993Sutula et al 1988), electroconvulsive shock (Gombos et al 1999;Vaidya et al 1999), tetanus toxin (Anderson et al 1999), alumina gel (Ribak et al 1998), pentylenetetrazol (Golarai et al 1992, in mutants with spontaneous seizures (Amano et al 1999;Qiao and Noebels 1993), and temporal lobe epilepsy (especially nontumor associated cases; Babb et al 1991;Cavazos et al 1991;Houser et al 1990;Sutula et al 1989). Mossy fiber sprouting has also been reported following lesions or deafferentation of the hippocampus, trauma, stroke, ischemia, and feline immunodeficiency virus (Arvidsson 2001;Frotscher and Zimmer 1983;Golarai et al 2001;Gould and Tanapat 1997;Hannesson et al 1997;Laurberg and Zimmer 1981;Liu et al 1998;Mitchell et al 1999;Mohapel et al 1997;Onodera et al 1990;Santhakumar et al 2001;Shetty and Turner 1999;West and Dewey 1984;Zimmer 1973). Although it has not been definitively proven, mossy fiber sprouting has often been considered to contribute to hippocampal hyperexcitability, particularly in temporal lobe epilepsy.…”

Section: Introductionmentioning

confidence: 99%

Electrophysiological Evidence of Monosynaptic Excitatory Transmission Between Granule Cells After Seizure-Induced Mossy Fiber Sprouting

Scharfman

Sollas

Berger

et al. 2003

Journal of Neurophysiology

140

104

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evidence of monosynaptic excitatory transmission between granule cells after seizure-induced mossy fiber sprouting. J Neurophysiol 90: 2536 -2547, 2003; 10.1152/jn.00251.2003. Mossy fiber sprouting is a form of synaptic reorganization in the dentate gyrus that occurs in human temporal lobe epilepsy and animal models of epilepsy. The axons of dentate gyrus granule cells, called mossy fibers, develop collaterals that grow into an abnormal location, the inner third of the dentate gyrus molecular layer. Electron microscopy has shown that sprouted fibers from synapses on both spines and dendritic shafts in the inner molecular layer, which are likely to represent the dendrites of granule cells and inhibitory neurons. One of the controversies about this phenomenon is whether mossy fiber sprouting contributes to seizures by forming novel recurrent excitatory circuits among granule cells. To date, there is a great deal of indirect evidence that suggests this is the case, but there are also counterarguments. The purpose of this study was to determine whether functional monosynaptic connections exist between granule cells after mossy fiber sprouting. Using simultaneous recordings from granule cells, we obtained direct evidence that granule cells in epileptic rats have monosynaptic excitatory connections with other granule cells. Such connections were not obtained when age-matched, saline control rats were examined. The results suggest that indeed mossy fiber sprouting provides a substrate for monosynaptic recurrent excitation among granule cells in the dentate gyrus. Interestingly, the characteristics of the excitatory connections that were found indicate that the pathway is only weakly excitatory. These characteristics may contribute to the empirical observation that the sprouted dentate gyrus does not normally generate epileptiform discharges.

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“…But group 4 (hypothermia, 7 days survival) LES and WS rats showed mild to severe CA1 neuronal loss, respectively. Although the severity of CA1 neuronal damage beyond 7 days of ischaemia was not evaluated in this study, Onodera et al [30] showed the marked atrophy of the CA1 sector and approximately 40% pyramidal cell loss in the CA3 after three months. Delayed neuronal cell death in cerebral ischaemia was tentatively incriminated in (1) that transient ischaemia disturbed gene expression of the cells, (2) that the cells gradually change their morphology and functions while maintaining homeostasis, and (3) that the relationship of the cells with the surrounding tissue was finally disturbed, leading to death after several months due to disruption of homeostasis [27].…”

Section: Failure Of Mild Hypothermiamentioning

confidence: 95%

Mild hypothermia fails to protect late hippocampal neuronal loss following forebrain cerebral ischaemia in rats

Taşdemiroğlu

1996

Acta neurochir

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Anaesthetized male rats (n = 86) from both Long-Evans strain (LES) (n = 43) and Wistar strain (WS) (n = 43) were utilized for the experiments. While three animals from each strain were used as control, 40 rats from each strain underwent up to 10 minutes forebrain ischaemia by bilateral common carotid artery (CCA) occlusion combined with systemic hypotension [Mean Arterial Blood Pressure (MABP) = 50 mm/Hg]. The animals from each strain were divided into four (n = 10) groups. In both strains, groups (n = 10) 1 and 2, temporalis muscle (TM) and body temperatures of the animals were kept at 36-37 degrees C during the experiments. The groups 1 and 2 were killed in 3 and 7 days after the ischaemic insult, respectively. The groups 3 and 4 were also killed 3 and 7 days after the ischaemic insult, but the forebrain ischaemia was carried out under mild cerebral hypothermia (TM temperature = 33 degrees C). Pyramidal neurons of the hippocampal CA1 region from each group was evaluated semiquantitatively. In WS, groups 1 and 2 showed moderate and severe neuronal loss in the CA1 region, respectively. However, in LES while the group 1 (3 days survival) did not show any neuronal loss, group 2 showed moderate neuronal loss of the CA1 region. While in group 3 (3 days survival, hypothermia) WS and LES, hypothermia protected the CA1 region, group 4 of LES showed mild neuronal loss. However WS, group 4 (7 days survival, hypothermia) showed severe neuronal loss of the CA1 region. It was concluded that mild hypothermia during ischaemic insults did not prevent the delayed postischaemic neuronal damage of the hippocampal CA1 region of both strains, and following 10 minutes forebrain ischaemia, male LES rats were found more resistant than male WS rats to neuronal loss of the CA1 region.

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Post-ischemic synaptic plasticity in the rat hippocampus after long-term survival: Histochemical and autoradiographic study

Cited by 43 publications

References 33 publications

Correlations Between Cholinesterase Activity and Cognitive Scores in Post-Ischemic Rats and Patients with Vascular Dementia

Correlations Between Cholinesterase Activity and Cognitive Scores in Post-Ischemic Rats and Patients with Vascular Dementia

Electrophysiological Evidence of Monosynaptic Excitatory Transmission Between Granule Cells After Seizure-Induced Mossy Fiber Sprouting

Mild hypothermia fails to protect late hippocampal neuronal loss following forebrain cerebral ischaemia in rats

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