Dendritic changes of the pyramidal neurons in layer V of sensory-motor cortex of the rat brain during the postresuscitation period

Akulinin, V. A.; Stepanov, S. S.; Semchenko, V. V.; Belichenko, Pavel V.

doi:10.1016/s0300-9572(97)00048-8

Cited by 24 publications

(20 citation statements)

References 34 publications

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“…73,74,[85][86][87][88] In cortical neurons that survived global ischemia, a reduction in dendrite complexity and loss of dendritic spines was observed. 89 Similar changes can be seen after brain cell injury as a result of excessive glutamatergic stimulation, one of the pathways linking ischemia and neuronal injury. 90,85 Effects on Synaptic Plasticity Under physiological conditions, synaptic strength is not fixed, but can be modulated.…”

Section: Evidence Of Postsynaptic Failurementioning

confidence: 86%

Ischemic Cerebral Damage

Hofmeijer¹,

Putten²

2012

Stroke

223

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Abstract-In the human brain, Ϸ30% of the energy is spent on synaptic transmission. Disappearance of synaptic activity is the earliest consequence of cerebral ischemia. The changes of synaptic function are generally assumed to be reversible and persistent damage is associated with membrane failure and neuronal death. However, there is overwhelming experimental evidence of isolated, but persistent, synaptic failure resulting from mild or moderate cerebral ischemia. Early failure results from presynaptic damage with impaired transmitter release. Proposed mechanisms include dysfunction of adenosine triphosphate-dependent calcium channels and a disturbed docking of glutamate-containing vesicles resulting from impaired phosphorylation. We review energy distribution among neuronal functions, focusing on energy usage of synaptic transmission. We summarize the effect of ischemia on neurotransmission and the evidence of long-lasting synaptic failure as a cause of persistent symptoms in patients with cerebral ischemia. Finally, we discuss the implications of synaptic failure in the diagnosis of cerebral ischemia, including the limited sensitivity of diffusion-weighted MRI in those cases in which damage is presumably limited to the synapses. (Stroke. 2012;43:607-615.)Key Words: brain metabolism Ⅲ cerebral ischemia Ⅲ synaptic failure T he human brain is metabolically expensive. Although it represents only 2% of the body weight, it accounts for 20% of oxygen consumption and 25% of glucose utilization. 1,2 Cerebral ischemia is a pathological condition in which blood flow to the brain is insufficient to meet these metabolic demands, causing a loss of neuronal function and viability. Ischemia may be focal if a brain artery is occluded or global, for example, after cardiac arrest.In the 1950s, the concept of perfusion thresholds was introduced. 3 It was shown that functional activity became impaired with moderately reduced perfusion (14 -35 mL/100 g/min), along with electroencephalographic and evoked potential disturbances, whereas loss of ion gradients across the plasma membrane and subsequent cell swelling occur at lower perfusion levels Ϸ4.8 to 8.4 mL/100 g/min (Figure 1). [3][4][5] In focal brain ischemia, the brain tissue that is perfused in the flow range between these 2 levels is now called the penumbra. 6 The penumbra is considered structurally intact and viable, but functionally silent. The dysfunction is, in principle, reversible by restoration of blood flow. However, if oxygen and glucose are not resupplied in time, irreversible damage occurs.Knowledge on the distribution of energy usage among different neuronal activities may contribute to understanding the successive loss of cell function and cell damage in cerebral ischemia. In the human brain, Ϸ30% of the energy is spent on synaptic transmission. 7 Disappearance of synaptic activity is the earliest consequence of cerebral ischemia 8 and failure of synaptic transmission has been proposed to account for electric silence in the penumbra. 3,6,8 -10 The changes of syna...

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Section: Evidence Of Postsynaptic Failurementioning

confidence: 86%

Ischemic Cerebral Damage

Hofmeijer¹,

Putten²

2012

Stroke

223

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“…10 Almost in accordance with our present study, the LMS study of Golgi silver impregnated spine and dendrites showed that the number of spines and thickness of dendrites decreased maximally in 4 to 7 days after the temporary ischemia and recovered around 5 weeks in the 2nd to 3rd cortical layers of the rat cerebral cortex. 13 Earlier studies on cultured Figure 4. A, Light-microscopy.…”

Section: Discussionmentioning

confidence: 99%

“…4 -6 Degenerated boutons and multiple synapse boutons (MSBs) in this region were investigated by electron microscopy (EM) after temporary ischemia, [7][8][9] as well as after temporary hypoxia/hypoglycemia in hippocampal slices. 10 Changes in spines and dendrites were studied by time-lapse microscopy after temporary anoxia/hypoglycemia in cell culture, 11,12 by light microscopy (LMS) of Golgi stain-impregnated sections of the 3rd to 5th cortical layers of the cerebral cortex after temporary ischemia, 13 and by EM after temporary hypoxia/glycemia in hippocampal slice. 10 Changes in CA-1 dendrites after temporary ischemia were investigated by light microscopy of horseradish peroxidase-injected specimens, 14 by EM after temporary ischemia in CA-1, 15,16 and by EM of Golgi stain-impregnated cerebral cortex after temporary ischemia for 20 minutes.…”

mentioning

confidence: 99%

Temporal Profiles of Axon Terminals, Synapses and Spines in the Ischemic Penumbra of the Cerebral Cortex

Ito

Kuroiwa

Nagasao

et al. 2006

Stroke

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Background and Purpose-Because the recovery process of axon terminals, synapses, and spine-dendrites in the ischemic penumbra of the cerebral cortex is obscure, we studied the temporal profile of these structures up to 12 weeks after the ischemic insult, using a gerbil model. Methods-Stroke-positive animals were selected according to their stroke index score during the first 10-minute left carotid occlusion done twice with 5-hour interval. The animals were euthanized at various times after the second ischemic insult. Ultra-thin sections including the 2nd to 4th cortical layers were obtained from the neocortex coronally sectioned at the infundibular level, in which the penumbra appeared. We counted the number of synapses, spines and multiple synapse boutons, measured neurite thickness, and determined the percent volume of the axon terminals and spines by Weibel point counting method. Results-The number of synapses, synaptic vesicles and spines and the total percent volume of the axon terminals and spines decreased until the 4th day. From 1 to 12 weeks after the ischemic insult, these values increased to or exceeded the control ones, and neuritic thickening and increase in number of multiple synapse boutons occurred. Conclusions-In the ischemic penumbra, the above structures degenerated, with a reduction in their number and size, until 4 days and then recovered from 1 to 12 weeks after the ischemic insult.

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“…In addition, neurogenesis and integration of newly differentiated neurons into neuronal circuits in the Ammon's horn may contribute to recovery of hippocampal-dependent cognitive functions (Bendel et al, 2005;Bernabeu & Sharp, 2000). Similarly, reductions of dendritic length, arborization, and dendritic spine density have also been described, among various cytoarchitectural adjustments, in sensorymotor cortex pyramidal neurons following global cerebral ischemia (Akulinin et al, 1997(Akulinin et al, , 1998(Akulinin et al, , 2004. These cytoarchitectural alterations could be influenced by the extent of neuronal remaining connections; thus, either reduction or increase of afferent connections may result in changes in dendritic arborizations and spine density (Fiala et al, 2002;Johansson & Belinchenko, 2002).…”

Section: Cellular Mechanisms Of Neuronal Plasticity and Repairmentioning

confidence: 98%

“…These dendritic restructuring (Neigh el al., 2004;Ruan el al., 2006) and reactive synaptogenesis (Briones et al, 2005;Crepel et al, 2003;Jourdain et al, 2002, Kovalenko et al, 2006 among other phenomena including the activation of a variety of potential growth-promoting processes (Arvidsson et al, 2001;Gobbo & O´Mara, 2004;Schmidt-Kastner et al, 2001), that occur in neurons surviving to the ischemic insult in vulnerable brain structures, seem to be a part of mechanisms of adaptive changes, probably accounting for neuronal conditions favoring synaptic plasticity and functional recovery. In fact, a long-term progressive continuous plastic reorganization of the dendritic tree and dendritic spines, initially altered by acute global cerebral ischemia, has been shown to occur in pyramidal neurons at layers 3 and 5 of the sensorymotor cortex of the rat (Akulinin et al, 1997(Akulinin et al, , 1998(Akulinin et al, , 2004. Thus, preservation or recovery of hippocampal-and pre-frontal cortex-dependent functions after global cerebral ischemia, may involve long-term cytoarchitectural modifications in those remaining hippocampal CA1 and prefronto-cortical (layers 3 and 5) pyramidal neurons, since their morpho-functional organization is critical for normal learning and memory performance (Block, 1999;McDonald & White, 1993;McNamara & Skelton, 1993;Olsen et al, 1994;Olvera-Cortés et al, 2002;Silva et al, 1998), on the basis of the major role played by the CA1 region for the output of information flowing through the hippocampus, via the tri-synaptic circuit (Herreras et al, 1987).…”

Section: Cellular Mechanisms Of Neuronal Plasticity and Repairmentioning

confidence: 99%