Light microscopic response of neuronal somata, dendrites and axons to post-mortem concussive head injury

Gallyas, Ferenc; Zoltay, Gabor; Horváth, Zsolt

doi:10.1007/bf00310026

Cited by 19 publications

(8 citation statements)

References 7 publications

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“…Sections obtained from immature rats killed 24 h after a seizure. Silver-stained neurons (Gallyas' dark-neuron method; Gallyas et al, 1992) are evident in the CA3c pyramidal cell layer in this high-magnification photomicrograph. The distribution of the argyrophilic neurons involved also CA3a and b, CA1, some hilar interneurons, and discrete nuclei in amygdala and perirhinal cortex .…”

Section: Resultsmentioning

confidence: 72%

“…The relative nature of silver uptake by different classes of intact and injured neurons and subcellular organelles has been discussed (Gallyas et al, 1990). Indeed, avidity to silver staining can be induced by subjecting the brain to postmortem trauma, indicating that this process is independent from the process of cell death (Gallyas et al, 1992). This fact, together with earlier studies (Chang and Baram, 1994), raised the question as to the interpretation of neuroanatomical methods used to demonstrate 'cell death'.…”

Section: Do Argyrophilia Acid-fuchsin Staining or In Situ End-labelimentioning

confidence: 99%

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Is neuronal death required for seizure-induced epileptogenesis in the immature brain?

Baram

Eghbal-Ahmadi

Bender

2002

Progress in Brain Research

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Do seizures cause neuronal death? At least in the immature hippocampus, this may not be the critical question for determining the mechanisms of epileptogenesis. Neuronal injury and death have clearly been shown to occur in most epilepsy models in the mature brain, and are widely considered a prerequisite to seizure-induced epilepsy. In contrast, little neuronal death occurs after even a severe and prolonged seizure prior to the third postnatal week. However, seizures early in life, for example prolonged experimental febrile seizures, can profoundly and permanently change the hippocampal circuit in a pro-epileptogenic direction. These seizure-induced alterations of limbic excitability may require transient structural injury, but are mainly due to functional changes in expression of gene coding for specific receptors and channels, leading to altered functional properties of hippocampal neurons. Thus, in some pro-epileptogenic models in the developing brain, neither the death of neurons nor death-induced abnormalities of surviving neurons may underlie the formation of an epileptic circuit. Rather, findings in the experimental prolonged febrile seizure model suggest that persistent functional alterations of gene expression ('neuroplasticity') in diverse hippocampal neuronal populations may promote pro-epileptogenic processes induced by these seizures. These findings also suggest that during development, relatively short, intense bursts of neuronal activity may disrupt 'normal' programmed maturational processes to result in permanent, selective alterations of gene expression, with profound functional consequences. Therefore, determining the cascade of changes in the programmed expression of pertinent genes, including their temporal and cell-specific spatial profiles, may provide important information for understanding the process of transformation of an evolving, maturing hippocampal network into one which is hyperexcitable.

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Section: Resultsmentioning

confidence: 72%

Section: Do Argyrophilia Acid-fuchsin Staining or In Situ End-labelimentioning

confidence: 99%

Is neuronal death required for seizure-induced epileptogenesis in the immature brain?

Baram

Eghbal-Ahmadi

Bender

2002

Progress in Brain Research

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“…However, such 'dark' neurons can also be generated by subjecting the brain to postmortem trauma, indicating that this process is independent from the process of cell death. 37 Indeed, neuronal counts carried out in the central nucleus of the amygdala, where ~30% of neurons became silver-stained after experimenral febrile seizures, demonstrated no loss of cells. 78 These findings suggest that the onset of the avidity to silver may not necessarily mean neuronal death: the changes or injury which render a cell argyrophilic may be reversible and not lead to cell loss.…”

Section: Do Prolonged Experimental Febrile Seizures Cause Neuronal Dementioning

confidence: 95%

Febrile Seizures and Mechanisms of Epileptogenesis: Insights from an Animal Model

Bender¹,

Dubé²,

Baram³

2004

Advances in Experimental Medicine and Biology

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Temporal lobe epilepsy (TLE) is the most prevalent type of human epilepsy, yet the causes for its development, and the processes involved, are not known. Most individuals with TLE do not have a family history, suggesting that this limbic epilepsy is a consequence of acquired rather than genetic causes. Among suspected etiologies, febrile seizures have frequently been cited. This is due to the fact that retrospective analyses of adults with TLE have demonstrated a high prevalence (20-->60%) of a history of prolonged febrile seizures during early childhood, suggesting an etiological role for these seizures in the development of TLE. Specifically, neuronal damage induced by febrile seizures has been suggested as a mechanism for the development of mesial temporal sclerosis, the pathological hallmark of TLE. However, the statistical correlation between febrile seizures and TLE does not necessarily indicate a causal relationship. For example, preexisting (genetic or acquired) 'causes' that result independently in febrile seizures and in TLE would also result in tight statistical correlation. For obvious reasons, complex febrile seizures cannot be induced in the human, and studies of their mechanisms and of their consequences on brain molecules and circuits are severely limited. Therefore, an animal model was designed to study these seizures. The model reproduces the fundamental key elements of the human condition: the age specificity, the physiological temperatures seen in fevers of children, the length of the seizures and their lack of immediate morbidity. Neuroanatomical, molecular and functional methods have been used in this model to determine the consequences of prolonged febrile seizures on the survival and integrity of neurons, and on hyperexcitability in the hippocampal-limbic network. Experimental prolonged febrile seizures did not lead to death of any of the seizure-vulnerable populations in hippocampus, and the rate of neurogenesis was also unchanged. Neuronal function was altered sufficiently to promote synaptic reorganization of granule cells, and transient and long-term alterations in the expression of specific genes were observed. The contribution of these consequences of febrile seizures to the epileptogenic process is discussed.

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“…Although these results were compatible with the "pressure wave" hypothesis, a concern remained that during the ϳ1 min delay between the impact and the beginning of the administration of the fixative, there could be some physiological process that may have contributed to the neuronal damage. Therefore, we took advantage of the fact that the Gallyas stain does not require the presence of living cells to reveal physical damage (van den Pol and Gallyas, 1990;Gallyas et al, 1992b,c), and we performed fluid percussion injury on animals Figure 4. Head injury-induced alterations in the interneuronal circuitry of the dentate gyrus.…”

Section: Mechanical Pressure Wave-induced Immediate Injury To Neuronsmentioning

confidence: 99%

Instantaneous Perturbation of Dentate Interneuronal Networks by a Pressure Wave-Transient Delivered to the Neocortex

et al. 1997

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Whole-cell patch-clamp recordings and immunocytochemical experiments were performed to determine the short-and longterm effects of lateral fluid percussion head injury on the perisomatic inhibitory control of dentate granule cells in the adult rat, with special reference to the development of traumainduced hyperexcitability. One week after the delivery of a single, moderate (2.0-2.2 atm) mechanical pressure wave to the neocortex, the feed-forward inhibitory control of dentate granule cell discharges was compromised, and the frequency of miniature IPSCs was decreased. Consistent with the electrophysiological data, the number of hilar parvalbumin (PV)-and cholecystokinin (CCK)-positive dentate interneurons supplying the inhibitory innervation of the perisomatic region of granule cells was decreased weeks and months after head injury. The initial injury to the hilar neurons took place instantaneously after the impact and did not require the recruitment of active physiological processes. Furthermore, the decrease in the number of PV-and CCK-positive hilar interneurons was similar to the decrease in the number of the AMPA-type glutamate receptor subunit 2/3-immunoreactive mossy cells, indicating that the pressure wave-transient causes injurious physical stretching and bending of most cells that are large and not tightly packed in a cell layer.These results reveal for the first time that moderate pressure wave-transients, triggered by traumatic head injury episodes, impact the dentate neuronal network in a unique temporal and spatial pattern, resulting in a net decrease in the perisomatic control of granule cell discharges.

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Light microscopic response of neuronal somata, dendrites and axons to post-mortem concussive head injury

Cited by 19 publications

References 7 publications

Is neuronal death required for seizure-induced epileptogenesis in the immature brain?

Is neuronal death required for seizure-induced epileptogenesis in the immature brain?

Febrile Seizures and Mechanisms of Epileptogenesis: Insights from an Animal Model

Instantaneous Perturbation of Dentate Interneuronal Networks by a Pressure Wave-Transient Delivered to the Neocortex

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