Prion protein deposition and abnormal synaptic protein expression in the cerebellum in Creutzfeldt–Jakob disease

Ferrer, Isidró; Puig, Berta; Blanco, R.; Martı́, Eulàlia

doi:10.1016/s0306-4522(00)00045-2

Cited by 57 publications

(42 citation statements)

References 56 publications

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“…It is a very reliable presynaptic marker (24). SYN accumulation in a form of disclosed large coarse pericellular reactivity indicates abnormal axon transport (8).…”

Section: The Presence Of Nse Immunoreactivity Indicates No Evidence Omentioning

confidence: 99%

Immunohistochemical investigation of neuronal injury in cerebral cortex of cobra-envenomed rats

Rahmy

Hassona

2004

J. Venom. Anim. Toxins incl. Trop. Dis

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ABSTRACT. The immunohistochemical expression of neuron-specific enolase, NSE (a cytoplasmic glycolytic enzyme of the neurons), synaptophysin, SYN (a major membrane glycoprotein of synaptic vesicles), and Bcl-2 (anti-apoptotic protein) were determined in cerebral cortex of rats envenomed with neurotoxic venom from Egyptian cobra. Male rats were intramuscularly (IM) injected with a single injection of either physiological saline solution or ½ LD 50 or LD 50 of cobra venom and sacrificed 24, 48, or 72 hr after envenoming.Formalin-fixed paraffin sections were immunohistochemically studied by avidin-biotinperoxidase complex method. Neuron histological structure and isolation of genomic DNA were also detected. The results showed a dose and time-dependent increase in NSE and SYN immunoreactivity in cerebral cortex of envenomed rats except in 72 hr high dose envenoming, where decreased SYN was observed. On the other hand, low dose venom induced high Bcl-2 expression 24 hr after envenoming, while the high dose decreased Bcl-2 protein expression. Temporal and spatial Bcl-2 expression was accompanied by DNA fragmentation in cerebral cortex of all envenomed rats, although no serious histological alterations were noticed. These results suggest that cobra venom may lead to neuronal injury and impairment of axonal transport as ascertained by alterations in NSE and SYN immunoreactivity. It could also indicate that venom alters the molecular machinery of apoptosis by inhibiting Bcl-2 expression; however, some vulnerable cells have the ability to overcome this by increasing Bcl-2 protein. These immunohistochemical investigations can be used as tools for detecting neuronal abnormalities even before the occurrence of any histological alterations in case of cerebral cortex neurotoxicity.

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“…It is a very reliable presynaptic marker (24). SYN accumulation in a form of disclosed large coarse pericellular reactivity indicates abnormal axon transport (8).…”

Section: The Presence Of Nse Immunoreactivity Indicates No Evidence Omentioning

confidence: 99%

Immunohistochemical investigation of neuronal injury in cerebral cortex of cobra-envenomed rats

Rahmy

Hassona

2004

J. Venom. Anim. Toxins incl. Trop. Dis

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“…The decrease of synaptophysin is almost certainly a reflection of the synaptic loss which occurs in the disease DeKosky et al, 1996). A similar explanation probably applies to the decline in synaptophysin expression seen in other degenerative disorders (Ince et al, 1995;Samuel et al, 1997;Ferrer et al, 2000), following experimental lesions (e.g., Masliah et al, 1991;Gonzales-Dunia et al, 2000), with aging Eastwood et al, 1994), and with age-associated memory impairment (Smith et al, 2000). Equally, the localized increases of synaptic proteins seen in temporal lobe epilepsy (Honer et al, 1994;Looney et al, 1999;Proper et al, 2000) are associated with synaptic sprouting (Marco and DeFelipe, 1997), and this relationship likely exists during lesion-induced plasticity too (Boschert et al, 1996;Bergmann et al, 1997).…”

Section: What Do Altered Synaptic Protein Levels In Schizophrenia Mean?mentioning

confidence: 95%

Neuropathological studies of synaptic connectivity in the hippocampal formation in schizophrenia

Harrison¹,

Eastwood²

2001

Hippocampus

201

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Cytoarchitectural changes in the hippocampal formation have been prominent among the various neuropathological abnormalities reported in schizophrenia. Replicated positive findings include decreased neuronal size and alterations in presynaptic and dendritic markers. These findings, in the absence of neurodegenerative changes, suggest that there are alterations in the neural circuitry in schizophrenia. These may represent the anatomical correlate of the aberrant functional connectivity described in neuroimaging studies, which in turn contributes to the psychotic and cognitive symptomatology of the disorder. The identity of the affected hippocampal circuits remains unclear; there is evidence for both glutamatergic and GABAergic involvement, and perhaps for a gradient of pathology in which changes are most apparent in CA4 and the subiculum, and least in CA1. The data, their interpretation, and their limitations are discussed, with particular emphasis upon molecular and immunological studies of synaptic protein gene expression.

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“…Several abnormalities have been observed in PrP 0/0 neurons in culture, including reduced Ca 2ϩ -dependent K ϩ currents (Colling et al, 1996;Herms et al, 2001;Mallucci et al, 2002) and cytoplasmic Ca 2ϩ levels (Herms et al, 2000). PrP is distributed on the neuron surface and in presynaptic terminals (Herms et al, 1999;Ferrer et al, 2000). Despite initial negative observations, there is now growing evidence that PrP regulates neuronal survival and differentiation (Steele et al, 2006) through its interaction with laminin and intracellular signaling cascades (Graner et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Altered Neuron Excitability and Synaptic Plasticity in the Cerebellar Granular Layer of Juvenile Prion Protein Knock-Out Mice with Impaired Motor Control

et al. 2008

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Prion protein deposition and abnormal synaptic protein expression in the cerebellum in Creutzfeldt–Jakob disease

Cited by 57 publications

References 56 publications

Immunohistochemical investigation of neuronal injury in cerebral cortex of cobra-envenomed rats

Immunohistochemical investigation of neuronal injury in cerebral cortex of cobra-envenomed rats

Neuropathological studies of synaptic connectivity in the hippocampal formation in schizophrenia

Altered Neuron Excitability and Synaptic Plasticity in the Cerebellar Granular Layer of Juvenile Prion Protein Knock-Out Mice with Impaired Motor Control

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