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Neuronal degeneration by suicide transport following injection of volkensin into rat cerebral cortex.

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We have examined the time course of neurodegeneration in subcortical nuclei and other cortical areas known to project to the rat parietal cortex, following unilateral injection of the suicide transport agent, volkensin, into the cortex of one side. Degenerating neurons, visualized by Gallyas silver

Glial reaction to volkensin-induced selective degeneration of central neurons.

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Volkensin, a highly toxic protein retrogradely transported through axons, was used to target primary neuronal death in brainstem precerebellar relays after injection in the cerebellar cortex of rats. The reaction of astrocytes and microglia was studied with immunohistochemistry in the inferior

Anatomical and neurochemical evidence for suicide transport of a toxic lectin, volkensin, injected in the rat dorsal hippocampus.

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Volkensin, a ribosome-inactivating toxic lectin which has been proposed as a 'suicide transport' agent in the CNS, was unilaterally injected in the rat dorsal hippocampus at a dose of 1.2 ng. Three to 5 days after the injection, degenerating neurons were observed at the electron microscope in the

Reinnervation of rat muscles via volkensin-affected and normal peripheral nerve conduits.

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Volkensin is a neurotoxic lectin which, when injected into a peripheral nerve is retrogradely transported to the cell body and causes it to die. Accordingly, volkensin-affected peripheral nerves rapidly degenerate. It is, however, not clear whether axonal growth can take place within these

The use of a neurotoxic lectin, volkensin, to induce loss of identified motoneuron pools.

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In this study we investigated degeneration of defined motor pools in the adult rat spinal cord and the associated changes in spinal cord in dorsal root ganglia and peripheral nerve. Degeneration of motoneurons was induced by the neurotoxic lectin, volkensin. This substance is taken up by the axons

Toxicity of ricin and volkensin, two ribosome-inactivating proteins, to microglia, astrocyte, and neuron cultures.

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Ricin and volkensin, two potent toxins belonging to the family of ribosome-inactivating proteins (RIPs), have been largely exploited in recent years in in vivo experiments of neuronal degeneration consequent to suicide transport or immunolesioning. We have determined both the toxicity of, and the

Suicide retrograde transport of volkensin in cerebellar afferents: direct evidence, neuronal lesions and comparison with ricin.

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Volkensin and ricin, either free or conjugated with colloidal gold, were injected into the cerebellar cortex of rats. The inferior olive and pontine nuclei were examined to verify the retrograde axonal transport of these two toxins, and the consequent neuronal damage. No evidence was obtained of a

Electron microscopic analysis of adrenalectomy-induced hippocampal granule cell degeneration in the rat: apoptosis in the adult central nervous system.

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As described in the preceding paper, adrenalectomy triggers hippocampal granule cell degeneration that begins within days after adrenalectomy, continues for months, and is the only apparent cell death anywhere within the brain. At the light microscopic level, granule cell degeneration is

Neuroplasticity and Repair in Rodent Neurotoxic Models of Spinal Motoneuron Disease.

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Retrogradely transported toxins are widely used to set up protocols for selective lesioning of the nervous system. These methods could be collectively named "molecular neurosurgery" because they are able to destroy specific types of neurons by using targeted neurotoxins. Lectins such as ricin,

Localization of striatal excitatory amino acid binding site subtypes to striatonigral projection neurons.

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Quantitative autoradiography was used to examine the cellular localization of excitatory amino acid binding sites in the striatum following selective lesion of striatonigral projection neurons. Degeneration of striatonigral neurons was induced unilaterally by injection of the suicide transport

Effects of suicide transport lesions of the striatopallidal or striatonigral pathways on striatal ultrastructure.

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In the basal ganglia, centrally active suicide transport agents produce selective lesions of the striatopallidal and striatonigral pathways based on receptor binding and neuropeptide mRNA studies. Anatomical analyses indicate a selective, albeit modest, loss of projection neurons. In the present

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