ricin/atrophy

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Response of glial cells and activation of complement following motorneuron degeneration induced by toxic ricin.

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Motor nerve transection in adult rats induce a series of metabolic and structural changes in the injured neurons as well as in surrounding glial cells; however, without substantial neuronal degeneration. In the present study we found, in contrast with axotomy, a massive neuronal death in the

Quantification of motor neuron loss and muscular atrophy in ricin-induced focal nerve injury.

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BACKGROUND Intrasciatic nerve injection of the Ricinus communis agglutinin (RCA or ricin) causes degeneration of motor neurons (MNs) with functional deficits, such as those that occur in amyotrophic lateral sclerosis (ALS). The objective of this study was to develop a new comprehensive platform for

Response of endogenous glial cells to motor neuron degeneration induced by toxic ricin.

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The injection of toxic lectin from Ricinus communis into the rat facial nerve resulted in suicide transport and rapid degeneration of facial motor neurons. The reaction of glial cells to neuronal death in comparison with nerve crush lesions was studied by using lectin-HRP conjugates derived from

Neural degeneration and non-neuronal cellular reactions in the hypoglossal nucleus following an intraneural injection of toxic ricin.

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The present study describes neuronal degeneration and its accompanying non-neuronal cellular reaction in the hypoglossal nucleus following an intraneural injection of Ricinus communis agglutinin-60 (RCA-60) into the hypoglossal nerve. The first noticeable structural changes were observed in neurons

Lethal ricin intoxication in two adult dogs: toxicologic and histopathologic findings.

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Two adult dogs with the same owner were intoxicated by ingestion of fertilizer composed of residual plant material of the castor bean plant (Ricinus communis L.). Both dogs died within 2 and 3 days, respectively, after the first signs of vomiting and abundant hemorrhagic diarrhea. Toxicologic and

Selective inhibition of neuronal protein synthesis by retrogradely transported ricin.

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The ability of the lectin, ricinus communis agglutinin I (ricin120), to undergo retrograde axonal transport and cause degeneration of neuronal cell bodies has been frequently exploited to establish the origin of peripheral axons. Since this cytotoxic action of ricin results from its inactivation of

A model of motor neuron loss: selective deficits after ricin injection.

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This study characterizes a model of motor neuron (MN) loss on the molecular, cellular, and behavioral levels. Injection of the toxic lectin Ricinus communis agglutinin I (RCA I or ricin) caused cellular deficit and loss of function by damaging the sciatic nerve. Since the sciatic nerve supplies

Dose- and time-dependent selective and non-selective effects of ricin (RCA 120) on rat primary sensory neurons.

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The distribution of degenerating fibers in the spinal cord was studied in Fink-Heimer-stained sections following treatment of the tibial nerve with ricinus communis agglutinin (RCA 120). The ricin was either injected into the nerve or applied in a capsule on the transected nerve. Short survival

Toxic ricin demonstrates a dual dental projection.

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Toxic ricin was used to study the central distribution of dental afferents in the cat. Following intrapulpal ricin injections ganglion cell degeneration is seen in the II and III ganglion divisions. Central argyrophilic degeneration occurs in the dorsal portion of all ipsilateral trigeminal nuclei.

Sequential changes in the permeability of the blood-nerve barrier over the course of ricin neuronopathy in the rat.

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We examined the sequential changes in the permeability of the BNB to a 4000-molecular-weight fluoresceinated dextran over an 18-week course of ricin neuronopathy. Neuronopathy was produced by injecting ricin into the tibial nerve of 18-day-old Long-Evans rats; permeability of the BNB in proximal

Ultrastructural observations of non-selective effects of ricin treatment (RCA-120) in the rat dorsal root ganglion.

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The effects of ricin (RCA-120) on non-injected dorsal root ganglion (DRG) cells, sharing the same DRG as the injected ones, were studied after ricin injections into the tibial nerve and B-HRP injections into the peroneal nerve. Numerous DRG cells containing B-HRP reaction product and exhibiting

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

Ultrastructure of degenerative changes following ricin application to feline dental pulps.

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The ultrastructure of degenerative changes within the ipsilateral trigeminal ganglion, and partes caudalis and interpolaris of the spinal trigeminal nucleus in the cat is described following the application of the potent toxin ricin to the tooth pulps of unilateral maxillary and mandibular posterior

Morphology of ricin and abrin exposed endothelial cells is consistent with apoptotic cell death.

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Cultures of bovine pulmonary endothelial (BPE) cells were exposed to LC70 doses of ricin or abrin (15.5 and 4.5 pM respectively) over a period of up to 40 h. The viability of the cultures (as determined by the neutral red (NR) dye retention assay) declined after 6 h exposure to the toxins. From 15 h

Toxicity and immunogenicity of monoclonal antimelanoma antibody-ricin A chain immunotoxin in rats.

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This study was performed to assess the subacute toxicity and immunogenicity in rats of XOMAZYME-MEL, an antimelanoma monoclonal antibody-ricin A chain immunotoxin. Female Sprague-Dawley rats received 14 consecutive daily i.v. injections of XOMAZYME-MEL at doses of 5 mg/kg/day, 1 mg/kg/day, or normal

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