Neuronal uptake of plasma proteins in cryogenic brain lesions

Løberg, E. M.; Brorson, Sverre‐Henning; Skjørten, F; Torvik, Ansgar

doi:10.1111/j.1699-0463.1992.tb04037.x

Cited by 3 publications

(2 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…1,4,12,25,28,29,[34][35][36]39,40 The distribution of albumin within the neurons in the present study was similar to that in other reports. [17][18][19][20][34][35][36] At the edge of the lesion, neuronal staining for albumin was of two types. The albumin immunostaining in some neurons was homogeneous, obscuring cytoplasmic and nuclear details, whereas in other neurons the staining was only cytoplasmic.…”

Section: Fate Of Extravasated Proteinsmentioning

confidence: 99%

See 1 more Smart Citation

Neurotoxicity of 1,3,5-Trinitrobenzene (TNB): Immunohistochemical Study of Cerebrovascular Permeability

et al. 1999

View full text Add to dashboard Cite

Abstract. 1,3,5-Trinitrobenzene (TNB) is a soil and water contaminant at certain military installations. Encephalopathy in rats given 10 daily oral doses of TNB has been reported. The lesion was bilaterally symmetric vacuolation and microcavitation in the cerebellar roof nuclei, vestibular nuclei, olivary nuclei, and inferior colliculi. The contribution of the blood-brain barrier (BBB) in the genesis of these lesions remains uncertain. One of the main goals of the present work was to evaluate the functional state of the BBB. Male Fischer 344 rats (five rats/group) were euthanatized after four, five, six, seven, eight, or 10 daily doses of TNB (71 mg/kg). A different set of rats (five rats/group) was allowed to recover for 10 or 30 days after receiving 10 doses of TNB. Integrity of the BBB was assessed by immunohistochemical staining for extravasated plasma albumin on paraffin-embedded sections. Rats euthanatized after four to eight doses had no lesions, and albumin extravasation in the susceptible regions of the brain was minimal. Rats receiving 10 daily doses of TNB had bilaterally symmetric vacuolation and microcavitation in the cerebellar nuclei, vestibular nuclei, and inferior colliculi in association with multifocal, often confluent foci of extravasated albumin in susceptible nuclei. Albumin was present in vascular walls, extracellular space, and neurons. Immunoreactivity in neurons was of two types: cytoplasmic staining representing pinocytic uptake and homogenous staining of the entire neuron (nucleus and cytoplasm) due to uncontrolled albumin leakage through the damaged cell membrane. In rats allowed to recover for 10 days, the microcavitated foci were infiltrated by glial and gitter cells. Albumin immunoreactivity was present as extracellular granular debris, and neuronal staining (for albumin) was mild. In rats allowed to recover for 30 days, immunoreactivity to albumin was not seen. This study demonstrates that TNB-mediated tissue damage is accompanied by breakdown of the BBB. The presence of vacuolation and associated extravasated serum proteins in TNB-treated rats is an indication of vasogenic brain edema, which appears to be a critical event in TNB toxicity. Additional studies are needed to determine the reason for selective regional vulnerability and brain microvasculature susceptibility to TNB.

show abstract

Section: Fate Of Extravasated Proteinsmentioning

confidence: 99%

“…Immunohistochemical staining for albumin in histologic sections is a well-established method for demonstrating extravasation and confirming vasogenic edema. [17][18][19][20][34][35][36] …”

mentioning

confidence: 99%

Neurotoxicity of 1,3,5-Trinitrobenzene (TNB): Immunohistochemical Study of Cerebrovascular Permeability

et al. 1999

View full text Add to dashboard Cite

show abstract

Antibody penetration into LR-White sections

Brorson¹,

Roos

rten³

1994

Micron

View full text Add to dashboard Cite

Early entry of plasma proteins into damaged neurons in brain infarcts

Løberg¹,

Hassel²,

Fonnum³

et al. 1994

APMIS

Self Cite

View full text Add to dashboard Cite

Entry of plasma proteins into damaged neurons has previously been demonstrated in various pathological conditions, but little is known about brain infarcts in this respect. In the present study, focal ischemic lesions were produced in rats by permanent occlusion of the middle cerebral artery (MCA). The animals were killed from 1 to 48 h postlesion. Leakage of plasma proteins across the blood‐brain barrier into the infarcted area was visualized with immunostaining 2–3 h after the occlusion. This is earlier than in most previous reports. Entry of plasma proteins into ischemic neurons was seen 3 h after permanent occlusion of the MCA, while reliable changes were not seen until 12–24 h in sections stained with hematoxylin and eosin (H & E). Ischemic neurons stained for plasma proteins irrespective of their morphological appearance. Even cells that appeared normal with H & E staining were positively labeled. The technique may be used to diagnose very early ischemic lesions.

show abstract

Neuronal uptake of plasma proteins in cryogenic brain lesions

Cited by 3 publications

References 21 publications

Neurotoxicity of 1,3,5-Trinitrobenzene (TNB): Immunohistochemical Study of Cerebrovascular Permeability

Neurotoxicity of 1,3,5-Trinitrobenzene (TNB): Immunohistochemical Study of Cerebrovascular Permeability

Antibody penetration into LR-White sections

Early entry of plasma proteins into damaged neurons in brain infarcts

Contact Info

Product

Resources

About