The post-mortem origin and mechanism of neuronal hyperchromatosis and nuclear pyknosis

Cammermeyer, Jan

doi:10.1016/0014-4886(60)90022-4

Cited by 126 publications

(27 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…However, these dissimilarities are not sufficient to negate the message of the present investigation, specified in the first sentence of the previous paragraph. The sporadic formation of "dark" (strikingly shrunken and hyperbasophilic) neurons as a result of post mortem mechanical injuries to unfixed or improperly fixed brains, and its avoidance by transcardial perfusion fixation and a 1-day delay of the brain autopsy, have long been known (Cammermeyer, 1960 and1961). Since these "dark" neurons have been regarded as artifacts, their ultrastructure has not been investigated so far.…”

Section: Comments On the Methods Used And The Results Obtainedmentioning

confidence: 99%

Gel-to-gel phase transition may occur in mammalian cells: Mechanism of formation of ?dark? (compacted) neurons

Gallyas

2004

Biology of the Cell

View full text Add to dashboard Cite

In the course of many diseases, individual non-apoptotic cells that are randomly distributed among undamaged cells in various mammalian tissues become shrunken and hyperbasophilic ("dark"). The light microscopic shrinkage is caused by a potentially reversible, dramatic compaction of all ultrastructural elements inside the affected cells, and escape of the excess water through apparently intact plasma membrane. In the case of neurons, the ultrastructural compaction rapidly involves the soma-dendrite domains in an all-or-nothing manner, and also mm-long axon segments. The present paper demonstrates that such ultrastructural compaction in neurons, which affects the whole soma-dendrite domain or long axon segments, can take place both immediately after an in vivo head injury and in rat brains perfusion-fixed for 30 min., and then chilled to just above the freezing point before the same kind of head injury was inflicted. This argues strongly against any enzyme-mediated compaction mechanism. On the analogy of gel-to-gel phase transitions in polymer chemistry, we hypothesize a pure physico-chemical compaction mechanism. Specifically, after initiation at a single site in each affected cell, the ultrastructural compaction is propelled throughout the whole cell on the domino principle by the free energy stored in the form of non-covalent interactions among the constituents of some cytoplasmic gel structure.

show abstract

Section: Comments On the Methods Used And The Results Obtainedmentioning

confidence: 99%

Gel-to-gel phase transition may occur in mammalian cells: Mechanism of formation of ?dark? (compacted) neurons

Gallyas

2004

Biology of the Cell

View full text Add to dashboard Cite

show abstract

“…Histologicamente, nos casos agudos há necrose laminar e segmentar dos neurônios corticais do telencé-falo, caracterizada por encarquilhamento e eosinofilia citoplasmática, cromatólise e picnose nuclear (neurônios vermelhos). Os neurônios necróticos não devem ser confundidos com os chamados "neurônios escuros" pretos ou azul-escuros, que são artefatos pós-mortais que são formados comumente por manipulação excessiva do encéfalo na retirada do crânio (Cammermeyer 1960, Jortner 2006. Edema também é uma alteração comum e consiste de aumento dos espaços perineuronais e perivasculares e formação de numerosos vacúolos no neurópilo (espongiose).…”

Section: Achados De Necropsia E De Histopatologiaunclassified

Polioencefalomalacia em ruminantes

Sant’Ana¹,

Lemos

Nogueira

et al. 2009

Pesq. Vet. Bras.

View full text Add to dashboard Cite

Polioencefalomalacia (PEM) de ruminantes é uma doença complexa. O termo indica um diagnóstico morfológico em que necrose neuronal grave resulta em amolecimento da substância cinzenta do cérebro. Interpretada no início como uma doença única, causada por deficiência de tiamina, acredita-se hoje que várias causas e diferentes mecanismos patogênicos, ou um único mecanismo patogênico disparado por diferentes agentes, sejam responsáveis pelo aparecimento da doença. Neste artigo, as possíveis causas e a patogênese de PEM em ruminantes são criticamente revisadas e discutidas. Também são revisadas a epidemiologia, os sinais clínicos, os achados macro e microscópicos e os métodos de diagnóstico, tratamento e controle.

show abstract

“…The hyperchromatic neurone or 'dark cell' has been the subject of numerous studies, including those of Scharrer (1938), Wolf and Cowaen (1949), Koenig and Koenig (1952), Cammermeyer (1960Cammermeyer ( , 1961Cammermeyer ( , 1962 and Cohen and Pappas (1969). This artefact is most frequently observed after a fresh neurosurgical biopsy specimen is fixed in formaldehyde, when the brain of a normal animal removed immediately after death is immersed in a fixative, or when a perfusion-fixed brain is removed immediately from the skull.…”

mentioning

confidence: 99%