Chromatolysis

[1] The term "chromatolysis" was initially used in the 1940s to describe the observed form of cell death characterized by the gradual disintegration of nuclear components; a process which is now called apoptosis.

[2] Chromatolysis is still used as a term to distinguish the particular apoptotic process in the neuronal cells, where Nissl substance disintegrates.

In 1885, researcher Walther Flemming described dying cells in degenerating mammalian ovarian follicles.

[2] Around the same time of Flemming's research, chromatolysis was also studied in the lactating mammary glands and in breast cancer cells.

From observing the regression of ovarian follicles in mammals, it was argued that a necessary cellular process existed to counterbalance the proliferation of cells by mitosis.

These budding fragments were termed "apoptotic bodies," thus coining the name "apoptosis" to describe this form of cell death.

For example, there is an increase in phosphorylated neurofilament proteins and cytoskeletal components, tubulin and actin, in neurons undergoing chromatolysis.

Changes in the cell body cytoskeleton seem to be responsible for enhanced nuclear eccentricity following axonal injury.

In one study groups of rats were injected with acrylamide for 3, 6, and 12 days and the A- and B-cell perikarya of their L5 dorsal root ganglion were examined.

The study involved the injection of large doses of lithium chloride into female Lewis rats over several day periods.

[7] Central chromatolysis has been observed in spinal anterior horn and motor neurons of patients with amyotrophic lateral sclerosis (ALS).

The most typical functional change in chromatolytic motor neurons is the significant reduction in size of the monosynaptic excitatory postsynaptic potentials (EPSPs).

[14] Most recent studies have observed chromatolysis in cells from rats that have been subjected to either copper or aluminum toxication, which are both hypothesized to be involved in the pathogenesis of Alzheimer's disease.

The symptoms of IBNC in cattle are clinically similar to those characterized by bovine spongiform encephalopathy, otherwise known as mad-cow disease.

IBNC has been characterized by severe neuronal, axonal, and myelin degradation, accompanied by non-supportive inflammation and changes in spongiform of various regions of grey matter.

Mild to severe degeneration of spinal cord tracks has been observed in patients with Marchiafava–Bignami disease and Wernicke–Korsakoff syndrome, both forms of encephalopathy linked to alcohol.

[9][20] It is clear that axotomy is one of the most direct inducers of chromatolysis and if further research were put into elucidating the specific pathways which associate axonal damage to chromatolysis, then potential therapies could be developed for halting the chromatolytic response of neurons and ameliorating the detrimental effects of degenerative diseases, such as Alzheimer's and ALS.

This drawing compares a normal neuron to one undergoing chromatolysis after axonal injury. Regeneration after axonal injury may occur.
A high magnification micrograph of the anterior horn of the spinal cord showing motoneurons with central chromatolysis visualized using hematoxylin and eosin staining. The chromatolytic cells in the image are those that appear swollen and are missing dark purple substance in the interior.
An image of an axotomized spinal motor neuron with Nissl bodies and lipofuscin . The pink structures are Nissl bodies and the blue and yellow structures are the lipofuscin granules. In chromatolysis of motor neurons, these pink structures dissolve. [ 8 ]