Factors restricting maximal preservation of neuronal glycogen after perfusion fixation with dimethyl sulfoxide and iodoacetic acid in Bouin's solution. Histochemical observations in the brain of the Netherlands dwarf rabbit.

Thirty seconds after an initial intracardial epinephrine injection, deeply anesthetized animals are perfused consecutively with saline, Bouin's and 100% ethanol solutions, each containing 1% or 5% DMSO (Me2SO) and 0.01 M iodoacetic acid. In the Netherlands dwarf rabbit and the guinea pig, a maximal preservation of dimedone PAS-stainable, saliva-digestible glycogen is achieved, without signs of polarization of glycogen, in many neuronal and neuroglial cells occupying either brain stem nuclei or occasionally narrow perivascular zones.

Argentophil neuronal perikarya and neurofibrils induced by postmortem trauma and hypertonic perfusates.

Argentophil neuronal perikarya and perikaryal neurofibrils similar to those illustrated in Ramón y Cajal's classical studies have in the present investigation been found to be manifestations of the chromophil neuron. Conclusive evidence of such association was obtained by silver impregnation with the Bodian technique of sections previously stained with cresyl violet. Regardless of the fixative used, silver-impregnated neurofibrils were evident when (1) normal tissues were fixed by immersion or unsuccessfully fixed by perfusion, (2) normal tissues were exposed and touched after death but before perfusion with the fixative, or (3) flow of perfusates was compromised by the effect of an experimental procedure, as well as when (4) a hypertonic saline solution was used in the first perfusate.

Is the solitary dark neuron a manifestation of postmortem trauma to the brain inadequately fixed by perfusion?

Dark neurons, classified as solitary because of their sparse occurrence, were discerned in the transitional zones between gray and white matter in various species of laboratory animals fixed by perfusion. These neurons, histologically indistinguishable from dark neurons in immersion fixed material, tended to develop when the saline perfusion was delayed or slow, the amount of the Bouin fixative was excessive, or the autopsy was performed shortly after the perfusion. Under these conditions, the white matter manifested a softer consistency and a paler color than the gray matter.

Cerebral and retinal fat emboli in normal animals fixed by perfusion.

The brains and retinas of laboratory animals fixed by perfusion occasionally contain isolated round fat emboli, which increase in number if the two organs are covered with oil during the autopsy. These emboli, in contrast to emboli induced by intravenous injection of oil, are present in smaller numbers, occur without adjacent aggregation of erythrocytes and do not cause widening of the occluded vascular channel. The fat emboli in the normal brain are attributed to connective tissue fat aggregating on the exposed cerebral surface and flowing through openings cut in the leptomeninges and the vascular walls during removal of the brain.

Factors contributing to denucleation of cerebral mast cells.

When mast cells, identified by metachromatic color in cresyl-echt-violet-stained paraffin sections, aggregate in large numbers, the intensity of cytoplasmic granulation varies. The intensely stained cytoplasmic granules of heavily granulated cells may be pushed over the microscopic section by the microntome blade either in the direction of cutting or against it. In the pale mast cells, in which a progressive pyknosis and atrophy of the nuclei by compaction of DNA particles take place, dislodgment and displacement of the pyknotic nuclei may occur in 1.

The effect of cortisone treatment and reoperation on reactive changes in the facial nucleus after axotomy.

The material, with few exceptions, consists of PAS-gallocyanin stained paraffin sections from 4- to 6-month-old male rabbits fixed by perfusion first with saline and then with Bouin's solution. (1) In animals treated with cortisone prior to and subsequent to axotomy, the neurons exhibit an accelerated dispersal and delayed reconstitution of Nissl substance (ribosomes). While mitotic activity is depressed at various sites, formation of new microglial cells is evident.