Behaviour of biogenic amines was studied in the brains of Mongolian gerbils subjected to unilateral occlusion of the common carotid artery. Assays on the hemispheres ipsilateral to occlusion revealed in symptom-positive animals a progressive decrease in norepinephrine and dopamine, and an increase in serotonin throughout the duration of an ischemic insult. In post-ischemic periods following the release of the clip, changes in biogenic amine levels generally conformed to the principles of a previously described “maturation” phenomenon, with delayed reactions occurring after the shorter ischemic insults.

Experimental cerebral ischemia in Mongolian gerbils. IV. Behaviour of biogenic amines.

The nerve cell body response to axotomy.

Trigeminal ganglia of normal rats and of adult rats subjected to unilateral transection of the infraorbital nerve were studied by light and electron microscopy. Counts of ganglion cells in ganglia on operated and unoperated sides were made following long postoperative survival times. The ultrastructural changes in ganglia of the operated side were studied from 3 to 70 days postoperatively. The quantitative observations show that a considerable loss of ganglion cells takes place on the operated side. The ultrastructural observations demonstrate the occurrence of ganglion cell degeneration, nerve fibre degeneration and phagocytosis by satellite and Schwann cells. The results are compatible with the view that degeneration of trigeminal afferents in the brain stem following lesions of peripheral trigeminal nerve branches is related to retrograde degeneration of trigeminal ganglion cells.

Nerve cell degeneration and death in the trigeminal ganglion of the adult rat following peripheral nerve transection.

Regulation of peripherin and neurofilament expression in regenerating rat motor neurons.

Following olfactory bulb removal in young and adult rats, many neurons in the primary olfactory cortex become markedly argyrophilic in silver impregnated preparations. Although argyrophilic neurons are found scattered throughout the pyramidal and multiform cell layers, the heaviest concentration is seen in the superficial part of the pyramidal layer.



Electron microscopic analysis reveals that argyrophilic neurons are undergoing rapid degeneration. The degenerative changes are similar in all affected cells, although some cells begin to disintegrate within 24 hours following bulbectomy, whereas others are just beginning to show pathological changes at three or four days. The first clear signs of cellular degeneration occur in the cytoplasm of the perikaryon and involve swelling of mitochondria and polysome disaggregation. An increase in the electron density of the cytoplasm follows and this is accompanied by the appearance of enlarged cisternae and disruption of the nuclear membrane. Degenerative changes in the nucleus usually are detected at a slightly later stage than in the cytoplasm. Nuclear changes are characterized by the proliferation of local aggregations of condensed chromatin, and the replacement of the nucleolus with large homogenous islands of electron dense material. In advanced stages of degeneration ribosomes are increased in density and become uniformly dispersed throughout the cytoplasm. Remnants of necrotic organelles are visible only at the cellular periphery, and phagocytosis of dying neurons by astrocytes and microglia follows quickly.



Evidence from HRP-studies indicates that cells in the olfactory cortex, which project directly to the bulb do not correspond to those which show fulminant necrosis following olfactory bulb removal. The majority of those which degenerate are located superficially, whereas the cells of origin of the centrifugal projection lie more deeply. Based on this dissociation, it is proposed that rapid cell death in the olfactory cortex is not caused by retrograde factors involving axotomy, but is due instead to transneuronal deafferentation that results from a sudden massive loss of input from the olfactory bulb.

Rapid transneuronal degeneration and death of cortical neurons following removal of the olfactory bulb in adult rats.

Described here are ultrastructural changes in neurons of feline red nucleus exhibiting axon reaction after unilateral rubropsinal tratotomy at the C-2 level and surviving 2 to 65 days. Ultrastructural alterations included neurofilamentous hyperplasia; proliferation of smooth ER; temporary disappearance of organized granular ER with partial substitution by haphazardly arranged, broad cisternal profiles; loss of rosette ribosomes and occurrence of single ribonucleoprotein granules or an intercisternal amorphous density; increased numbers of subsurface cisterns and allied structures, often disposed in stacks; vesiculation and vacuolation of Golgi cisternae; prevalence of autophagic bodies derived in part from Golgi complexes; probable mitochondrial hyperplasia and various qualitative changes in these organelles; an increase in lipofuscin. Dendritic changes paralleled those of perikarya save that proliferation of subsurface cisterns and autophagic bodies was absent. Abnormalities of myelinated axons and boutons occurred and may have originated from retrograde degeneration of cortical neurons induced by lateral funiculotomy. Some perikarya were devoid of axosomatic boutons. Ultrastructural changes varied with the length of postoperative survival and were, at least partly, reversible. Chromatolysis was detectable light microscopically before ultrastructural abnormality appeared. The bearing of transneuronal mechanisms on axon reaction of central neurons and the protective effect of section of axons beyond the site of origin of collaterals are discussed.

J. Ernest Mincy

Papers

Ultrastructure of axonal reaction in red nucleus of cat.