CHROMATOLYSIS RECONSIDERED: A NEW VIEW OF THE REACTION OF THE NERVE CELL BODY TO AXON INJURY

Author(s):  
Bernice Grafstein
2010 ◽  
Vol 6 (1) ◽  
pp. 3-10 ◽  
Author(s):  
Ennio Pannese

In sensory ganglia each nerve cell body is usually enveloped by a satellite glial cell (SGC) sheath, sharply separated from sheaths encircling adjacent neurons by connective tissue. However, following axon injury SGCs may form bridges connecting previously separate perineuronal sheaths. Each sheath consists of one or several layers of cells that overlap in a more or less complex fashion; sometimes SGCs form a perineuronal myelin sheath. SGCs are flattened mononucleate cells containing the usual cell organelles. Several ion channels, receptors and adhesion molecules have been identified in these cells. SGCs of the same sheath are usually linked by adherent and gap junctions, and are functionally coupled. Following axon injury, both the number of gap junctions and the coupling of SGCs increase markedly. The apposed plasma membranes of adjacent cells are separated by 15–20 nm gaps, which form a potential pathway, usually long and tortuous, between connective tissue and neuronal surface. The boundary between neuron and SGC sheath is usually complicated, mainly by many projections arising from the neuron. The outer surface of the SGC sheath is covered by a basal lamina. The number of SGCs enveloping a nerve cell body is proportional to the cell body volume; the volume of the SGC sheath is proportional to the volume and surface area of the nerve cell body. In old animals, both the number of SGCs and the mean volume of the SGC sheaths are significantly lower than in young adults. Furthermore, extensive portions of the neuronal surface are not covered by SGCs, exposing neurons of aged animals to damage by harmful substances.


1985 ◽  
Vol 47 (5) ◽  
pp. 735-738 ◽  
Author(s):  
E. Nasi ◽  
D. Tillotson
Keyword(s):  

Nature ◽  
1980 ◽  
Vol 286 (5775) ◽  
pp. 816-817 ◽  
Author(s):  
D. Tillotson ◽  
A. L. F. Gorman
Keyword(s):  

1980 ◽  
Vol 87 (1) ◽  
pp. 23-43
Author(s):  
W. R. Schlue ◽  
J. W. Deitmer

Potassium-sensitive double-barrelled microelectrodes were used to measure the potassium content of extracellular spaces in leech ganglia, both intact and with the ganglion capsule opened. When the ganglion capsule was opened, the extracellular concentrations of potassium in the ganglion were similar to that of the bathing medium (4 mM). With intact ganglia the extracellular potassium concentration in the neuropile averaged 6.3 +/− 0.7 mM and in the nerve cell body region 5.8 +/− 0.6 mM. The potential measured in these parts of the ganglion was between +2 and −8 mV, averaging −1.9 mV. The change of potassium concentration in the extracellular spaces following increase or decrease in the concentration of potassium ions in the bath declined exponentially. This rate of change, which would be expected of a first-order diffusion process, was found in both the neuropile and the nerve cell body region. In a medium containing 5 × 10(−4) M ouabain, the potassium concentration in both parts of the ganglion increased transiently by an average of 3.8 +/− 1.0 mM in the neuropile and 1.2 +/− 0.4 mM in the nerve cell body region. Negatively charged polyelectrolytes in extracellular spaces of leech ganglia could affect the distribution of potassium ions to give a Donnan distribution. It is also possible, that the endothelial layer influences the extracellular potassium concentration in a ganglion under resting conditions.


The distribution of motor nerve cell bodies in the metathoracic ganglion of the cockroach Periplaneta americana was mapped and displayed in three dimensions. A dense ring of ribonucleic acid ( RNA ) appears in the perinuclear cytoplasm of a nerve cell body whose axon has been cut in a peripheral nerve trunk. Using this RNA ring as the primary marker, 5 cell maps of ganglia from different animals were constructed to indicate which motor nerve cell body sends its axon out a particular peripheral nerve trunk. We count about 3000 neurons in the ganglion, and of these about 230 are above 20 /an in diameter. About 100 of these larger cells are generally arranged in bilaterally symmetrical pairs. These cell pairs have been assigned numbers and can be identified from one animal to another. Nerve cell bodies associated with nerves 3 through 6 send their axons out the ipsilateral nerve trunks. Cells associated with nerve 2 send their axons out the contralateral nerve trunk. This study may provide a basis for understanding the structural and metabolic organization responsible for the particular behavioural capacities of certain populations of neurons.


It is possible to reveal all the terminal boutons on the ventral horn cells of the spinal cord after fixation with formalin, mordanting (Weigert-Pal), embedding in carbowax and staining with haematoxylin or by a silver method. The boutons are more numerous than has been supposed and cover the greater part of the surface of the nerve cell body and dendrites. Electron micrographs after osmium fixation show a thin membrane at the surface of the nerve cell body and dendrites. The boutons are closely apposed to this surface and are themselves covered by thin membranes. At the region of contact there is usually no separation visible, with the relatively low magnification used, between pre- and post-synaptic membranes. The boutons contain many bodies that absorb electrons strongly and are presumably mitochondria. The pre-synaptic nerve fibres are provided with relatively thick sheaths, except where they swell out to form boutons. The protoplasm of glia cells fills up all the space between the neuronal elements. No large tissue spaces or intercellular matrix appear. Exchanges between the neurons and capillaries presumably take place through the glial protoplasm.


Neurosurgery ◽  
2009 ◽  
Vol 65 (suppl_4) ◽  
pp. A74-A79 ◽  
Author(s):  
Peter M. Richardson ◽  
Tizong Miao ◽  
Dongsheng Wu ◽  
Yi Zhang ◽  
John Yeh ◽  
...  

Abstract OBJECTIVE Peripheral nerve injury causes retrograde changes in the damaged neurons, which are beneficial to axonal regeneration. Better understanding of the mechanisms of induction and mediation of these conditioning responses would help to design strategies to invoke stronger regenerative responses in neurons in situations when these responses are inadequate. METHODS Relevant literature is reviewed. RESULTS Experimental preparations that measure the influence of peripheral axotomy on regeneration in the central axons of primary sensory neurons are useful to examine mechanisms of conditioning neurons. Despite 4 decades of speculation, the nature of the damage signals from injured nerves that initiate axonal signals to the nerve cell body remains elusive. Members of the family of neuropoietic cytokines are clearly implicated, but what induces them is unknown. Multiple changes in gene regulation in axotomized neurons have been described, and dozens of growth-associated genes have been identified: neurotrophic factors, transcription factors, molecules participating in axonal transport, and molecules active in the growth cone. The mechanisms of interaction of a few regeneration-associated molecules with the signaling cascades that lead to actin and tubulin remodeling at the growth cone are understood in some detail. In animals, viral gene therapy to deliver regeneration-associated genes to neurons or other local measures to induce these genes can improve regeneration. A few pharmacological agents, administered systemically, have small beneficial effects on axonal regeneration. CONCLUSION Advances in laboratory research have provided knowledge of cell body responses to axotomy with clinical relevance.


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