Neurons chromatolysis

Effects in Laboratory Animals. As highlighted in other chapters, the central toxicities during and after repeated stimulant bingeing may be related to neuronal or terminal destruction and/or depletion of neurotransmitter in the brain. In monkeys and cats, the report by Duarte-Escalante and Ellinwood (1970) of neuronal chromatolysis associated with decreased catecholamine histofluorescence following chronic METH intoxication has been followed by extensive neurochemical demonstrations of damage to the monoamine pathways by chronic stimulants (Seiden and Ricaurte 1987). 

Effects In Humans. Neither postmortem nor functional cerebrospinal fluid (CSF) studies in humans provide firm evidence for similar, long-term damages or alterations to monoaminergic neurons in chronic stimulant abusers. In part, the lack of demonstrable neurochemical changes may well be due to the obvious preclusion of well-controlled prospective experimentation in humans, as well as to variability in critical variables (e.g., individual sensitivity or pattern of abuse) encountered in clinical research. Possible relationship of the various complications of stimulant abuse including hyperpyrexia, seizure, anoxia, and metabolic exhaustion to neuronal chromatolysis, terminal destruction, and monoamine and enzymatic depletion have not been systematically explored in human autopsy eases. It should be also noted that, under nonperturbed conditions, overt behavioral deficits are rare in... 

FIGURE BO-2 Wallerian degeneration in the PNS. After an axon is injured, resulting chromatolysis, i.e. stress reaction and increased protein synthesis, occurs in the neuronal cell body, with axonal and myelin degeneration distal to the injury. Growth-permissive Schwann cells secrete growth factors that stimulate axons to regenerate. 

The somata of neurons respond to axotomy by chromatolysis in the adult 112 those of neonates are more sensitive and degenerate.113 The release of neurotoxins from reactive glia in damaged neuropil (see above) also causes neuronal cell death. Within wounds there are elevated titres of the excitotoxic amino acids, glutamate and aspartate,114 released from damaged neurons and glia,115 which activate A-methyl-D-aspartate (NMDA) receptors on neurons. The resulting raised intracellular levels... 

Grant G, Wisten B, Berkley KJ, Aldskogius H (1982) The location of cerebellar projecting neurons within the lumbosacral spinal cord in the cat. An anatomical study with HRP and retrograde chromatolysis. J. Comp. Neurol, 204, 336-348. 

The lesions of the nervous system start in the cortex and progressively invade the midbrain and the medulla. The first symptoms are paresthesias, pain in the back, vertigo, headaches, general fatigue, and sensorial perversion associated with depression, melancholy, and suicidal tendencies. These symptoms may develop into a more characteristic psychiatric syndrome, with hallucinations, schizophrenia, and maniac dementia. At autopsy, the brain reveals edema, congestion of the cortex, and loss of ganglion cells. The neurons show chromatolysis. 

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