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Journal of Neuroscience, Vol 8, 2887-2894, Copyright © 1988 by Society for Neuroscience
Catecholamine toxicity in cerebral cortex in dissociated cell culture
PA Rosenberg
Department of Neurology, Children's Hospital, Boston, Massachusetts 02115.
Identification of endogenous toxins and characterization of the mechanisms
by which toxins produce cell injury and death may help understand both
normal modeling of cell populations and connections in the CNS as well as
abnormal cell loss. The toxicity of catecholamines intrinsic to the CNS was
investigated using the model system of rat cerebral cortex in dissociated
cell culture. All catecholamines tested, including norepinephrine (NE),
dopamine, and epinephrine, were toxic to neurons as well as glia at a
concentration of 25 microM when added to cultures 24 hr after plating.
Toxicity was evident after 48 hr exposure to NE, as monitored by loss of
cells from the cultures. Toxicity did not seem to be mediated by adrenergic
receptors because, although the beta-adrenergic agonist isoproterenol (but
not the alpha-adrenergic agonist phenylephrine) was similar in its toxic
effect to NE, the beta- adrenergic antagonist atenolol did not block the
toxic effect of NE. Toxicity could be mimicked by hydrogen peroxide, a
product of the oxidative degradation of catecholamines. Toxicity of NE was
blocked by catalase. The neurotoxin 6-hydroxydopamine (6-OHDA), supposedly
selective for catecholaminergic neurons, was found to be toxic over the
same concentration range as NE. These results suggest that endogenous
catecholamines may play a role in normal and abnormal cell death, and
suggest that caution be used in relying on the specificity of 6-OHDA and
other supposedly selective neurotoxins.
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