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Postnatal development of monoamine neurotransmitters and receptors in the occipital cortex of the cat
Author(s) -
Jonsson G.,
Kasamatsu T.
Publication year - 1985
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/0736-5748(85)90098-x
Subject(s) - monoamine neurotransmitter , citation , neuroscience , cortex (anatomy) , psychology , library science , biology , receptor , computer science , genetics , serotonin
After injury of their axon damaged neurons shift their metabolic activity into a reparative mode aimed at survival and recovery by axonal regeneration or, alternatively they prepare themselves for death and undergo degeneration. It is proposed that these metabolic shifts are the result of initial specific biophysical and biochemical changes which are initiated immediately after the injury. We obtained evidence that within minutes after axotomy, changes in calcium ion fluxes become essential for the rapid activation of the enzyme transglutaminase, selectively in the nuclear fraction. This calcium-activated enzyme catalyzes the covalent binding of polyamines to glutamine residues on peptide chains and may thereby lead to cross-links between them. These findings imply that polyamine-dependent post-translational modification of nuclear proteins may play a regulatory role at the genom level after axonal injury. This notion is supported by the demonstration that inhibition of polyamine biosynthesis results in the selective death of axonally damaged neurons while undamaged neurons remain intact.