Zen-Brain Reflections by James H. Austin

Author:James H. Austin
Language: eng
Format: mobi, epub, pdf
Published: 2011-11-25T20:06:00+00:00

Item: The ACH nerve cells in the brainstem are highly resistant to the toxic side effects of NO'. In fact, ACH nerve cells cultured from the parabrachial nuclei are some 300 times more resistant than are ACH cells from the medial septal region [Z:165].27 During near-death states, when there is a terminal flurry of excitation/inhibition, when an extra release of NO' reaches levels that would prove toxic elsewhere, and when many anoxic regions of the brain have shut down, these surviving ACH nerve cells could still be contributing to the phenomena of near-death experiences [Z:164-169, 443, 452].

Unhappily for healthy seniors who could need help forming new memories, experiments suggest that NO' reduces the growth of new nerve cells (neurogenesis) in adult rat brain.2s Various kinds of oxidative damage have been linked increasingly with degenerative diseases of the human nervous system. The evidence suggests that reactive oxygen species selectively nitrate a second amino acid, tyrosine. The result is that certain proteins will now have their properties changed by this new moiety, 3-nitrotyrosine. Antibodies which detect this altered tyrosine are now available. They can serve to target localized nerve cells that have had their proteins modified by an unusual local exposure to NO'.29 This could be a useful chemical "fingerprint" for NO'.

NO' has important implications with regard to neuronal plasticity. The influence that NO' has in changing the brain is not limited to certain forms of ("shorter") long-term potentiation in the hippocampus. NO' may also be involved in different, very long-term potentiation changes that also affect the brain [Z:181, 677]. For example, NO' can enhance the growth factor responses of a cell by virtue of its ability to increase both a moiety called p2l ras and certain kinases. This effect that NO' has on gene transcription does not require cGMP.3"

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