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pocampal neurogenesis by 42%. A similar effect is revealed after chronic
self-administration of heroin. Because adrenalectomy and corticosterone
replacement have no effect on neurogenesis, the opiate suppression is not
mediated by changes in circulating levels of glucocorticoids. These fi ndings
suggest that opiates may infl uence hippocampal function via regulation of
neurogenesis in the adult rat hippocampus.
5. Functional Roles of Adult Neural Progenitor Cells
The adult brain has long been thought to be entirely postmitotic. Hence,
functional roles of adult neural progenitors in the CNS are unclear at present.
It has been suggested that they are vestiges of evolution from more primitive
organisms, such as fi sh (41) , in which organ and tissue self-renewal provides
survival advantages in an inhospitable environment. However, along with
emerging studies on this issue, some functional roles of adult neurogenesis can
be speculated and tested. Under physiological conditions, neurogenesis may
replace cells programmed for death with fully functional cells, even though this
repopulation is considered to be very limited in adult brains. More importantly,
the adult mammalian nervous system retains the capacity of adapting new
demands of brain functions, such as learning, memory, and neural plasticity in
response to environmental changes. It is possible that the local generation of
new neuronal and non-neuronal cells in the responsible brain structures could
participate in the acquisition or integration of new memories and neuroadapta-
tion. As to region-specifi c roles, the SVZ is more likely a stem-cell factory
conveniently located in the brain. Through proliferation, it manufactures
progenitor cells infi nitely and delivers them to their destinations in the whole
brain (42 , 43) . As compared to the SVZ, neurogenesis in the hippocampus can
directly add new granule cells in the dentate gyrus whenever a call is made for
new memory or neuroadaptive formation.
Under pathophysiological conditions, inducible cytogenesis can play dual
roles in a given pathophysiological process. First, cytogenesis can be provoked
to process aberrant functions. For example, the neurons that are formed through
normal ongoing neurogenesis do not send processes to the CA3 region of
the hippocampus (44 , 45) . However, epilepsy-induced neurogenesis sends
axon collaterals back onto the dentate gyrus that forms recurrent collaterals
contributing to enhanced local activity for epilepsy (44) . Second and more
signifi cantly, cytogenesis can be stimulated to repair (rescue or compensate) for
cell loss in chronic neurodegenerative diseases, such as Parkinson's disease. In
this case, repopulation of missing cells by increased endogenous neurogenesis
in the diseased site could be an ideal “self-repair.” The newborn cells after
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