Biomedical Engineering Reference
In-Depth Information
differentiation in situ may partly or completely take on the exact function of
the cells they replace. Further studies are needed to explore anatomical and
functional “self-repair” of this kind in various neurodegenerative diseases, and
results from these studies may bring about a new therapy for those diseases.
6. Implications in Psychostimulant Dependence and Medication
With limited studies, how drug exposure influences brain cytogenesis
and how altered cytogenesis contributes to addictive properties of drugs of
abuse can only be hypothesized at present. As described in the preceding,
amphetamine exposure decreases total cell proliferation in the striatum (13) .
Morphine, heroin, and methamphetamine decrease hippocampal neurogenesis
(36 , 40) . However, alteration in proliferation of a given population of cells in the
affected areas remains unidentifi ed. It is possible that one specifi c phenotype of
neuronal and/or non-neuronal cells is either increased or decreased in response
to drug stimulation. In this case, a decreased generation of cells that normally
exert an inhibitory infl uence on the formation of drug addiction may result in
disinhibition of addictive processes. On the contrary, an increased generation
of cells that are involved in the mediation of drug effects may facilitate drug
addiction. In sum, drugs may develop their dependence via altering cytogenesis
activity in adult brain. Future studies can be pursued to address (1) effects of
drug exposure on the generation of a specifi c phenotype of cells in the adult
forebrain, and (2) underlying mechanisms of altered neurogenesis/gliogenesis
in the regulation of long-term drug actions.
The therapeutic potential of targeting neural progenitor cells for the treatment
of drug addiction is obvious. Again, however, concrete suggestions will have
to wait until future studies can elucidate changes in cytogenesis in response
to drug exposure and how those changes regulate drug actions. In the future,
it is expected that pharmacological agents can be developed to inhibit or
facilitate the new generation of specifi c phenotype of cells, depending on the
cell function in drug addiction. Reprogrammed endogenous cell birth through
exogenously administered agents could then prevent drug dependence and
addiction.
In summary, recent convincing evidence has shown a profound infl uence
of drug exposure on neurogenesis/gliogenesis in the affected brain areas
in adult animals. Altered cytogenesis may participate in the modulation of
addictive properties of drugs. More studies are needed to defi ne the underlying
mechanisms of the drug effects and contribution of neural progenitors to drug
actions in order to develop an effective therapy for drug addiction by targeting
neural stem cells.
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