Genetic Models of Schizophrenia, Volume 179 (Progress in Brain Research) by Akira Sawa

Author:Akira Sawa
Language: eng
Format: mobi
ISBN: 9780444534309
Publisher: Elsevier Science
Published: 2009-12-27T22:00:00+00:00

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mutant huntingtin gene with an inserted CAG

References

repeat, show a robust reduction in striatal

PDE10A mRNA and protein levels, as well as a

Barad, M., Blouin, A. M., & Cain, C. K. (2004). Like

smaller decrease in PDE1B expression (Hebb et

extinction, latent inhibition of conditioned fear in mice is

blocked by systemic inhibition of L-type voltage-gated

al., 2004; Hu et al., 2004). Interestingly, the calcium channels. Learning & Memory, 11, 536–539.

reduction in PDE10A expression preceeds onset

Bender, A. T., & Beavo, J. A. (2006). Cyclic nucleotide

of motor symptoms. A slight reduction in PDE4A

phosphodiesterases: Molecular regulation to clinical use.

mRNA also occurs in the more severe R6/2

Pharmacological Reviews, 58, 488–520.

mouse, but only at the early age of 3 weeks when

Brandon, N. J., & Rotella, D. P. (2007). Potential CNS

applications for phosphodiesterase enzyme inhibitors. In J. E.

striatal PDE4A mRNA expression is highest

Macor (Ed.), Annual reports in medicinal chemistry (Vol. 42,

(Hebb et al., 2004). Consistent with these observa-

Chapter 1) (pp. 3–12). USA: Elsevier . pp.

tions in rodents, PDE10A protein is decreased in

Clapcote, S. J., Lipina, T. V., Millar, J. K., Mackie, S., Christie, S.,

tissue from Huntington’s patients (Hebb et al.,

Ogawa, F., et al. (2007). Behavioral phenotypes of Disc1

2004). It is possible that this downregulation of

missense mutations in mice. Neuron, 54, 387–402.

Cygnar, K. D., & Zhao, H. (2009). Phosphodiesterase 1C is

striatal PDE levels may be an attempt to compen-

dispensable for rapid response termination of olfactory

sate for the mutant huntingtin, because adminis-

sensory neurons. Nature Neuroscience, 12, 454–462.

tration of either PDE4 or PDE10 inhibitors

DeMarch, Z., Giampa, C., Patassini, S., Bernardi, G., & Fusco,

ameliorates neuropathology and behavioral defi-

F. R. (2008). Beneficial effects of rolipram in the R6/2 mouse

cits observed in the R6/2 and quinolinic acid model

model of Huntington's disease. Neurobiology of Disease, 30,

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for Huntington’s disease (DeMarch et al., 2007,

DeMarch, Z., Giampa, C., Patassini, S., Martorana, A.,

2008; Giampa et al., 2009a, b).

Bernardi, G., & Fusco, F. R. (2007). Beneficial effects of

rolipram in a quinolinic acid model of striatal excitotoxicity.

Neurobiology of Disease, 25, 266–273.

Dlaboga, D., Hajjhussein, H., & O’Donnell, J. M. (2006).

Conclusion

Regulation of phosphodiesterase-4 (PDE4) expression in

mouse brain by repeated antidepressant treatment: Compar-

ison with rolipram. Brain Research, 1096, 104–112.

Studies in genetically modified animal models

Dlaboga, D., Hajjhussein, H., & O’Donnell, J. M. (2008).

have greatly contributed to our understanding of

Chronic

haloperidol

and

clozapine produce different

how each PDE family contributes uniquely to the

patterns of effects on phosphodiesterase-1B,

4B, and

function of the nervous system. For example, it is

10A expression in rat striatum. Neuropharmacology, 54,

745–754.

interesting to note that deletion of PDE1B and

Ehrman, L. A., Williams, M. T., Schaefer, T. L., Gudelsky,

PDE10A results in nearly opposite phenotypes,

G.A., Reed, T. M., Fienberg, A. A., et al. (2006).

despite the fact that both are a dual-specificity

Phosphodiesterase 1B differentially modulates the effects

PDEs with enriched expression in the striatum.

of methamphetamine on locomotor activity and spatial

Although our understanding is growing, much

learning through DARPP32-dependent pathways: Evidence

from PDE1B-DARPP32 double-knockout mice. Genes,

work remains. Genetic models are lacking for a

Brain, & Behavior, 5, 540–551.

great many of the PDE family isoforms and only a

Engels, P., Abdel’Al, S., Hulley, P., & Lubbert, H. (1995).

single spliceform model exists (PDE10A2 / ).

Brain distribution of four rat homologues of the Drosophila

Further, of the genetic models that do exist for

dunce cAMP phosphodiesterase.

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