Methylazoxymethanol acetate does not fully block cell genesis in the young and aged dentate gyrus.

David Dupret, Marie-Françoise Montaron, Elodie Drapeau, Catherine Aurousseau, Michel Le Moal, Pier-Vincenzo Piazza, Djoher Nora Abrous
European Journal of Neuroscience. 2005-08-01; 22(3): 778-783
DOI: 10.1111/j.1460-9568.2005.04262.x

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1. Eur J Neurosci. 2005 Aug;22(3):778-83.

Methylazoxymethanol acetate does not fully block cell genesis in the young and
aged dentate gyrus.

Dupret D(1), Montaron MF, Drapeau E, Aurousseau C, Le Moal M, Piazza PV, Abrous
DN.

Author information:
(1)INSERM U588, University of Bordeaux II, Institute F Magendie, 146 rue
Léo-Saignat, 33077 Bordeaux Cedex, France.

During adulthood, new neurons are continuously added to the mammalian dentate
gyrus (DG). An increasing number of studies have correlated changes in rates of
dentate neurogenesis with memory abilities. One study based on subchronic
treatment with the toxin methylazoxymethanol acetate (MAM) has provided causal
evidence that neurogenesis is involved in hippocampal-dependent trace
conditioning. In contrast, spatial learning is not impaired following MAM
treatment. We hypothesized that this was due to the small residual number of new
cells produced following MAM treatment. In the present experiment, we attempted
to achieve a higher level of reduction of adult-generated cells following MAM
treatment in young and aged rats. We found only a partial reduction of
adult-generated cells in the DG. More importantly, independently of the age of
the animals, MAM treatment at a dose necessary to reduce neurogenesis altered the
overall health of the animals. In conclusion, the behavioural results obtained
following subchronic treatment with high doses of MAM in adulthood must be
interpreted with extreme caution.

DOI: 10.1111/j.1460-9568.2005.04262.x
PMID: 16101760 [Indexed for MEDLINE]

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