MAO A knockout attenuates adrenocortical response to various kinds of stress

NK Popova, LN Maslova, EA Morosova… - …, 2006 - Elsevier
NK Popova, LN Maslova, EA Morosova, VV Bulygina, I Seif
Psychoneuroendocrinology, 2006Elsevier
The effect of a lack of the gene encoding monoamine oxidase A (MAO A) in transgenic Tg8
mice on the corticosterone response to restraint, cold, water deprivation-induced, or social
acute stress as well as chronic variable stress was studied. It was found that Tg8 mice with
genetic MAO A knockout and wild-type C3H/HeJ (C3H) strain showed similar plasma
corticosterone resting level. MAO A knockout mice differed from C3H mice by attenuated
response to restraint (60min), cold (4° C, 60min), and water deprivation (48h) as well as to a …
The effect of a lack of the gene encoding monoamine oxidase A (MAO A) in transgenic Tg8 mice on the corticosterone response to restraint, cold, water deprivation-induced, or social acute stress as well as chronic variable stress was studied. It was found that Tg8 mice with genetic MAO A knockout and wild-type C3H/HeJ (C3H) strain showed similar plasma corticosterone resting level. MAO A knockout mice differed from C3H mice by attenuated response to restraint (60min), cold (4°C, 60min), and water deprivation (48h) as well as to a chronic (15 days) variable stress. No difference between Tg8 and C3H strains in the response to psychosocial stress (encounters for 30min of six previously isolated mice) has been found. ACTH administration to dexamethasone-pretreated mice produced a similar corticosterone effect in Tg8 and C3H mice, indicating that the decreased stress response in MAO A-deficient mice was due rather to the central mechanisms regulating stress-induced ACTH release than to adrenocortical responsiveness to ACTH.
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