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Angiotensin-(1-7)/Mas axis modulates fear memory and extinction in mice.

Abstract：

:Inappropriate defense-alerting reaction to fear is a common feature of neuropsychiatric diseases. Therefore, impairments in brain circuits, as well as in molecular pathways underlying the neurovegetative adjustments to fear may play an essential role on developing neuropsychiatric disorders. Here we tested the hypothesis that interfering with angiotensin-(1-7) [Ang-(1-7)]/Mas receptor axis homeostasis, which appears to be essential to arterial pressure control, would affect fear memory and extinction. Mas knockout (MasKO) mice, in FVB/N background, showed normal cued fear memory and extinction, but increased freezing in response to context. Next, as FVB/N has poor performance in contextual fear memory, we tested MasKO in mixed 129xC57BL/6 background. MasKO mice behaved similarly to wild-type (WT), but memory extinction was slower in contextual fear conditioning to a weak protocol (1CS/US). In addition, delayed extinction in MasKO mice was even more pronounced after a stronger protocol (3CS/US). We showed previously that Angiotensin II receptor AT1 antagonist, losantan, rescued object recognition memory deficit in MasKO mice. Here, losartan was also effective. Memory extinction was accelerated in MasKO mice after treatment with losartan. In conclusion, we showed for the first time that Ang-(1-7)/Mas axis may modulate fear memory extinction. Furthermore, we suggest MasKO mice as an animal model to study post-traumatic stress disorder (PTSD).

journal_name

Neurobiol Learn Mem

journal_title

Neurobiology of learning and memory

authors

Lazaroni TL,Bastos CP,Moraes MF,Santos RS,Pereira GS

doi

10.1016/j.nlm.2015.11.012

subject

Has Abstract

pub_date

2016-01-01 00:00:00

pages

27-33

eissn

1074-7427

issn

1095-9564

pii

S1074-7427(15)00221-X

journal_volume

127

pub_type

杂志文章

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