Differential histone acetylation in the Amygdala leads to fear memory consolidation and extinction

Abstract

<p>In the present study, a fear-conditioning model in rats was used to gauge the changes in the histone acetylation level in the<br />different nuclei of amygdala during fear memory consolidation and its extinction. It was found by immunohistochemical<br />examination of Amygdala that during the fear memory consolidation histone H3 acetylation level was significantly<br />increased in the Central amygdala (CeA), the output of the fear circuitry, as compared to the unconditioned group and<br />subsequently, when this fear memory was extinguished during fear extinction, the histone H3 acetylation levels decreased<br />significantly as compared to the conditioned group. However, in another nuclei of the amygdala, the intercalated cells<br />(ITCs) the Acetyl H3 levels increased during extinction and but not in the conditioned group as compared to the<br />unconditioned group. The p-ERK and p-CREB levels also significantly varied in the different nuclei of amygdala<br />between the two groups and showed correlation with the Histone acetylation changes observed in these groups. In<br />conclusion the present study points out that the memory formation, during fear memory consolidation and its extinction,<br />may be dependent on differential neuronal activity under epigenetic control through acetylation at k-9 residue of histone<br />H3, in different regions of the amygdala as evident by the p-ERK and p-CREB activation, which are the markers for<br />activity of neurons and memory formation.</p>

Differential Histone Acetylation in Sub-Regions of Bed Nucleus of the Stria Terminalis Underlies Fear Consolidation and Extinction

“…This is consistent with earlier reports which have shown that the CS responsiveness of the STMA neurons is similar to that of CeM,8889 both having innervations from prelimbic cortex (PL), a region playing an active role in fear acquisition 9091. However, there was an increase in the levels CBP, Acetyl H3/H4 and c-fos in the STLP but not in the STMA and STLP following extinction as compared to the conditioned group and naïve control.…”

Mouse Model of Weak Depression Exhibiting Suppressed cAMP Signaling in the Amygdala, Lower Lipid Catabolism in Liver, and Correlated Gut Microbiota

“…Based on the results of the transcriptome analysis, we predicted the suppression of the cAMP signaling in the amygdala of SH mice, which was confirmed by the lower level of CREB phosphorylation observed in the medial amygdala ( Figures 6B,C ). There are emerging pieces of evidence that activation of the cAMP signaling in the amygdala facilitates the consolidation of social memory ( Viosca et al, 2009 ; Tronson et al, 2012 ; Cowansage et al, 2013 ; Ranjan et al, 2015 ; Hamidkhaniha et al, 2019 ). Accordingly, the impaired memory and social interaction observed in SH mice could be attributable to the repression of the cAMP signaling in the amygdala.…”

“…With reference to the neuronal response to stressors, cyclic adenosine monophosphate (cAMP) signaling has been proposed to play an essential role in the amygdala. By the use of cAMP analog injection or phosphodiesterase (PDE) gene knock out, it has been shown that activation of cAMP signaling in the amygdala was necessary for fear memory consolidation by the amygdala ( Viosca et al, 2009 ; Tronson et al, 2012 ; Cowansage et al, 2013 ; Ranjan et al, 2015 ). Corticotropin-releasing hormone is one of the candidates for extra-cellular stimuli that trigger cAMP signaling, but several neurotransmitters, such as noradrenaline, are also considered to be involved ( Keil et al, 2016 ).…”