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In this article it states that:

Increased promoter methylation of the serotonin transporter gene predicted increased threat related amygdala activity.

I'm finding this somewhat difficult to understand. Increased promoter methylation would imply that the serotonin transporter gene is less expressed, so less serotonin is taken up by the presynaptic neuron, leading to increased serotonin levels in the synaptic cleft. Surely the increased serotonin levels would lead to decreased amygdala response to threat? After all, selective serotonin reputable inhibitors (SSRIs) are used to treat anxiety disorders and depression by reducing uptake of serotonin and increasing serotonin levels as well.

It seems like these two are suggesting two contrasting effects for the same cause? Have I misunderstood something?

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From my limited understanding...

First off, you're definitely interpreting this correctly. The authors note:

[…] methylation of the proximal promoter of human SLC6A4 predicts threat-related amygdala reactivity, possibly reflecting decreased serotonin transporter gene expression and, consequently, reduced regional serotonin reuptake.

However, it's definitely true that increased serotonin signaling is associated with increased amygdala reactivity (e.g., Fakra et al., 2009).

Moreover, SSRI administration in neurotic (Simplicio et al., 2013) and healthy (Bigos et al., 2008) adults seems to initially increase amydgala reactivity to threatening faces. Simplicio et al. interpret this as facilitating "a process of decreasing emotional avoidance," which would be adaptive in the long-term through greater exposure (and habituation to) "benign 'threat' cues" like faces.

Both Fakra et al. (2009) and Bigos et al. (2008) suggest that acute effects of increased 5HT on amygdala reactivity may have to do with delayed effects on prefrontal cortex, which would otherwise exhibit control over amygdala reactivity. More specifically, Bigos et al. argue:

While acute 5-HT reuptake blockade may potentiate stimulus-dependent amygdala reactivity, likely through stimulation of excitatory postsynaptic 5-HT receptors located on apical dendrites of glutamatergic neurons (McDonald and Mascagni, 2007), chronic blockade may lead to a more general increase in 5-HT neurotransmission via downregulation of negative feedback 5-HT autoreceptors (Blier and de Montigny, 1999). This shift toward generally increased neurotransmission after chronic reuptake blockade may allow 5-HT to potentiate the response of pyramidal neurons in prefrontal circuits, via volume transmission at excitatory 5-HT receptors localized extrasynaptically (Jansson et al, 2001; Sharp et al, 2007), thereby mediating top-down regulation of the amygdala (Hariri and Holmes, 2006).

So SSRIs might have long-term adaptive consequences via effects on prefrontal cortex, otherwise not seen acutely.

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