Quoting from the above article (http://www.cfids-cab.org/rc/Cho-1.pdf):

Serotonergic system
Most of the existing evidence has suggested a hyperserotonergic state or upregulated serotonin receptors among CFS patients, in contrast to the hyposerotonergic state seen in major depression, although this has mainly been indirect evidence from neuroendocrine challenge studies.

Two published studies have now measured directly the status of cerebral serotonin receptors in CFS. In the first, Cleare et al. [28��] showed decreased 5-HT1A receptor binding throughout the brain using positron emission tomography (PET), the reduction being most marked in the hippocampi bilaterally. The authors noted that it is possible that 5-HT1A receptor downregulation is a response to increased levels of synaptic serotonin, but also noted alternative explanations.

For example, although Cleare et al. studied only non-depressed CFS patients, patients who do have depression show downregulation of 5-HT1A receptors even after treatment; since many CFS sufferers (including most of those studied by Cleare et al.) have a past history of depression, this is one possible explanation.

Similarly, the effect on the serotonin system of the behavioural consequences of CFS (such as sleep disturbance and inactivity) remains unclear.

In a second PET study in non-depressed CFS subjects, this time of the density of cerebral serotonin transporters, Yamamoto et al. [29] found reduced receptor binding in the rostral anterior cingulate of CFS patients and found that this correlated inversely with the level of reported pain (i.e. lower binding was related to higher pain scores) but not to other symptoms. These authors also point out that the reduced serotonin reported could be secondary to increased serotonin synaptic levels, or to changes in blood flow or neuronal density in these areas.

This article shows that in Chronic Fatigue Syndrome there is a reduction in serotonin signaling. This occurs via a reduction in serotonin receptors.

Reading the article is tricky. The two studies speculated that the reduction in serotonin receptors may be due to either increased serotonin in the synapse or changes in blood flow or changes in neuronal density in the studied areas.

As an aside, the problem of doing imaging studies is that most of what is imaged is glial activity, NOT neuronal activity. Glial cells can produce all of the receptors that neurons have and can also produce all of the signals that neurons can produce. And the connections between glial cells and neurons and other glial cells are not considered synaptic, though the glial cells called astrocytes do participate in synaptic transmission – they control the synapse itself. Thus, interpreting imaging studies to represent neuron circuits is most likely to be full of errors.

Note that the authors give alternative explanations to the reason that serotonin receptors are reduced in CFS. Concluding that there is a “hyperserotonergic state” in CFS is blatantly wrong and not demonstrated by the studies. In fact, if serotonin receptors are reduced, then any increase in serotonin in the synapse is actually negated and serotonin signaling is not increased, rather it is decreased. Also, the actual level of serotonin in the synapse is not even actually measured in the studies. Asserting serotonin is high is purely speculative.

Note that since lower serotonin receptor binding correlates with increased pain, which often accompanies CFS, one can actually instead conclude that serotonin signaling is reduced in CFS.

Serotonin signaling, furthermore, is influenced by other signals – such as thyroid hormone, norepinephrine, estradiol, immune system cytokines, dopamine, etc. etc. The authors did not add abnormalities in these other systems as additional reasons that serotonin density can be reduced.

In summary, the article, itself, indicates that serotonin signaling is reduced in CFS. The data shows reduced serotonin receptor binding.