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Decreased tryptophan availability but normal post-synaptic 5-HT2c receptor sensitivity in chronic fatigue syndrome
C M Vassallo1, E Feldman, T Peto
1University Department of Psychiatry, Warneford Hospital, Oxford.
Psychological Medicine
|May 16, 2001
Summary
Patients with Chronic Fatigue Syndrome (CFS) do not have heightened post-synaptic serotonin receptor sensitivity. This suggests that abnormal prolactin responses in CFS are due to increased pre-synaptic serotonin neuron activity.
Area of Science:
- Neuroscience
- Endocrinology
- Sleep Medicine
Background:
- Chronic Fatigue Syndrome (CFS) is linked to abnormal prolactin (PRL) responses to serotonin (5-HT) releasing agents.
- The underlying cause in CFS remains unclear: increased 5-HT release or heightened receptor sensitivity?
Purpose of the Study:
- To investigate post-synaptic 5-HT receptor sensitivity in CFS patients.
- To compare the effects of a 5-HT receptor agonist on PRL and sleep in CFS and controls.
- To assess tryptophan availability in CFS.
Main Methods:
- Administered m-chlorophenylpiperazine (mCPP), a 5-HT receptor agonist, to CFS patients and controls.
- Measured plasma PRL response and changes in slow wave sleep (SWS) via polysomnography.
- Analyzed plasma amino acid levels, focusing on tryptophan.
Main Results:
- mCPP equally increased plasma PRL in both CFS patients and controls.
- mCPP-induced reduction in SWS did not differ between groups.
- CFS patients exhibited significantly lower plasma-free tryptophan levels.
Conclusions:
- Post-synaptic 5-HT2c receptor sensitivity is not elevated in CFS.
- The heightened PRL response to fenfluramine in CFS likely stems from increased pre-synaptic 5-HT neuron activity.
- Increased peripheral tryptophan availability is an unlikely cause for this abnormality.