Effects of tryptophan depletion on carbon dioxide provoked panic in panic disorder patients

Schruers, Koen; Klaassen, Tim; Pols, Henk; Overbeek, Thea; Deutz, N.E.P.; Griez, Eric

doi:10.1016/s0165-1781(00)00117-7

Cited by 91 publications

(94 citation statements)

References 28 publications

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“…57 The evidence in panic disorder had been mixed; however, three recent studies have shown that ATD increases the vulnerability of PD patients to provocation with flumazenil, 58 5% CO 2 59 and 35% CO 2 . 60 The latter study found a possible protective effect of the control condition (which often raises plasma Trp levels).…”

Section: Acute Tryptophan Depletionmentioning

confidence: 85%

Monoamine depletion in psychiatric and healthy populations: review

2003

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A number of techniques temporarily lower the functioning of monoamines: acute tryptophan depletion (ATD), alpha-methyl-para-tyrosine (AMPT) and acute phenylalanine/tyrosine depletion (APTD). This paper reviews the results of monoamine depletion studies in humans for the period 1966 until December 2002. The evidence suggests that all three interventions are specific, in terms of their short-term effects on one or two neurotransmitter systems, rather than on brain protein metabolism in general. The AMPT procedure is somewhat less specific, affecting both the dopamine and norepinephrine systems. The behavioral effects of ATD and AMPT are remarkably similar. Neither procedure has an immediate effect on the symptoms of depressed patients; however, both induce transient depressive symptoms in some remitted depressed patients. The magnitude of the effects, response rate and quality of response are also comparable. APTD has not been studied in recovered major depressive patients. Despite the similarities, the effects are distinctive in that ATD affects a subgroup of recently remitted patients treated with serotonergic medications, whereas AMPT affects recently remitted patients treated with noradrenergic medications. The evidence also suggests that ATD and APTD affect different cognitive functions, in particular different memory systems. Few studies investigated cognitive effects of the procedures in patients. Patients who are in remission for longer may also be vulnerable to ATD and AMPT, but the relationship with prior treatment is much weaker. For these patients, individual vulnerability markers are the more important determinants of depressive response, making these techniques potentially useful models of vulnerability to depression. Molecular Psychiatry (2003) 8, 951-973.

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Section: Acute Tryptophan Depletionmentioning

confidence: 85%

Monoamine depletion in psychiatric and healthy populations: review

2003

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“…Specifically, Miller et al (2000) found that TD caused a greater panic and anxiogenic response and a higher rate of panic attacks after 5% CO 2 inhalation in PD patients, but not in healthy subjects. Another study in patients by Schruers et al (2000) demonstrated a significant increase in anxiety and panic symptoms induced by 35% CO 2 inhalation in the TD group, compared to the placebo condition. Conversely, Schruers et al (2002) found that increasing 5-HT by the acute administration of 200 mg 5-HTP restrained panic responses to 35% CO 2 challenge in patients with PD, but not in healthy subjects.…”

Section: Challenge Studiesmentioning

confidence: 94%

Serotonin Function in Panic Disorder: Important, But Why?

Maron

Shlik

2005

Neuropsychopharmacol

109

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The essential role of serotonin (5-hydroxytryptamine (5-HT)) system in the neurobiology and pharmacotherapy of panic disorder (PD) continues to be a topic of intensive interdisciplinary research. Interest in the involvement of 5-HT in PD has been fuelled by clinical studies demonstrating that medications increasing the synaptic availability of 5-HT, such as selective 5-HT re-uptake inhibitors, are effective in the treatment of PD. Rival theories of 5-HT deficiency vs excess have attempted to explain the impact of 5-HT function in PD. In the past decade, knowledge of the role of 5-HT in the neurobiology of PD has expanded dramatically due to much new research including experimental, treatment, brain-imaging, and genetic studies. The current review attempts to summarize the new data and their implications. The challenge and treatment studies generally confirm the specific inhibitory influence of 5-HT on panicogenesis. The brainimaging studies in PD patients demonstrate functional and clinically relevant alterations in various elements of 5-HT system affecting the neurocircuitry of panic. The findings of genetic association studies suggest that certain 5-HT-related genes may contribute to the susceptibility to PD; however, these data are rather limited and inconsistent. It appears that, even if not the primary etiological factor in PD, the 5-HT function conveys important vulnerability, as well as adaptive factors. A better understanding of these processes may be critical in achieving progress in the treatment of patients suffering from PD.

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“…TRP (L-tryptophan) is an essential amino acid which is converted to 5-hydroxy-tryptophan (L-5-HTP), which is in turn converted to 5-hydroxytryptamine (5-HT or serotonin), so it was expected that lower TRP would decrease availability of 5-HT and amplify the panicogenic effects of the challenge. This was confirmed by Klaasen et al, 97 Miller et al, 98 and Schruers et al, 99 who verified that consumption of the TRP-free amino acid solution led to a severe depletion of TRP serum levels (of about 80%). This depletion caused no panic or anxiety before the CO 2 challenge in PD patients or healthy controls, but provoked stronger panic responses to CO 2 in patients with PD, as manifested by higher levels of subjective anxiety and neurovegetative symptoms.…”

Section: Serotonin Modulationmentioning

confidence: 64%

The carbon dioxide challenge test in panic disorder: a systematic review of preclinical and clinical research

Amaral

Spadaro

Pereira³

et al. 2013

Rev. Bras. Psiquiatr.

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This systematic review assesses the current state of clinical and preclinical research on panic disorder (PD) in which the carbon dioxide (CO 2 ) challenge was used as a trigger for panic attacks (PAs). A total of 95 articles published from 1984 to 2012 were selected for inclusion. Some hypotheses for PD evolved greatly due to the reproducibility of PAs in a controlled environment using the safe and noninvasive CO 2 test. The 35% CO 2 protocol was the method chosen by the majority of studies. Results of the test report specific sensitivity to hypercapnia in PD patients of the respiratory PD subtype. The CO 2 challenge helped assess the antipanic effects of medication and nonpharmaceutical approaches such as physical exercise and cognitive behavioral therapy. The test was also used in studies about the genetic component of PD, in which twins and relatives of PD patients were analyzed.

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Effects of tryptophan depletion on carbon dioxide provoked panic in panic disorder patients

Cited by 91 publications

References 28 publications

Monoamine depletion in psychiatric and healthy populations: review

Monoamine depletion in psychiatric and healthy populations: review

Serotonin Function in Panic Disorder: Important, But Why?

The carbon dioxide challenge test in panic disorder: a systematic review of preclinical and clinical research

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