Effects of Alpha-Methyl-Para-Tyrosine-Induced Catecholamine Depletion in Patients with Seasonal Affective Disorder in Summer Remission

Lam, Raymond W.; Tam, Edwin M.; Grewal, Arvinder; Yatham, Lakshmi N.

doi:10.1016/s0893-133x(01)00337-2

Cited by 38 publications

(24 citation statements)

References 29 publications

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“…In a sample of nine SAD patients in summer remission, all patients relapsed after AMPT. 91 In a sample of eight recovered bipolar patients who were stable on lithium, there was no mood effect during AMPT administration. However, manic symptoms increased 24-48 h after discontinuation of AMPT.…”

Section: Acute Tryptophan Depletionmentioning

confidence: 97%

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: 97%

Monoamine depletion in psychiatric and healthy populations: review

2003

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“…Recently, an enhanced 5-HTT turnover rate (defined as the number of uptake events of one 5-HTT molecule per sec- [113] , although these results could not be replicated in another study [114] . However, two catecholamine depletion studies in BLT-treated remitted patients [115] and patients during summer remission [116] suggest a possible role of norepinephrine and dopamine in the pathophysiology of SAD. A number of genetic studies aimed at investigating vulnerabilities to SAD and seasonality.…”

Section: Role Of Monoaminesmentioning

confidence: 99%

Bright-Light Therapy in the Treatment of Mood Disorders

et al. 2011

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Bright-light therapy (BLT) is established as the treatment of choice for seasonal affective disorder/winter type (SAD). In the last two decades, the use of BLT has expanded beyond SAD: there is evidence for efficacy in chronic depression, antepartum depression, premenstrual depression, bipolar depression and disturbances of the sleep-wake cycle. Data on the usefulness of BLT in non-seasonal depression are promising; however, further systematic studies are still warranted. In this review, the authors present a comprehensive overview of the literature on BLT in mood disorders. The first part elucidates the neurobiology of circadian and seasonal adaptive mechanisms focusing on the suprachiasmatic nucleus (SCN), the indolamines melatonin and serotonin, and the chronobiology of mood disorders. The SCN is the primary oscillator in humans. Indolamines are known to transduce light signals into cells and organisms since early in evolution, and their role in signalling change of season is still preserved in humans: melatonin is synthesized primarily in the pineal gland and is the central hormone for internal clock circuitries. The melatonin precursor serotonin is known to modulate many behaviours that vary with season. The second part discusses the pathophysiology and clinical specifiers of SAD, which can be seen as a model disorder for chronobiological disturbances and the mechanism of action of BLT. In the third part, the mode of action, application, efficacy, tolerability and safety of BLT in SAD and other mood disorders are explored.

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“…This is evident from the finding that inhibition of synthetic enzymes for norepinephrine (NE) or serotonin results in a rapid return of symptoms in depressed patients treated successfully with desipramine or fluoxetine, respectively (Charney, 1998;Miller et al, 1996a). Further, inhibition of catecholamine synthesis with a-methyl-p-tyrosine (AMPT) increases depressive symptoms in patients with seasonal affective disorder (Lam et al, 2001). Similarly, reduction of serotonin synthesis with parachlorophenylalanine or a tryptophan-free amino-acid drink reverses symptom remission induced by serotonin reuptake inhibitors (SRIs; Salomon et al, 1993).…”

Section: Introductionmentioning

confidence: 99%

Norepinephrine Transporter Regulation Mediates the Long-Term Behavioral Effects of the Antidepressant Desipramine

Zhao

Baros

Zhang

et al. 2008

Neuropsychopharmacol

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The relationship between the ability of repeated desipramine treatment to cause downregulation of the norepinephrine transporter (NET) and produce antidepressant-like effects on behavior was determined. Treatment of rats with 15 mg/kg per day desipramine reduced NET expression, measured by 3 H-nisoxetine binding and SDS-PAGE/immunoblotting, in cerebral cortex and hippocampus and reduced the time of immobility in the forced-swim test. The antidepressant-like effect on forced-swim behavior was evident 2 days following discontinuation of desipramine treatment when plasma and brain levels of desipramine and its major metabolite desmethyldesipramine were not detectable. Reduced NET expression resulted in reduced norepinephrine uptake, measured in vitro, and increased noradrenergic neurotransmission, measured in vivo using microdialysis. Overall, the dose-response and time-of-recovery relationships for altered NET expression matched those for production of antidepressant-like effects on behavior. The importance of increased noradrenergic neurotransmission in the persistent antidepressant-like effect on behavior was confirmed by demonstrating that it was blocked by inhibition of catecholamine synthesis with a-methyl-p-tyrosine. The present results suggest an important role for NET regulation in the long-term behavioral effects of desipramine and are consistent with clinical data suggesting that enhanced noradrenergic neurotransmission is necessary, but not sufficient, for its antidepressant actions. Understanding the mechanisms underlying NET regulation in vivo may suggest novel targets for therapeutic intervention in the treatment of depression.

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Effects of Alpha-Methyl-Para-Tyrosine-Induced Catecholamine Depletion in Patients with Seasonal Affective Disorder in Summer Remission

Cited by 38 publications

References 29 publications

Monoamine depletion in psychiatric and healthy populations: review

Monoamine depletion in psychiatric and healthy populations: review

Bright-Light Therapy in the Treatment of Mood Disorders

Norepinephrine Transporter Regulation Mediates the Long-Term Behavioral Effects of the Antidepressant Desipramine

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