Serotonin Function in Panic Disorders

Charney, Dennis S.

doi:10.1001/archpsyc.1986.01800110045006

Cited by 85 publications

(7 citation statements)

References 95 publications

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“…Similar to several prior studies of panic patients (Appleby et al, 1981;Grunhaus et al, 1983;Liebowitz et al, 1985Liebowitz et al, , 1986Carr et al, 1986;Charney and Heninger, 1986;Roy-Byrne et al, 1986a), baseline prolactin levels in our study were normal. Although prior studies (Appleby et al, 1981;Liebowitz et al, 1985Liebowitz et al, , 1986Charney and Heninger, 1986) found sex differences, with prolactin in women higher than in men, we found no sex difference. Lactate produced a rise in prolactin (Appleby et al, 1981;Liebowitz et al, 1985Liebowitz et al, , 1986Cart et al, 1986).…”

Section: Discussionsupporting

confidence: 91%

“…Male patients who had attacks may have had a more vigorous prolactin response to lactate than male patients who did not, although this was not reported as significant (Appleby et al, 1981;Liebowitz et al, 1985Liebowitz et al, , 1986; female patients did not show this effect. Patients and normals had equal magnitude increases in prolactin after tryptophan administration (Charney and Heninger, 1986). Finally, patients showed a normal response to the cold pressor test (Graunhaus et al, 1983), but a reduced prolactin response to TRH, only in female patients (Roy-Byrne et al, 1986a).…”

Section: Discussionmentioning

confidence: 99%

“…Studies in panic have included resting conditions (Nesse et al, 1984), normal activity (Hamlin et al, 1983;Ballenger et al, 1984;Nesse et al, 1985b) and pharmacologically (Appleby et al, 1981;Charney et al, 1984Charney et al, , 1985Liebowitz et al, 1985Liebowitz et al, , 1986Carr et al, 1986) and situationally induced (Ko et al, 1983) panic attacks. Challenge tests in panic patients which did not produce panic attacks have also been studied (Grunhaus et al, 1983;Nesse et al, 1984;Charney and Heninger, 1986;Roy-Byrne et al, 1986a,b). However, despite the presence of at least some spontaneous panic attacks as a sine qua non for the DSM-III-defined diagnosis of panic disorder (American Psychiatric Association, 1980), no studies of endocrine changes associated with spontaneous panic attacks have been reported.…”

Section: Introductionmentioning

confidence: 99%

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Endocrine and physiological changes during “spontaneous” panic attacks

Cameron

Lee

Curtis

et al. 1987

Psychoneuroendocrinology

123

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Eight patients with DSM-III-defined panic attacks were compared to four normal subjects on hormonal and physiological variables measured at six predetermined times through 24 hr and also during nine "spontaneous" attacks. Levels at predetermined times were not different, other than a reduction of urinary unconjugated epinephrine in patients. Plasma prolactin was elevated at the peak of most of the attacks and correlated with attack severity. Plasma cortisol and growth hormone, and heart rate, were elevated during some attacks, and plasma norepinephrine showed small increases. Significant plasma epinephrine and MHPG changes were not observed.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Endocrine and physiological changes during “spontaneous” panic attacks

Cameron

Lee

Curtis

et al. 1987

Psychoneuroendocrinology

123

View full text Add to dashboard Cite

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“…Thus, the present data disagree with the supposed hyperactivity of the noradrenergic system as a prerequi site for the expression of panic attacks [16]. Further more, our results are also at variance with previous find ings indicating reduced plasma levels of MHPG after alprazolam treatment [9], Reduced plasma levels of MHPG are, however, suggested to be a result of alprazo lam-induced inhibition of a centrally mediated sympa thetic discharge [17], On the other hand, our data con cerning CSF 5-HIAA levels agree with those of Charney and Heninger [18] indicating that alprazolam treatment in panic patients did not affect the tryptophan-induced increase of plasma prolactin used as an index of seroton ergic function.…”

Section: Discussionsupporting

confidence: 84%

Long-Term Effects of Alprazolam and Imipramine on Cerebrospinal Fluid Monoamine Metabolites and Neuropeptides in Panic Disorder

Lepola¹,

Jolkkonen²,

Rimón³

et al. 1989

Neuropsychobiology

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Cerebrospinal fluid (CSF) homovanillic acid, 5-hydroxyindoleacetic acid, 3-methoxy-4-hydroxyphenylglycol, and somatostatin and β-endorphin levels were measured in 12 patients with panic disorder before and after 7 months of treatment with alprazolam or imipramine. The concentrations of CSF monoamine metabolites and neuropeptides were at baseline of the same order of magnitude in panic patients and controls. Neither alprazolam nor imipramine changed metabolite or neuropeptide levels in CSF despite clinical improvement in both treatment groups. According to present CSF data, the antipanic actions of alprazolam and imipramine do not involve the monoaminergic or peptidergic systems studied.

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“…Specifically, Charney et al (1982) showed that intravenous infusion of L-tryptophan was not accompanied by anxiety symptoms, although it induced significant increases in prolactin and growth hormone in healthy subjects as compared to placebo injection. Later they also established that the ability of tryptophan to increase prolactin levels was not different between the PD patients and healthy subjects and was not influenced by alprazolam treatment (Charney and Heninger, 1986). Notably, a clinical observation was made that oral tryptophan augmentation did not potentiate the beneficial effect of 10-week treatment with clomipramine on phobic avoidance, phobic fears or the incidence of panic attacks in a small sample of patients with agoraphobia or social phobia (Pecknold et al 1982).…”

Section: Experimental Studiesmentioning

confidence: 99%

Tryptophan Research in Panic Disorder

Maron

Shlik

Nutt

2008

Int J�Tryptophan�Res

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A considerable body of evidence suggests the involvement of serotonin neurotransmission in the pathogenesis of panic disorder. Research on pathways and functions of tryptophan, an essential amino acid converted into serotonin, may advance our understanding of serotonergic actions in panic disorder and related phenomena. The investigative approaches in this fi eld include manipulations of tryptophan availability as well as genetic association and functional brain imaging studies. In this review we examine the principle fi ndings of these studies and propose further research directions.Keywords: tryptophan, panic disorder, anxiety, challenge, gene Panic disorder (PD) is a prevalent and serious illness in need of a better understanding of its neurobiological basis to improve treatment outcomes. The pathogenesis, clinical manifestations and treatment effects of PD are thought to be substantially related to the functions of serotonin or 5-hydroxytryptamine (5-HT) neurotransmission. The crucial role of 5-HT in PD has been suggested by clinical studies demonstrating that medications specifi cally increasing the synaptic availability of 5-HT, especially the selective 5-HT re-uptake inhibitors (SSRIs), are particularly effective in the treatment of PD (Nutt, 1998). Extensive experience with SSRIs in the treatment of PD and the effect of tryptophan depletion (TD) to undermine this action underscored the necessity of increased synaptic availability of 5-HT for achieving remission. Furthermore, growing data from experimental and neuroimaging studies have suggested that altered availability of brain 5-HT is associated with PD; however the exact mechanisms of a possible disturbance in 5-HT metabolism are not fully understood . 5-HT is synthesized from the essential amino acid tryptophan via intermediate metabolite, 5-hydroxytryptophan (5-HTP), and stored in reserpine-sensitive vesicles until released into the synaptic cleft by nerve impulses. The conversion of tryptophan into 5-HTP is regulated by tryptophan hydroxylase (TPH), the rate limiting enzyme in biosynthesis of 5-HT. In the next step, 5-HTP is decarboxylated by aromatic acid decarboxylase to 5-HT. Unlike 5-HTP, tryptophan can be shunted into kynurenine via tryptophan 2,3-dioxygenase, making tryptophan unavailable for 5-HT production (Birdsall, 1998;Ruddick et al. 2006). TPH can be inhibited by numerous factors, including stress, insulin resistance, vitamin B6 deficiency, and insuffi cient magnesium, that may increase the conversion of tryptophan to kynurenine. Under normal conditions, the enzyme TPH is only about 50% saturated in brain, therefore the synthesis of 5-HT is dependent on the availability of free plasma tryptophan, whereas alterations in its availability correlate with the amount of synthesized 5-HT (Schaechter and Wurtman, 1990). Presently, the central 5-HT pathways remain the main targets in the research on the neurobiology of PD. In this paper we review the studies focusing on the role of tryptophan and discuss research directions in this are...

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Serotonin Function in Panic Disorders

Cited by 85 publications

References 95 publications

Endocrine and physiological changes during “spontaneous” panic attacks

Endocrine and physiological changes during “spontaneous” panic attacks

Long-Term Effects of Alprazolam and Imipramine on Cerebrospinal Fluid Monoamine Metabolites and Neuropeptides in Panic Disorder

Tryptophan Research in Panic Disorder

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