Plasma Levels of Tricyclic Antidepressants in Panic Disorder

1984 ◽  
Vol 13 (2) ◽  
pp. 93-96 ◽  
Author(s):  
Donald R. Sweeney ◽  
Mark S. Gold ◽  
A. L. C. Pottash ◽  
David Martin
Keyword(s):  
Panic Disorder ◽  
Depressive Disorder ◽  
Mechanism Of Action ◽  
Plasma Levels ◽  
Tricyclic Antidepressants ◽  
Dramatic Improvement ◽  
Low Doses

Five patients with panic disorder were placed on low doses of imipramine. All patients had shown dramatic improvement after three weeks of treatment, when plasma levels of imipramine and desipramine were measured. Plasma levels corresponded to the low doses being administered. This result implies that the mechanism of action of tricyclic antidepressants is different in patients with panic disorder than in patients with depressive disorder.

5-HT1A receptor binding in panic disorder; comparison with depressive disorder and healthy volunteers using PET and [11C]WAY-100635

NeuroImage ◽  
2000 ◽  
Vol 11 (5) ◽  
pp. S189 ◽  
Author(s):  
P. Sargent ◽  
J. Nash ◽  
S. Hood ◽  
E. Rabiner ◽  
C. Messa ◽  
...  
Keyword(s):  
Panic Disorder ◽  
Depressive Disorder ◽  
Healthy Volunteers ◽  
Receptor Binding ◽  
Way 100635

Mechanism of action of narcolepsy medications

CNS Spectrums ◽  
2014 ◽  
Vol 19 (S1) ◽  
pp. 25-34 ◽  
Author(s):  
Chandan R. Gowda ◽  
Leslie P. Lundt
Keyword(s):  
Neuronal Activity ◽  
Mechanism Of Action ◽  
Tricyclic Antidepressants ◽  
Sodium Oxybate ◽  
Side Effect Profile ◽  
First Line ◽  
Excessive Sleepiness ◽  
Gamma Hydroxybutyrate ◽  
Clinical Strategies ◽  
Tuberomamillary Nucleus

The medications used to treat narcolepsy are targeted toward alleviating symptoms such as excessive sleepiness and cataplexy. The cause of this neurological sleep disorder is still not completely clear, though a destruction of hypocretin/orexin neurons has been implicated. The destruction of these neurons is linked to inactivity of neurotransmitters including histamine, norepinephrine, acetylcholine, and serotonin, causing a disturbance in the sleep/wake cycles of narcoleptic patients. Stimulants and MAOIs have traditionally been used to counteract excessive daytime sleepiness and sleep attacks by inhibiting the breakdown of catecholamines. Newer drugs, called wake-promoting agents, have recently become first-line agents due to their better side-effect profile, efficacy, and lesser potential for abuse. These agents similarly inhibit reuptake of dopamine, but have a novel mechanism of action, as they have been found to increase neuronal activity in the tuberomamillary nucleus and in orexin neurons. Sodium oxybate, a sodium salt of gamma-hydroxybutyrate (GHB), is another class that is used to treat many symptoms of narcolepsy, and is the only U.S. Food and Drug Administration (FDA)-approved medication for cataplexy. It has a different mechanism of action than either stimulants or wake-promoting agents, as it binds to its own unique receptor. Antidepressants, like selective serotonin re-uptake inhibitors (SSRIs) and tricyclic antidepressants (TCAs), have also been used, as similar to stimulants, they inhibit reuptake of specific catecholamines. In this article, we seek to review the mechanisms behind these classes of drugs in relation to the proposed pathophysiology of narcolepsy. Appropriate clinical strategies will be discussed, including specific combinations of medications that have been shown to be effective.

FC23-04 - Anti-neuropeptide y plasma immunoglobulins are distinctly associated with altered mood and appetite in depressive disorder

2011 ◽  
Vol 26 (S2) ◽  
pp. 1942-1942
Author(s):  
F.D. Garcia ◽  
Q. Coquerel ◽  
J.-C. do Rego ◽  
A. Cravezic ◽  
E. Kiive ◽  
...  
Keyword(s):  
Depressive Disorder ◽  
Neuropeptide Y ◽  
Plasma Levels ◽  
Forced Swim Test ◽  
Study Groups ◽  
Mild Depression ◽  
High Affinity ◽  
Swim Test ◽  
Moderate Depression ◽  
Immobility Time

IntroductionNeuropeptide Y(NPY) has potent antidepressant and orexigenic properties suggesting that altered NPY signaling can be relevant to etiology of altered mood and appetite commonly co-occurring in depressive disorder.ObjectiveStudy if plasma levels and affinities of anti-NPY immunoglobulins(autoAbs) are affected in depression.MethodsPlasma levels of NPY-reactive total/free IgG, IgM and IgA autoAbs were measured by ELISA in 14 patients with mild and in 9 patients with moderate depression and 20 controls. Affinity of autoAbs was assayed by the plasmon resonance. Depressant-like effect of human autoAbs was studied in mice using forced-swim test(FST) after IV injections of patients’ and controls’ IgG. Effects of affinity anti-NPY to antagonize NPY-induced antidepressant and orexigenic effects were studied in mice.ResultsPlasma levels of NPY total IgG autoAbs were lower in patients with moderate depression than in patients with mild depression and healthy controls. MADRS scores correlated negatively with levels of NPY free autoAbs but not with their affinity values were not significantly among study groups. Body mass index(BMI) correlated negatively with affinities of NPY IgG autoAbs. Immobility time in FST was increased by I.V. injection of IgG of patients and controls and correlated negatively with levels of NPY total IgG autoAbs. Low and high affinity NPY IgG autoAbs antagonized NPY-induced anti-immobility effect. Higher affinity autoAbs antagonized more NPY-induced food intake.ConclusionThese data suggest that changes of plasma levels of anti-NPY autoAbs are relevant to altered mood while changes of their affinity may be involved in altered appetite in depressive disorder.

Hormone secretion stimulated by ethanol-induced cell swelling in normal rat adenohypophysial cells

1991 ◽  
Vol 260 (6) ◽  
pp. E946-E950 ◽  
Author(s):  
N. Sato ◽  
X. B. Wang ◽  
M. A. Greer
Keyword(s):  
Effective Dose ◽  
Cell Volume ◽  
Mechanism Of Action ◽  
Plasma Levels ◽  
Hormone Secretion ◽  
Cell Swelling ◽  
Normal Rat ◽  
Rapid Passage ◽  
Stimulating Hormone

Ethanol has been reported to affect endocrine functions, but its mechanism of action is unclear. To evaluate the hypothesis that cell swelling induced by ethanol permeation through the plasmalemma triggers hormone secretion, we studied the effect of ethanol on both hormone secretion and cell volume in acutely dispersed rat adenohypophysial cells under isotonic and hypertonic conditions. Isotonic ethanol caused a prompt cell swelling and an explosive secretory burst of prolactin and thyrotropin, which were proportional to the concentration of ethanol between 10 and 120 mM. The lowest effective dose of isotonic ethanol was 10 mM, which is below the plasma levels of legal intoxication (16 mM). Removal of medium Ca2+ enhanced the isotonic ethanol-induced increases in both cell volume and secretion. Hypertonic ethanol was ineffective in these effects. These data indicate that, in normal rat adenohypophysial cells, cell swelling caused by the rapid passage of ethanol through the plasmalemma is a potent mechanism for stimulating hormone secretion and this induced secretion is negatively modulated by extracellular Ca2+.

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