The Effects of Electric Convulsive Treatments on Nitrogen, Calcium, and Phosphorus Metabolism in Psychiatric Patients

Flach, Frederic F.; Liang, Edward; Stokes, Peter E.

doi:10.1192/bjp.106.443.638

Cited by 13 publications

(2 citation statements)

References 4 publications

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“…In addition, changes in serum or CSF calcium levels have been reported in patients with depression not directly associated with endocrine dysfunction 32–40. Conversely, reduced plasma, serum, or CSF calcium levels accompany improvement of depressive symptomatology after either electroconvulsive shock or antidepressant drug treatment 33–35,39,41–43. Finally, calcium channel antagonists have been reported to be antidepressant in an anecdotal report 44,45…”

Section: Major Depression and Excitatory Amino Acidsmentioning

confidence: 99%

Glutamate and Depression

Paul¹,

Skolnick²

2003

Annals of the New York Academy of Sciences

359

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The past decade has seen a steady accumulation of evidence supporting a role for the excitatory amino acid (EAA) neurotransmitter, glutamate, and its receptors in depression and antidepressant activity. To date, evidence has emerged indicating that N-methyl-d-aspartate (NMDA) receptor antagonists, group I metabotropic glutamate receptor (mGluR1 and mGluR5) antagonists, as well as positive modulators of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors have antidepressant-like activity in a variety of preclinical models. Moreover, antidepressant-like activity can be produced not only by drugs modulating the glutamatergic synapse, but also by agents that affect subcellular signaling systems linked to EAA receptors (e.g., nitric oxide synthase). In view of the extensive colocalization of EAA and monoamine markers in nuclei such as the locus coeruleus and dorsal raphe, it is likely that an intimate relationship exists between regulation of monoaminergic and EAA neurotransmission and antidepressant effects. Further, there is also evidence implicating disturbances in glutamate metabolism, NMDA, and mGluR1,5 receptors in depression and suicidality. Finally, recent data indicate that a single intravenous dose of an NMDA receptor antagonist is sufficient to produce sustained relief from depressive symptoms. Taken together with the proposed role of neurotrophic factors in the neuroplastic responses to stressors and antidepressant treatments, these findings represent exciting and novel avenues to both understand depressive symptomatology and develop more effective antidepressants.

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Section: Major Depression and Excitatory Amino Acidsmentioning

confidence: 99%

Glutamate and Depression

Paul¹,

Skolnick²

2003

Annals of the New York Academy of Sciences

359

View full text Add to dashboard Cite

show abstract

“…Clinical studies have shown that Ca is associated with a mental disorders ( 33 , 34 ). Rare studies have directly examined the relationship between Ca intake and depression separately ( 35 , 36 ).…”

Section: Introductionmentioning

confidence: 99%

Association between dietary calcium and depression among American adults: National health and nutrition examination survey

Shen

Liu

et al. 2023

Front. Nutr.

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BackgroundThere is only limited evidence for an association between calcium (Ca) and depression, and the relationship was inconsistent. Therefore, the aim of this study was to assess the relationship between dietary Ca and the risk of depressive symptoms in individuals over the age of 18 in the US.MethodsWe extracted 14,971 participants from the US National Health and Nutrition Examination Survey (NHANES) 2007–2016 to probe their associations. Dietary Ca intake was measured through 24 h dietary recall method. Patients with the Patient Health Questionnaire-9 (PHQ-9) ≥ 10 scores were believed to have depressive symptoms. The association between dietary Ca and depressive symptoms was investigated using multivariate logistic regression, sensitivity analysis, and restricted cubic spline regression.ResultsIn this study, 7.6% (1,144/14,971) of them had depressive symptoms. After adjusting for sex, age, race, poverty to income ratio (PIR), marital status, education, body mass index (BMI), caffeine intake, carbohydrates intake, total energy intake, smoking status, alcohol consumption, physical activity, diabetes, hypertension, severe cardiovascular disease (CVD), cancer, serum vitamin D, serum Ca, and Ca supplement, the adjusted ORs value [95% confidence interval (CI)] of depression for the lowest category (Q1 ≤ 534 mg/day) vs. Q2–Q4 of Ca intake were 0.83 (0.69–0.99), 0.97 (0.65–0.95), and 0.80 (0.63–0.98) with the p for trend (p = 0.014). The relationship between dietary Ca intake and depressive symptoms was linear (non-linear p = 0.148). None of the interactions were significant except among races (p for interaction = 0.001).ConclusionAssociation between dietary Ca and the prevalence of depressive symptoms in US adults. And Ca intake was negatively associated with the risk of depressive symptoms. As Ca intake increased, the prevalence of depressive symptoms decreased.

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Antidepressant activity and calcium signaling cascades

Paul

2001

Human Psychopharmacology

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Although antidepressant treatments produce clear effects on monoaminergic neuronal function, the link between these effects and therapeutic response to treatment is controversial. Previous studies have demonstrated that antagonists of the NMDA receptor-gated calcium ionophore result in antidepressant-like responses in rodents and humans. Likewise, antidepressant treatments produce regionally selective adaptation of the NMDA receptor suggestive of diminished capacity to gate calcium into receptive neurons. Similarly, voltage-dependent calcium channel antagonists have been reported to produce antidepressant-like effects in rodents. A major target of increases in subcellular calcium concentration is nitric oxide synthase (NOS) which liberates NO in response to stimulation. Recently, we have demonstrated that nitric oxide synthase antagonists produced antidepressant-like response in both in vivo preclinical screening procedures and in post-mortem in vitro studies of beta-adrenoceptor density. We propose: 1) that interruption of the Ca(2+)-calmodulin-NOS-guanylyl cyclase subcellular signaling pathway at any point will produce antidepressant-like effects; 2) that the acute actions of antidepressants in preclinical screening procedures are a consequence of their ability to disrupt Ca(2+)-calmodulin-NOS-guanylyl cyclase signaling; 3) that chronic but, not acute treatment with antidepressants results in adaptation of the Ca(2+)-calmodulin-NOS-guanylyl cyclase signaling pathway; 4) that this adaptation is necessary for the achievement of the therapeutic actions of antidepressants and; 5) that major depression is accompanied by an alteration (hyperactivity?) of subcellular Ca(2+) signaling. Copyright 2001 John Wiley & Sons, Ltd.

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The Effects of Electric Convulsive Treatments on Nitrogen, Calcium, and Phosphorus Metabolism in Psychiatric Patients

Cited by 13 publications

References 4 publications

Glutamate and Depression

Glutamate and Depression

Association between dietary calcium and depression among American adults: National health and nutrition examination survey

Antidepressant activity and calcium signaling cascades

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