Calcium Metabolism in States of Depression

Flach, Frederic F.

doi:10.1192/bjp.110.467.588

Cited by 35 publications

(4 citation statements)

References 8 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

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“…While serum magnesium in manic-depressive patients does not seem to show any consistent changes (11)(12)(13)(14), urinary excretion was found to be increased during recovery form depression (15), in contrast to urinary calcium which was decreased during recovery from depression (5,6).…”

Section: Introductionmentioning

confidence: 96%

“…The possibility therefore exists that such an influence may have certain bearing on the effect of lithium in manic-depressive psychosis, because calcium is important both for the impulse propagation along the nerve cell (3) and for the synaptic transmission (4). Furthermore, calcium metabolism may be changed in manic-depressive patients (5,6), and changes in calcium metabolism are often accompanied by mental disturbances (7,8).…”

Section: Introductionmentioning

confidence: 99%

Lithium Effects on Magnesium Metabolism in Rats

Plenge

Oj³

1973

Int Pharmacopsychiatry

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“…As to calcium we found lower excretions after recovery than during depression, but the difference was not statistically significant. In the studies of Flach (1964), Fluch & Faragalla (1966, and Fischback (1971) a similar change in calcium excretion was found, and in all of the three the difference was highly significant. On the other hand, Coirault et al (1959) found just the opposite, i. e. an increase in urinary calcium during recovery from depression.…”

Section: Discussionmentioning

confidence: 58%