• Mood stabilizers-lithium and certain anticonvulsants such as valproate and carbamazepine as well as atypical antipsychotics such as aripiprazole-are the mainstay of long-term pharmacologic relapse prevention. (wikipedia.org)
  • Interference with the cytoskeleton also failed to affect the intracellular calcium signal that occurred when external calcium was re-admitted to cells in which the calcium stores had been previously depleted by exposure to thapsigargin/ionomycin in calcium-free external solution. (ox.ac.uk)
  • Excess calcium can deplete its vital sister mineral, magnesium, from the body and, as a result, can bring about symptoms of magnesium depletion. (happybodies.com)
  • Physical or emotional stress and alcohol consumption can deplete the body of this important mineral. (happybodies.com)
  • Exposure to Li+, which reduces InsP3 levels by interfering with inositol monophosphatase, also failed to alter I(CRAC). (ox.ac.uk)
  • Sleep deprivation and extreme stressors like heat and cold can deplete catecholamine levels. (nootropicsexpert.com)
  • Coupling to Ca mobilisation In many cells a2-ARs have been shown to couple to production of inositol-1,4,5- trisphosphate [4,29,30] and Ca"" mobilisation [3,30-35]. (forexsignalx.com)
  • However, some products do not contain all of these ingredients and some may include others, such as biotin, para-aminobenzoic acid (PABA), choline bitartrate, and inositol. (medlineplus.gov)
  • Mood stabilizers-lithium and certain anticonvulsants such as valproate and carbamazepine as well as atypical antipsychotics such as aripiprazole-are the mainstay of long-term pharmacologic relapse prevention. (wikipedia.org)
  • The simplest answer is that our modern food supply (including organic food) simply doesn't contain the magnesium it should due to highly depleted soil conditions. (pureprescriptions.com)
  • Depleted soil conditions in combination with present day food processing methods have led to a decline in the nutritional content and value of foods. (amerilifevitamin.com)
  • Neurotransmitters Based on the hypothesis of neurochemical imbalance in mood disorders, a number of studies have investigated the genes encoding elements of neurotransmitter systems, in particular monoamines, in lithium response. (medscape.com)
  • showed no association between MAO-A and COMT variants and lithium response in 201 subjects diagnosed with mood disorders. (medscape.com)
  • In light of the evidence of genetic load for lithium-responsive BD, [ 24 , 56 , 57 ] case-control and family studies have been performed to identify molecular predictors of treatment response and to shed light on the genetic architecture of BD. (medscape.com)
  • In this section, we selectively review candidate gene studies focusing on neurotransmitters, neurotrophins, metabolic targets of lithium and transcription factor systems. (medscape.com)
  • Here we also present the results of lithium pharmacogenomic GWAS and gene- and protein-expression studies. (medscape.com)
  • [ 64 ] Association studies on genes encoding serotonin receptors do not support a major involvement of genetic variation with response to lithium prophylaxis in BD. (medscape.com)
  • [ 79-82 ] In regards to lithium response, some studies have suggested that the Val allele of the functional polymorphism rs6265 (Val66Met) predicts a poor response to lithium. (medscape.com)