Neural and developmental actions of lithium: A unifying hypothesis

@article{Berridge1989NeuralAD,
  title={Neural and developmental actions of lithium: A unifying hypothesis},
  author={Michael John Berridge and C. Peter Downes and Michael R. Hanley},
  journal={Cell},
  year={1989},
  volume={59},
  pages={411-419}
}

Lithium and synaptic plasticity.

Findings demonstrate that lithium directly inhibits, in a non-competitive fashion, the activity of glycogen synthase kinase (GSK)-3beta, a serine/threonine kinase highly expressed in the central nervous system, which raises the possibility for developing new therapeutic approaches for the treatment of bipolar disorders.

Bipolar disorder: leads from the molecular and cellular mechanisms of action of mood stabilisers

The results suggest that regulation of signalling pathways may play a major part in the long-term actions of mood stabilisers and may exert underappreciated neuroprotective effects.

Phosphoinositide metabolism, lithium and manic depressive illness

It is likely that the enzyme IMPase, other that being the key point in initiating lithium's therapeutic effects, may also play a critical role in the physiology underlying manic depressive illness.

Signal transduction pathways. Molecular targets for lithium's actions.

The identification of key components of signal transduction pathways (in particular, guanine nucleotide-binding proteins [G proteins], adenylyl cyclases, and protein kinase C isozymes) as targets for lithium's actions are reviewed to integrate these effects with the large body of data emphasizing alterations in various neurotransmitter systems.

Neural network dysfunction in bipolar depression: clues from the efficacy of lamotrigine.

In healthy volunteers, lamotrigine had a facilitatory effect on the BOLD response to TMS (transcranial magnetic stimulation) of the prefrontal cortex, and in vitro, lamOTrigine enhanced the power of gamma frequency network oscillations induced by kainic acid in the rat hippocampus, an effect that was not observed with valproic acid.

Neurobiology of lithium: an update.

The accumulated preclinical and clinical evidence for the action of lithium in the brain is critically examined and areas that may be most productive for future investigation are suggested, i.e., membrane transport systems, neurotransmitter receptor regulation, second messenger generating systems, protein kinase C (PKC) regulation, and gene expression.

Signalling pathways in the brain: cellular transduction of mood stabilisation in the treatment of manic-depressive illness.

Chronic lithium administration produces a reduction in the expression of PKC alpha and epsilon, as well as a major PKC substrate, MARCKS, which has been implicated in long-term neuroplastic events in the developing and adult brain.

Lithium: the pharmacodynamic actions of the amazing ion

Support is provided for a role for the inhibition of glycogen synthase kinase 3 and inositol monophosphatase in the pharmacodynamic actions of lithium, and how inhibition of these enzymes by lithium can lead to downstream effects of clinical relevance, both for mood disorders and neurodegenerative diseases.

Lithium and valproic acid: parallels and contrasts in diverse signaling contexts.

Long‐term action of lithium: A role for transcriptional and posttranscriptional factors regulated by protein kinase C

Evidence is presented to show that chronic lithium exerts significant transcriptional and posttranscriptional effects, and that these actions of lithium may be mediated via protein kinase C (PKC)‐induced alterations in nuclear transcription regulatory factors responsible for modulating the expression of proteins involved in long‐term neural plasticity and cellular response.
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