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Review
. 2018;16(5):519-532.
doi: 10.2174/1570159X15666170828170921.

Neuron-glia Interaction as a Possible Pathophysiological Mechanism of Bipolar Disorder

Jairo Vinicius Pinto  1   2 , Ives Cavalcante Passos  1   2 , Diego Librenza-Garcia  1   2 , Grasiela Marcon  1   2 , Maiko Abel Schneider  2 , Joao Henrique Conte  1 , Joao Pedro Abreu da Silva  1 , Luiza Pereira Lima  1 , Andre Quincozes-Santos  3 , Marcia Kauer-Sant Anna  1   2 , Flavio Kapczinski  4
Affiliations
Review

Neuron-glia Interaction as a Possible Pathophysiological Mechanism of Bipolar Disorder

Jairo Vinicius Pinto et al. Curr Neuropharmacol. 2018.

Abstract

Accumulating evidence has shown the importance of glial cells in the neurobiology of bipolar disorder. Activated microglia and inflammatory cytokines have been pointed out as potential biomarkers of bipolar disorder. Indeed, recent studies have shown that bipolar disorder involves microglial activation in the hippocampus and alterations in peripheral cytokines, suggesting a potential link between neuroinflammation and peripheral toxicity. These abnormalities may also be the biological underpinnings of outcomes related to neuroprogression, such as cognitive impairment and brain changes. Additionally, astrocytes may have a role in the progression of bipolar disorder, as these cells amplify inflammatory response and maintain glutamate homeostasis, preventing excitotoxicity. The present review aims to discuss neuron-glia interactions and their role in the pathophysiology and treatment of bipolar disorder.

Keywords: Bipolar disorder; astrocyte; brain-blood barrier; glia; mania; microglia; neuron; oligodendrocyte..

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Figures

Fig. (1)
Fig. (1)
Tripartite synapses model. AMPA: α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor; CB1R: cannabinoid receptor type 1; AEA: N-arachidonoylethanolamine (anandamide); EAAT1: excitatory amino acid transporter subtype 1; EAAT2: excitatory amino acid transporter subtype 2; Gln: glutamine; GlnT: glutamine transportes; Glu: glutamate; mGluR1: metabotropic glutamate receptor 1; mGluR2: metabotropic glutamate receptor 2; mGluR3: metabotropic glutamate receptor 3; NMDA: N-methyl-D-aspartate receptor. (The color version of the figure is available in the electronic copy of the article).
Fig. (2)
Fig. (2)
Blood-brain barrier model. A blood-brain barrier model showing its components: astrocyte endfeet, pericytes, basement membrane, endothelium and the gap junctions. (The color version of the figure is available in the electronic copy of the article).
Fig. (3)
Fig. (3)
Blood-brain barrier disruption. A model of blood-brain barrier disruption showing cytokines and the blood-brain barrier components: astrocyte endfeet, pericytes, basement membrane, endothelium, and the gap junctions. IL-6: interleukin-6; TNF-α: tumor necrosis factor-alpha. (The color version of the figure is available in the electronic copy of the article).
See this image and copyright information in PMC

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