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. Author manuscript; available in PMC: 2009 Apr 30.
Published in final edited form as: Neuropsychopharmacology. 2008 Oct 15;34(1):18–54. doi: 10.1038/npp.2008.172

Figure 10.

Figure 10

Glutamate–glutamine shuttle between glutamatergic nerve terminals and astroglia in the CNS. Increased expression of GLUL and SLC1A2 genes in schizophrenia and bipolar disorder (Shao and Vawter, 2008; Vawter et al, 2006a; Choudary et al, 2005; Beasley et al, 2006) and increased expression of GLS (Bruneau et al, 2005; Gluck et al, 2002) have been reported in schizophrenia, whereas decreased SLC1A2 and AGXT2L1 mRNA and GLUL mRNA and protein levels in major depressive disorder in the anterior cingulate were reported (Shao and Vawter, 2008; Vawter et al, 2006a; Choudary et al, 2005; Beasley et al, 2006). These molecules contribute to the transport, synthesis, and recycling of glutamate after synaptic release (Magistretti et al, 1999). Glutamate does not cross the blood–brain barrier and its presence in the CNS is from the glia-derived precursor, glutamine. SLC1A2 (solute carrier family 1 (glial high-affinity glutamate transporter, member 2)), AGXT2L1 (alanine-glyoxylate aminotransferase 2-like 1), GLUL (glutamate-ammonia ligase (glutamine synthetase)), SLC38A1 (solute carrier family 38, member 1), and GLS (glutaminase) are involved in this process and, as shown by arrows, are mostly increased in schizophrenia.