GABA and GHB Neurotransmitters in Plants and Animals - Communication in Plants: Neuronal Aspects of Plant Life - page 180

concomitant overproduction of GHB may alter cell function by impairing
its redox state (Gupta et al. 2003; Visser et al. 2002; Nakamura et al. 2001)
or interfere with mitochondrial metabolism (Taberner et al. 1972; Godin et
al. 1969), which might in turn lead to the amplification of oxidative stress
(Genova et al. 2004).
12.3.4
The GABA Shunt, GHB,
andtheRedoxStateinPlants
Arecentstudyin Arabidopsis showed that SSADH deficiency leads to detri-
mental effects on plant development under stress conditions (Bouché et
al. 2003). The light-fluence-dependent appearance of necrotic lesions on
leaves, and the accumulation of ROI in SSADH-deficient plants, particu-
larly under high-fluence light, or in response to other stresses (e.g., heat
shock) suggested a redox related function of the GABA shunt in plants
(Bouché et al. 2003). Moreover, under conditions where SSADH is not func-
tional, there might be a toxic accumulation of by-products of the TCA cycle
and/or the GABA shunt. Similar to the situation in mammals, GHB might
accumulate under these conditions, and cause tissue toxicity. Recently, an
Arabidopsis GHBDH cDNA was identified and characterized by functional
complementation of an SSADH-deficient yeast mutant (Breitkreuz et al.
2003). The encoded enzyme synthesizes GHB from its precursor SSA. Re-
cent evidence also showed the accumulation of GHB in plants in response
to hypoxic conditions (Allan et al. 2003; Breitkreuz et al. 2003). Earlier,
Busch and Fromm (1999) showed that Arabidopsis SSADH is negatively
regulated by NADH to NAD + ratios as well as by adenylate composition,
AMP:ADP:ATP. Alterations in these metabolite ratios are characteristic of
hypoxic condition (Wigge et al. 1993; Shelp et al. 1995). Therefore, we may
speculate that a decrease in SSADH activity would boost GHB production
as a consequence of the accumulation of the common unstable precursor
SSA (Fig. 12.1). Moreover, similar to bacteria, increase in NADH/ROI in
hypoxic cells would inhibit the 2-OGDH, leading to redirection of Glu and
2OG through the GABA shunt.
The ssadh mutant in Arabidopsis provided an opportunity for further
studies of the physiological role of the GABA shunt and GHB in plants.
In a recent pharmacological and metabolic study on Arabidopsis ssadh
mutants, Fait et al. (2005) showed that GHB is abundant in the ssadh
mutant. High-fluence light further increased GHB content in the mutant,
which was associated with ROI accumulation and the appearance of lesions
on the leaves. These observations suggested that (1) the increased level of
GHB in the mutant is likely caused by the metabolic block resulting from