References

13 The Arabidopsis thaliana Glutamate-like Receptor Family(AtGLR) 191
Gilliham, unpublished), possibly indicating a desensitisation of response
(Everts, et al. 1999; Sun et al. 2002). Unpublished results of Qi et al (2005)
suggestthatglutamatedesensitisedtheresponsetoglycineinthehypocotyl,
but not vice versa, whereas no such specificity in desensitisation response
has been observed in roots (M. Gilliham, unpublished). De novo synthesis
of proteins may be required for full recovery of the response, since recovery
is inhibited by cycloheximide (Meyerhoff et al. 2005).
Neither response is initiated by GABA, NMDA, AMPA or KA, supporting
the divergence of AtGLRandiGluRbeforetheydevelopeduniqueligand
specificity (Chiuetal.1999).However,DNQXand6-cyano-7-nitroquinoxaline-2,3-dione
(CNQX) can abolish the glutamate-induced and/or the glycine-induced
[Ca2+ ]cyt increase (Dubos et al. 2003; Meyerhoff et al. 2005).
The cold-shock-induced rise in [Ca2+ ]cyt is unaffected by DNQX (or previous
application of glutamate) (Dubos et al. 2003), indicating separate Ca2+ response pathways but also specificity in the CNQX/DNQX antagonism.
TheNMDA/glutamatesitebindingiGluRantagonistAP-5alsoblocksboth
Em depolarisation and the Ca2+ -dependent microtubule depolymerisation
induced by glutamate (Sivaguru et al. 2003), however, its effect on [Ca2+ ]cyt
has not been measured directly. Interestingly NMDA also depolymerises
microtubules despite not inducing a [Ca2+ ]cyt or an Em response (Sivaguru
et al. 2003), suggesting that caution must be exercised when using iGluR agonists/antagonists
as indication of AtGLR involvement in these processes.
It should also be noted that NMDA-type iGluRs, the only iGluR subtype to
bind glycine, are not inhibited by CNQX/DNQX which bind at the glutamate
binding site of AMPA/KA iGluR.
L-glutamatealsoinducedtheinfluxofNa + and Ca2+ in a small percentage
of patch-clamped protoplasts derived from Arabidopsis root cells by
activating ‘spiky’ inward currents at hyperpolarised potentials with external
Ca2+ or less erratic currents with Na + (Demidchik et al. 2004). Glycine
can also activate an instantaneous current in patch-clamped protoplasts
derived from wheat root cells (M. Gilliham, unpublished). The effect of
glutamate on unidirectional influx of Na + into Arabidopsis roots was inconclusive
(Demidchik et al. 2004). Because Na + influx is mainly via NSCCs,
which are permeable to other monovalent cations, the movement of Na + ,
K + ,Cs + ,andNH + 4 , although not dependent upon a glutamate-induced
depolarisation may contribute to it.
Sivaguru et al. (2003) have suggested that AtGLRs are involved in root
responses to toxic Al3+ .TheyproposethatAl3+ , known to induce organic
anion release in some species (Ma and Furukawa 2003), stimulates glutamate
release, which activates Ca2+ influx via plasma-membrane-localised
AtGLR, leading to Em depolarisation and microtubule depolymerisation.
They observed that 5-nitro-2-(3-phenylpropylamino)-benzoate (NPPB),
known to inhibit the Al3+ -activated organic anion channel of the root