Ls. Kane et al., Uptake and metabolism of glutamate at non-synaptic regions of crayfish central nerve fibers: Implications for axon-glia signaling, NEUROSCIENC, 97(3), 2000, pp. 601-609
In crayfish and squid giant nerve fibers, glutamate appears to be an axon-g
lia signaling agent. We have investigated glutamate transport and metabolis
m by crayfish central nerve fibers in order to identify possible mechanisms
by which glutamate could subserve this non-synaptic signaling function. Ac
cumulation of radiolabeled L-glutamate by desheathed cephalothoracic nerve
bundles was temperature and Na+ dependent, linear with time for at least 8
h and saturable at about 0.5-1 mM L-glutamate. Most accumulated radiotracer
was associated with the periaxonal glial sheath and remained as glutamate.
Compounds known to block glutamate transport in invertebrate peripheral ne
rves or mammalian brain slices or cell cultures were also effective on cray
fish central nerve fibers. Tissue radiotracer levels were only 3% of contro
l levels when 1 mM p-chloromercuriphenylsulfonate was present, and 13%, 20%
, 26%, 38% and 42% of control levels, respectively, when L-cysteate, L-cyst
eine sulfinate, L-aspartate, D-aspartate or DL-threo-beta-hydroxyaspartate
was present. L-Glutamine, GABA, N-methyl-DL-aspartate, alpha-aminoadipate a
nd D-glutamate were without inhibitory effect on tissue tracer accumulation
. Radiolabeled D-aspartate was an equivalent non-metabolized substitute for
radiolabeled L-glutamate. D-Aspartate, p-chloromercuriphenylsulfonate and
GABA had comparable effects on isolated medial giant nerve fibers.
These studies indicate that L-glutamare is taken up primarily by the periax
onal glia of crayfish central nerve fibers by a low-affinity, saturable, Na
+-dependent transport system and is retained by the fibers primarily in tha
t form. Our results suggest that the glia are not only the target of the gl
utamate signal released from non-synaptic regions of the crayfish medial gi
ant axon during high-frequency stimulation, but that they are also the prim
ary site of its inactivation. (C) 2000 IBRO. Published by Elsevier Science
Ltd.