P. Hochstrate et Wr. Schlue, CA2-CELLS AND NEURONS CAUSED BY PHARMACOLOGICALLY DISTINCT GLUTAMATE RECEPTORS( INFLUX INTO LEECH GLIAL), Glia, 12(4), 1994, pp. 268-280
The effect of glutamatergic agonists on the intracellular free Ca2+ co
ncentration ([Ca2+](i)) of neuropile glial cells and Retzius neurones
in intact segmental ganglia of the medicinal leech Hirudo medicinalis
was investigated by using iontophoretically injected fura-2. In physio
logical Ringer solution the [Ca2+](i) levels of both cell types were a
lmost the same (glial cells: 58 +/- 30 nM, n = 51; Retzius neurones: 6
1 +/- 27 nM, n = 64). In both cell types glutamate, kainate, and quisq
ualate induced an increase in [Ca2+](i) which was inhibited by 6,7-din
itroquinoxaline-2,3-dione (DNQX). This increase was caused by a Ca2+ i
nflux from the extracellular space because the response was greatly di
minished upon removal of extracellular Ca2+. The glutamate receptors o
f neuropile glial cells and Retzius neurones differed with respect to
the relative effectiveness of the agonists used, as well as with regar
d to the inhibitory strength of DNQX, In Retzius neurones the agonist-
induced [Ca2+](i) increase was abolished after replacing extracellular
Na+ by organic cations or by mM amounts of Ni2+, whereas in glial cel
ls the [Ca2+](i) increase was largely preserved under both conditions.
It is concluded that in Retzius neurones the Ca2+ influx is predomina
ntly mediated by voltage-dependent Ca2+ channels, whereas in neuropile
glial cells the major influx occurs via the ion channels that are ass
ociated with the glutamate receptors. (C) 1994 Wiley-Liss, Inc.