Effects of glutamatergic agonists and antagonists on membrane potential and intracellular Na+ activity of leech glial and nerve cells

Glutamate receptor 5/6/7-like and glutamate transporter-1-like immunoreactivity in the leech central nervous system

“…In contrast, whole-mounted tissue exposed to NMDAR 1 antiserum did not differ from controls (not shown), indicating that the antibody did not detect the NMDAR 1 epitope in the leech CNS. Thus, non-NMDA receptor-like but not NMDA receptor-like immunoreactivity was present in leech ganglia, which is consistent with previous physiological and pharmacological studies (Ballanyi et al, 1989;Brodfuehrer and Cohen, 1990;Dörner et al, 1990Dörner et al, , 1994Deitmer and Munsch, 1992;Dierkes et al, 1996).…”

“…Ample physiological and pharmacological evidence exists for the ability of vertebrate macroglia to respond to glutamate (Hertz, 1979;Teichberg, 1991;Steinhä user and Gallo, 1996). In the leech, physiological and pharmacological studies have demonstrated that neuropil glia respond to exogenously applied glutamate and its agonists; these glia are also susceptible to non-NMDA receptor antagonism (Ballanyi et al, 1989;Ballanyi and Schlue, 1990;Dörner et al, 1990Dörner et al, , 1994Deitmer and Munsch, 1992;Hochstrate and Schlue, 1994;Munsch et al, 1994;Rose et al, 1995;Dierkes et al, 1996;Deitmer and Schneider, 1997;Munsch and Deitmer, 1997). Hence, GluR 5/6/7-like immunoreactivity within the neuropil may also be associated with the processes of neuropil glia.…”

“…Non-N-methyl-D-aspartate (NMDA) antagonists also block synaptic input to each of these cells, as well as to two additional members of the swim oscillator-cells 115 and 28 Thorogood et al, 1996). In addition, exposure to glutamate agonists directly induces membrane depolarization of leech DE-3 and L motor neurons, Retzius and effector AP and AE cells, and neuropil glia (Mat Jais et al, 1984;Brodfuehrer and Cohen, 1990;Deitmer and Munsch, 1992;Dörner et al, 1994;Thorogood et al, , 1996Dierkes et al, 1996). Agonist-induced excitation of neuropil glia and DE-3 are also blocked by non-NMDA antago-nists (Deitmer and Munsch, 1992;Thorogood et al, 1996).…”

Na+/K+-pump and neurotransmitter membrane receptors

“…Despite this, to date no invertebrate glutamate receptors have been described that are modulated by Na + /K + -pump. However, glutamate and non-NMDA glutamate agonists depolarize leech glial and Retzius cells, altering intracellular Na + activity and inducing an after-hyperpolarization (Dorner et al 1994). This after-hyperpolarization is blocked by 100 µM ouabain and when external sodium is partially replaced with lithium.…”

Comparison of Effects of Endogenous and Exogenous Excitatory Amino Acids on Retzius Nerve Cells of the Leech

“…DIERKES et al (1996) applied Kainate on RNCL in concentration of 10 -4 mol/l which produced depolarization comparable to that of 10 -4 mol/l L-BOAA in our experiments. DÖRNER et al (1994) constructed dose response curves for Kainate and L-glu on RNCL that are almost identically positioned as our dose response curves for L-BOAA and L-glu. Furthermore, investigations of the ionic mechanism of action of Kainate (DÖRNER et al 1990;LÖHRKE & DEITMER 1996;MULLER et al 2003) are in agreement with the ionic mechanism of action of L-BOAA reported by CEMERIKIC et al (2001).…”