PMID- 9089698
OWN - NLM
STAT- MEDLINE
DCOM- 19970721
LR  - 20190914
IS  - 0168-0102 (Print)
IS  - 0168-0102 (Linking)
VI  - 27
IP  - 1
DP  - 1997 Jan
TI  - Intracellular Ca2+, Na+ and H+ transients evoked by kainate in the leech giant 
      glial cells in situ.
PG  - 45-56
AB  - The membrane responses to the glutamate receptor agonist kainate and the 
      subsequent changes in intracellular Ca2+, H+ and Na+ concentration were measured 
      in giant glial cells of the leech central nervous system using ion-selective 
      microelectrodes and microfluorimetry of Fura-2. The membrane depolarization or 
      membrane inward current of exposed neuropile glial cells in situ, evoked by 2-20 
      microM kainate, were reversibly blocked by 6-cyano-7-dinitroquinoxaline-2,3-dione 
      (CNQX), (50-100 microM) and by Ni2+ (2 mM), but not by methoxyverapamil (D600, 
      500 microM), which blocked voltage-gated Ca2+ influx. Local iontophoretic 
      application of kainate on to the somatic membrane of single neuropile glial cells 
      in situ, resulted in CNQX-sensitive depolarization and rises in intraglial Ca2+ 
      concentration similar to those observed with bath-application of the agonist, 
      indicating the presence of non-N-methyl-D-aspartate-type (NMDA) glutamate 
      receptors in the somatic membrane of these cells. In voltage-clamped glial cells 
      bath-application of kainate (5-10 microM) evoked inward currents and an increase 
      in the membrane conductance,. while the intracellular Ca2+ increased (up to 200 
      nM). This increase in Ca2+i was not affected by substitution of Na+ by Li+, 
      indicating that it is not due to reversed Na+/Ca2 exchange following 
      intracellular Na+ accumulation. The intracellular Na+ concentration increased (up 
      to 40 mM), and the intracellular pH decreased (0.2-0.3 pH units) in 
      voltage-clamped glial cells following bath application of kainate. All these 
      changes of the concentration of intracellular cations were reversibly suppressed 
      by CNQX and Ni2+. The results indicate that Ca2+, Na+ and H+ enter leech 
      neuropile glial cells presumably through non-selective cation channels, activated 
      by the non-NMDA glutamate receptor agonist kainate.
FAU - Munsch, T
AU  - Munsch T
AD  - Abteilung fur Allgemeine Zoologie, FB Biologie, Universitat Kaiserstautern, 
      Germany.
FAU - Deitmer, J W
AU  - Deitmer JW
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Ireland
TA  - Neurosci Res
JT  - Neuroscience research
JID - 8500749
RN  - 0 (Receptors, Glutamate)
RN  - 39WPC8JHR8 (Gallopamil)
RN  - 6OTE87SCCW (6-Cyano-7-nitroquinoxaline-2,3-dione)
RN  - 77521-29-0 (alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid)
RN  - 7OV03QG267 (Nickel)
RN  - 9NEZ333N27 (Sodium)
RN  - SIV03811UC (Kainic Acid)
RN  - SY7Q814VUP (Calcium)
RN  - TSN3DL106G (Fura-2)
SB  - IM
MH  - 6-Cyano-7-nitroquinoxaline-2,3-dione/pharmacology
MH  - Animals
MH  - Calcium/*metabolism
MH  - Electric Conductivity
MH  - Fura-2
MH  - Gallopamil/pharmacology
MH  - Ganglia, Invertebrate/*physiology
MH  - *Hydrogen-Ion Concentration
MH  - In Vitro Techniques
MH  - Kainic Acid/*pharmacology
MH  - Kinetics
MH  - Leeches
MH  - Membrane Potentials/drug effects
MH  - Microelectrodes
MH  - Neuroglia/drug effects/*physiology
MH  - Nickel/pharmacology
MH  - Patch-Clamp Techniques
MH  - Receptors, Glutamate/physiology
MH  - Sodium/*metabolism
MH  - alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid/pharmacology
EDAT- 1997/01/01 00:00
MHDA- 1997/01/01 00:01
CRDT- 1997/01/01 00:00
PHST- 1997/01/01 00:00 [pubmed]
PHST- 1997/01/01 00:01 [medline]
PHST- 1997/01/01 00:00 [entrez]
AID - S0168-0102(96)01127-3 [pii]
AID - 10.1016/s0168-0102(96)01127-3 [doi]
PST - ppublish
SO  - Neurosci Res. 1997 Jan;27(1):45-56. doi: 10.1016/s0168-0102(96)01127-3.