EFFECTS OF STRONGLY ANISOSMOTIC AND NACL DEFICIENT SOLUTIONS ON MUSCIMOL AND GLUTAMATE EVOKED WHOLE-CELL CURRENTS IN FRESHLY DISSOCIATED HIPPOCAMPAL-NEURONS
M. Vreugdenhil et al., EFFECTS OF STRONGLY ANISOSMOTIC AND NACL DEFICIENT SOLUTIONS ON MUSCIMOL AND GLUTAMATE EVOKED WHOLE-CELL CURRENTS IN FRESHLY DISSOCIATED HIPPOCAMPAL-NEURONS, Brain research, 670(1), 1995, pp. 89-96
Sudden exposure of dissociated hippocampal neurons to strongly hypo- o
r hyperosmotic solutions suppresses voltage gated Na+, K+ and Ca2+ cur
rents. We investigated whether ligand gated ion currents were similarl
y shut down by exposure to anisosmotic solutions. The effect of hypo-o
smotic, NaCl deficient (mannitol-substituted), or hyper-osmotic test s
olutions delivered from a flow pipette was tested on voltage gated Ca2
+ currents and on currents and conductance changes evoked by brief adm
inistration of either the GABA(A)-agonist muscimol or glutamate. Hyper
-osmotic solution caused cells to shrink, but cell membrane capacitanc
e did not change. Muscimol-induced conductance increases were depresse
d by hypo-osmotic and by NaCl deficient solutions and often by hyper-o
smotic solution. Voltage gated Ca2+ currents were depressed by anisosm
otic, but not by NaCl deficient isosmotic solution. NMDA- and non-NMDA
evoked conductance increases were depressed by hyperosmotic solution;
hypo-osmotic and NaCl deficient solutions were not tested on glutamat
e induced currents. Ligand gated currents are suppressed by anisosmoti
c solutions more slowly than are voltage gated channels. The changes c
aused by anisosmotic and NaCl deficient solutions were much greater th
en expected from calculated electrochemical effects and are probably t
he result of change in receptor controlled channels.