MODULATION OF N-METHYL-D-ASPARTIC ACID RECEPTORS BY EXTRACELLULAR CALCIUM IN IMMATURE AND ADULT HIPPOCAMPAL SLICES - WHOLE-CELL RECORDINGS IN CA3 PYRAMIDAL CELLS

Citation
Ja. Gorter et Rj. Brady, MODULATION OF N-METHYL-D-ASPARTIC ACID RECEPTORS BY EXTRACELLULAR CALCIUM IN IMMATURE AND ADULT HIPPOCAMPAL SLICES - WHOLE-CELL RECORDINGS IN CA3 PYRAMIDAL CELLS, Neuroscience letters, 194(3), 1995, pp. 209-213
Citations number
28
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
03043940
Volume
194
Issue
3
Year of publication
1995
Pages
209 - 213
Database
ISI
SICI code
0304-3940(1995)194:3<209:MONARB>2.0.ZU;2-P
Abstract
Lowering extracellular calcium concentration [Ca2+](o) in rat hippocam pal slices can lead to an induction of epileptiform activity. It has b een shown that this effect is more pronounced in slices of neonatal ra ts (postnatal day, PND 8-19) than in mature slices (>PND 40) and it ha s been suggested that unique N-methyl-D-aspadic acid (NMDA) receptor p roperties of immature rat hippocampal pyramidal cells contribute to th is developmental effect. In a voltage clamp experiment we tested NMDA receptor properties in hippocampal pyramidal cells by measuring NMDA r eceptor mediated currents evoked by iontophoretic applied NMDA in the basal dendrites of CA3 pyramidal neurons, We found that lowering extra cellular calcium from 2 to 1 mM, increases NMDA evoked inward current in pyramidal cells around the resting membrane potential. However, thi s effect is observed in slices of neonatal as well as in slices of mat ure rats, suggesting that there is no difference in NMDA receptor sens itivity to extracellular Ca2+ between these two age groups, The modula tion of the NMDA receptor by extracellular calcium at physiological co ncentrations can have important consequences in pathological condition s during which extracellular calcium reaches low levels. Because this 'hypocalcemic' condition induces a larger current influx via the NMDA receptor channel at resting membrane potentials, it can further enhanc e cellular excitability and contribute to sustain epileptiform activit y.