FIG. 2.

NMDA regulation of Ca²⁺ levels in the SCN. Bath application of NMDA (50 μM, 60 s) produced Ca²⁺ transients in most cells (94%) within the SCN (P < 0.001, n = 64). These NMDA-induced Ca²⁺ transients were blocked by treatment with the NMDA GluR antagonist AP5 (50 μM, P < 0.001, n = 32) and were enhanced by the removal of magnesium (Mg²⁺) from the extracellular solution (P < 0.001, n = 39). Finally, because Ca²⁺ influx through voltage-activated channels might be a major source of NMDA-evoked Ca²⁺ increases, some experiments were run in the presence of the TTX and methoxyverapamil (D600). In the presence of these channel blockers and the absence of Mg²⁺, bath application of NMDA (50 μM) still produced significant Ca²⁺ transients (P < 0.001, n = 83). Data collected during day from 10–15-day-old rats.