Table 1.

Quantitation of [Ca²⁺]_i before and during low-Mg²⁺ treatment (SE) and the development of “epilepsy” 2 days later in the presence or absence of various pharmacological additions

Condition	[Ca2+]i, nM†	Epilepsy‡	SE spike frequency§
Control	165  ±  10	No	0
Low-Mg2+ (SE)	577  ±  35	Yes	12  ±  4.4
+ Low Ca2+ (0.2 mM)	177  ±  18**	No	10  ±  3.2
+ BAPTA (100 μM)	160  ±  8**	No	14  ±  5.1
+ APV (25 μM)	293  ±  24**	No	16  ±  3.8
+MK-801 (10 μM)	287  ±  25**	No	11  ±  2.9
+CNQX (10 μM)	433  ±  10**	Yes	9  ±  3
+NBQX (10 μM)	422  ±  56**	Yes	8  ±  2.4
+Nifedipine (5 μM)	441  ±  19*	Yes	13  ±  4.1
+TTX (1 μM)	157  ±  17**	No	0

^†The [Ca²⁺]_i quantitation was determined from the average [Ca²⁺]_i for individual neurons under each condition by using a Ca²⁺ calibration curve (17). The data represent the mean ± SE for each determination (n = 10). Each of the additions to the SE condition lowered [Ca²⁺]_i in a statistically significant manner (∗, P < 0.03; ∗∗, P < 0.005; Students t test). 

^‡The presence or absence of spontaneous recurrent seizures (epilepsy) at 2 days after a 3-hr low-Mg²⁺ treatment under each condition was determined by intracellular whole-cell current-clamp recordings of individuals neurons (n = 10) for more than 10 min each to determine the presence or absence of epileptiform activity. Cells either manifested epileptiform discharges or overt seizure activity (Yes) or showed no evidence of hyperexcitability (No). The development of epileptigenesis in these preparations was “all or none” in that no transition excitability states were observed at the 2-day time point. Representative examples of epileptic discharges (B, G–J) and nonexcitable recordings (A, C–F) are shown in Fig. 2. The results demonstrate that the decrease in [Ca²⁺]_i produced by multiple treatment conditions during SE were not equally effective in inducing epileptogenesis and were specific to the NMDA receptor-activated Ca²⁺-transduction pathway. 

^§The data represent the mean ± SE of spike frequency for spike discharges during low-Mg²⁺ treatment for each experimental condition (n = 8). Spike frequency was determined as described previously. In each condition where low Mg²⁺ produced continuous epileptiform discharges, the discharges were continuous and persistent at the same amplitude as shown in Fig. 1 for the duration of the low Mg²⁺ treatment. There were no statistical differences between the spike frequencies of these conditions (Student’s t test).