Figure 2

Roles of mitochondria, Na⁺ /Ca²⁺ exchanger (NCX), and neuronal size. The recovery of [Ca²⁺]_c from transients induced by application of high K⁺ solution (50 mM for 0.3 s) in thapsigargin-treated neurons was measured by recovery rate constant (τ) and by the time to achieve 95% recovery to baseline (T₉₅). Blockade of mitochondrial function by combined application of antimycin (1 μM) and oligomycin (10 μM) for 3 min had no effect compared baseline values (BL) in the same neurons (A). Block of NCX by equimolar replacement of bath Na⁺ with N-methyl-d-glucamine (NMDG) also had no effect on recovery of transients (B). Neuronal groups with either large (diameter 39 ± 4 μm) or small (26 ± 3 μm) profiles did not differ in PMCA function (C). Mean ± SD; numbers in bars indicate n; no differences when tested by paired T-test (A, B) and simple T-test (C).