Barium Plateau Potentials of CA1 Pyramidal Neurons Elicit All-or-None Extracellular

23 In many brain regions, synchronous neural activity causes a rapid rise in extracellular 24 pH. In the CA1 region of hippocampus, this population alkaline transient (PAT) enhances 25 responses from postsynaptic, pH-sensitive NMDA receptors. Recently, we demonstrated that 26 the plasma membrane Ca2+-ATPase (PMCA), a ubiquitous transporter that exchanges internal 27 Ca2+ for external H+, is largely responsible for the PAT. It has also been shown that a PAT can 28 be generated after replacing extracellular Ca2+ with Ba2+. The cause of this PAT is unknown, 29 however, since the ability of the mammalian PMCA to transport Ba2+ is unclear. If the PMCA 30 did not carry Ba2+, a different alkalinizing source would have to be postulated. Here, we 31 address this issue in mouse hippocampal slices, using concentric (high-speed, low-noise) pH 32 microelectrodes. In Ba2+-containing, Ca2+-free ACSF, a single antidromic shock to the alveus 33 elicited a large (0.1-0.2 unit pH), “all-or-none” PAT in the CA1 cell body region. In whole-cell 34 current clamp of single CA1 pyramidal neurons, the same stimulus evoked a prolonged plateau 35 potential that was similarly all-or-none. Using this plateau as the voltage command in other 36 cells, we recorded Ba2+-dependent surface alkaline transients (SATs). The SATs were 37 suppressed by adding 5 mM extracellular HEPES, and abolished when carboxyeosin (a PMCA 38 inhibitor) was in the patch pipette solution. These results suggest that the PAT evoked in the 39 presence of Ba2+ is due to the PMCA, and that this transporter is responsible for the PAT 40 whether Ca2+ or Ba2+ is the charge carrying divalent cation. 41