Barium plateau potentials of CA1 pyramidal neurons elicit all-or-none extracellular alkaline shifts via the plasma membrane calcium ATPase.
In many brain regions, synchronous neural activity causes a rapid rise in extracellular pH. In the CA1 region of hippocampus, this population alkaline transient (PAT) enhances responses from postsynaptic, pH-sensitive N-methyl-d-aspartate (NMDA) receptors. Recently, we showed that the plasma membrane Ca(2+)-ATPase (PMCA), a ubiquitous transporter that exchanges internal Ca(2+) for external H(+), is largely responsible for the PAT. It has also been shown that a PAT can be generated after replacing extracellular Ca(2+) with Ba(2+). The cause of this PAT is unknown, however, because the ability of the mammalian PMCA to transport Ba(2+) is unclear. If the PMCA did not carry Ba(2+), a different alkalinizing source would have to be postulated. Here, we address this issue in mouse hippocampal slices, using concentric (high-speed, low-noise) pH microelectrodes. In Ba(2+)-containing, Ca(2+)-free artificial cerebrospinal fluid, a single antidromic shock to the alveus elicited a large (0.1-0.2 unit pH), "all-or-none" PAT in the CA1 cell body region. In whole cell current clamp of single CA1 pyramidal neurons, the same stimulus evoked a prolonged plateau potential that was similarly all-or-none. Using this plateau as the voltage command in other cells, we recorded Ba(2+)-dependent surface alkaline transients (SATs). The SATs were suppressed by adding 5 mM extracellular HEPES and abolished when carboxyeosin (a PMCA inhibitor) was in the patch pipette solution. These results suggest that the PAT evoked in the presence of Ba(2+) is caused by the PMCA and that this transporter is responsible for the PAT whether Ca(2+) or Ba(2+) is the charge carrying divalent cation.
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 lar...متن کامل
21 In hippocampus, synchronous activation of CA1 pyramidal neurons causes a rapid, 22 extracellular, population alkaline transient (PAT). It has been suggested that the plasma 23 membrane Ca 2+-ATPase (PMCA) is the source of this alkalinization, as it exchanges 24 cytosolic Ca 2+ for external H +. Evidence supporting this hypothesis, however, has thus far 25 been inconclusive. We addressed this...متن کامل
Rapid rise of extracellular pH evoked by neural activity is generated by the plasma membrane calcium ATPase.
In hippocampus, synchronous activation of CA1 pyramidal neurons causes a rapid, extracellular, population alkaline transient (PAT). It has been suggested that the plasma membrane Ca(2+)-ATPase (PMCA) is the source of this alkalinization, because it exchanges cytosolic Ca(2+) for external H(+). Evidence supporting this hypothesis, however, has thus far been inconclusive. We addressed this long-s...متن کامل
Autocrine boost of NMDAR current in hippocampal CA1 pyramidal neurons by a PMCA-dependent, perisynaptic, extracellular pH shift.
The plasma membrane Ca(2+)-ATPase (PMCA) is found near postsynaptic NMDARs. This transporter is a Ca(2+)-H(+) exchanger that raises cell surface pH. We tested whether the PMCA acts in an autocrine fashion to boost pH-sensitive, postsynaptic NMDAR currents. In mouse hippocampal slices, NMDAR EPSCs in a singly activated CA1 pyramidal neuron were reduced when buffering was augmented by exogenous c...متن کامل
Altered neuronal calcium homeostasis is widely hypothesized to underlie cognitive deficits in normal aging subjects, but the mechanisms that underlie this change are unknown, possibly due to a paucity of direct measurements from aging neurons. Using CCD and two-photon calcium imaging techniques on CA1 pyramidal neurons from young and aged rats, we show that calcium influx across the plasma memb...متن کامل