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J Physiol Volume 579, Number 1, 85-99, February 15, 2007 DOI: 10.1113/jphysiol.2006.123901
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NEUROSCIENCE

Presynaptic plasma membrane Ca2+ ATPase isoform 2a regulates excitatory synaptic transmission in rat hippocampal CA3

Thomas P. Jensen1, Adelaida G. Filoteo2, Thomas Knopfel3 and Ruth M. Empson1,4

1 School of Biological Sciences, Royal Holloway University of London, Egham, Surrey TW20 0EX, UK
2 The Program in Molecular Neuroscience, Department of Biochemistry and Molecular Biology, Mayo Graduate School, Mayo Clinic, Rochester, MN 55905, USA
3 Laboratory for Neuronal Circuit Dynamics, RIKEN Brain Science Institute, Wako-ishi, Saitama, 351-0198, Japan
4 Department of Physiology, University of Otago School of Medical Sciences, Dunedin, New Zealand

Plasma membrane calcium ATPase isoforms (PMCAs) are expressed in a wide variety of tissues where cell-specific expression provides ample opportunity for functional diversity amongst these transporters. The PMCAs use energy derived from ATP to extrude submicromolar concentrations of intracellular Ca2+ ([Ca2+]i) out of the cell. Their high affinity for Ca2+ and the speed with which they remove [Ca2+]i depends upon splicing at their carboxy (C)-terminal site. Here we provide biochemical and functional evidence that a brain-specific, C-terminal truncated and therefore fast variant of PMCA2, PMCA2a, has a role at hippocampal CA3 synapses. PMCA2a was enriched in forebrain synaptosomes, and in hippocampal CA3 it colocalized with the presynaptic marker proteins synaptophysin and the vesicular glutamate transporter 1, but not with the postsynaptic density protein PSD-95. PMCA2a also did not colocalize with glutamic acid decarboxylase-65, a marker of GABA-ergic terminals, although it did localize to a small extent with parvalbumin-positive presumed inhibitory terminals. Pharmacological inhibition of PMCA increased the frequency but not the amplitude of mEPSCs with little effect on mIPSCs or paired-pulse depression of evoked IPSCs. However, inhibition of PMCA activity did enhance the amplitude and slowed the recovery of paired-pulse facilitation (PPF) of evoked EPSCs. These results indicated that fast PMCA2a-mediated clearance of [Ca2+]i from presynaptic excitatory terminals regulated excitatory synaptic transmission within hippocampal CA3.

(Received 7 November 2006; accepted after revision 6 December 2006; first published online 14 December 2006)
Corresponding author R. M. Empson: Department of Physiology, University of Otago School of Medical Sciences, Dunedin, New Zealand. Email: ruth.empson{at}stonebow.otago.ac.nz






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