Glutamatergic synaptic responses and long-term potentiation are impaired in the CA1 hippocampal area of calbindin D28k-deficient mice

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Abstract
The contribution of the cytosolic calcium binding protein calbindin D28K (CaBP) to glutamatergic neurotransmission and synaptic plasticity was investigated in hippocampal CA1 area of wild‐type and antisense transgenic CaBP‐deficient mice, with the use of extracellular recordings in the ex vivo slice preparation. The amplitude of non‐N‐methyl‐D‐aspartate receptor (non‐NMDAr)‐mediated extracellular field excitatory postsynaptic potentials (fEPSPs) recorded in control medium was significantly greater in CaBP‐deficient mice, whereas the afferent fiber volley was not affected. In contrast, the amplitude of NMDAr‐mediated fEPSPs isolated in a magnesium‐free medium after blockade of non‐NMDAr and GABAergic receptors was significantly depressed in these animals. No alteration in the magnitude of paired‐pulse facilitation was found, indicating that the presynaptic calcium mechanisms controlling glutamate release were not altered in CaBP‐deficient mice. The magnitude and time course of the short‐term potentiation (STP) of fEPSPs induced by a 30 Hz conditioning stimulation, which was blocked by the NMDAr antagonist 2‐amino‐5‐phosphonovalerate acid (2‐APV), was not impaired in the transgenic mice, whereas long‐term potentiation (LTP) induced by a 100 Hz tetanus was not maintained. The long‐term depression (LTD) induced by low‐frequency stimulation (1 Hz, 15 min) in the presence of the GABA antagonist bicuculline was not altered. These results argue for a contribution of CaBP to the mechanisms responsible for the maintenance of long‐term synaptic potentiation, at least in part by modulating the activation of NMDA receptors. Synapse 33:172–180, 1999.