Ca2+ buffer saturation underlies paired pulse facilitation in calbindin-D28k-containing terminals
Ca2+ buffer saturation was proposed as a mechanism of paired pulse facilitation (PPF). However, whether it operates under native conditions remained unclear. Here we show that saturation of the endogenous fast Ca2+ buffer calbindin-D28k (CB) plays a major role in PPF at CB-containing synapses. Paire...
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| Veröffentlicht in: | Neuron (Cambridge, Mass.) Mass.), 2003-04, Vol.38 (1), p.79-88 |
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| creator | Blatow, Maria Caputi, Antonio Burnashev, Nail Monyer, Hannah Rozov, Andrei |
| description | Ca2+ buffer saturation was proposed as a mechanism of paired pulse facilitation (PPF). However, whether it operates under native conditions remained unclear. Here we show that saturation of the endogenous fast Ca2+ buffer calbindin-D28k (CB) plays a major role in PPF at CB-containing synapses. Paired recordings from synaptically connected interneurons and pyramidal neurons in the mouse neocortex revealed that dialysis increased the amplitude of the first response and decreased PPF. Loading the presynaptic terminals with BAPTA or CB rescued the effect of the CB washout. We extended the study to the CB-positive facilitating excitatory mossy fiber-CA3 pyramidal cell synapse. The effects of different extracellular Ca2+ concentrations and of EGTA indicated that PPF in CB-containing terminals depended on Ca2+ influx rather than on the initial release probability. Experiments in CB knockout mice confirmed that buffer saturation is a novel basic presynaptic mechanism for activity-dependent control of synaptic gain. |
| doi_str_mv | 10.1016/s0896-6273(03)00196-x |
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However, whether it operates under native conditions remained unclear. Here we show that saturation of the endogenous fast Ca2+ buffer calbindin-D28k (CB) plays a major role in PPF at CB-containing synapses. Paired recordings from synaptically connected interneurons and pyramidal neurons in the mouse neocortex revealed that dialysis increased the amplitude of the first response and decreased PPF. Loading the presynaptic terminals with BAPTA or CB rescued the effect of the CB washout. We extended the study to the CB-positive facilitating excitatory mossy fiber-CA3 pyramidal cell synapse. The effects of different extracellular Ca2+ concentrations and of EGTA indicated that PPF in CB-containing terminals depended on Ca2+ influx rather than on the initial release probability. 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| subjects | Action Potentials - drug effects Action Potentials - physiology Animals Binding sites Buffers Calbindin 1 Calbindins Calcium - pharmacology Chelating Agents - pharmacology Dialysis Egtazic Acid - analogs & derivatives Egtazic Acid - pharmacology Experiments Extracellular Space - metabolism Hypotheses Interneurons - metabolism Mice Mice, Inbred C57BL Mice, Knockout Mossy Fibers, Hippocampal - metabolism Neocortex - cytology Neuronal Plasticity - physiology Neurons Neurosciences Organ Culture Techniques Pyramidal Cells - metabolism S100 Calcium Binding Protein G - genetics S100 Calcium Binding Protein G - metabolism Software Synapses - metabolism |
| title | Ca2+ buffer saturation underlies paired pulse facilitation in calbindin-D28k-containing terminals |
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