Transmitter release modulation in nerve terminals of rat neocortical pyramidal cells by intracellular calcium buffers

• Published in: The Journal of physiology 1998-11, Vol.513 (1), p.135-148
• Main Authors: Ohana, Ora, Sakmann, Bert
• Format: Article
• Language: English
• Subjects: Algorithms; Animals; Calcium - metabolism; Chelating Agents - pharmacology; Egtazic Acid - analogs & derivatives; Egtazic Acid - pharmacology; Electric Stimulation; Electrophysiology; Excitatory Postsynaptic Potentials - drug effects; In Vitro Techniques; Membrane Potentials - physiology; Neocortex - cytology; Neocortex - metabolism; Nerve Endings - metabolism; Neurotransmitter Agents - metabolism; Original; Patch-Clamp Techniques; Pyramidal Cells - metabolism; Rats; Rats, Wistar
• ISSN: 0022-3751; 1469-7793
• DOI: 10.1111/j.1469-7793.1998.135by.x

Dual whole-cell voltage recordings were made from synaptically connected layer 5 (L5) pyramidal neurones in slices of the young (P14-P16) rat neocortex. The Ca 2+ buffers BAPTA or EGTA were loaded into the presynaptic neurone via the pipette recording from the presynaptic neurone to examine their effect on the mean and the coefficient of variation (c.v.) of single fibre EPSP amplitudes, referred to as unitary EPSPs. The fast Ca 2+ buffer BAPTA reduced unitary EPSP amplitudes in a concentration dependent way. With 0.1 m m BAPTA in the pipette, the mean EPSP amplitude was reduced by 14 ± 2.8% (mean ± s.e.m. , n = 7) compared with control pipette solution, whereas with 1.5 m m BAPTA, the mean EPSP amplitude was reduced by 72 ± 1.5% ( n = 5). The concentration of BAPTA that reduced mean EPSP amplitudes to one-half of control was close to 0.7 m m . Saturation of BAPTA during evoked release was tested by comparing the effect of loading the presynaptic neurone with 0.1 m m BAPTA at 2 and 1 m m [Ca 2+ ] o . Reducing [Ca 2+ ] o from 2 to 1 m m , thereby reducing Ca 2+ influx into the terminals, decreased the mean EPSP amplitude by 60 ± 2.2% with control pipette solution and by 62 ± 1.9% after loading with 0.1 m m BAPTA ( n = 7). The slow Ca 2+ buffer EGTA at 1 m m reduced mean EPSP amplitudes by 15 ± 2.5% ( n = 5). With 10 m m EGTA mean EPSP amplitudes were reduced by 56 ± 2.3% ( n = 4). With both Ca 2+ buffers, the reduction in mean EPSP amplitudes was associated with an increase in the c.v. of peak EPSP amplitudes, consistent with a reduction of the transmitter release probability as the major mechanism underlying the reduction of the EPSP amplitude. The results suggest that in nerve terminals of thick tufted L5 pyramidal cells the endogenous mobile Ca 2+ buffer is equivalent to less than 0.1 m m BAPTA and that at many release sites of pyramidal cell terminals the Ca 2+ channel domains overlap, a situation comparable with that at large calyx-type terminals in the brainstem.