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Associative mossy fibre LTP induced by pairing presynaptic stimulation with postsynaptic hyperpolarization of CA3 neurons in rat hippocampal slice
Author(s) -
Sokolov Maxim V.,
Rossokhin Alexej V.,
M. Kasyanov Alexander,
Gasparini Sonia,
Berretta Nicola,
Cherubini Enrico,
Voronin Leon L.
Publication year - 2003
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.2003.02563.x
Subject(s) - hyperpolarization (physics) , excitatory postsynaptic potential , neuroscience , postsynaptic potential , long term potentiation , chemistry , ltp induction , glutamate receptor , metabotropic glutamate receptor , membrane potential , post tetanic potentiation , inhibitory postsynaptic potential , biophysics , biology , receptor , biochemistry , organic chemistry , nuclear magnetic resonance spectroscopy
Whole cell recordings of excitatory postsynaptic potentials/currents (EPSPs/EPSCs) evoked by minimal stimulation of commissural–associative (CF) and mossy fibre (MF) inputs were performed in CA3 pyramidal neurons. Paired responses (at 50 ms intervals) were recorded before, during and after hyperpolarization of the postsynaptic membrane (20–30 mV for 15–35 min). Membrane hyperpolarization produced a supralinear increase of EPSPs/EPSCs amplitude in MF‐inputs. Synaptic responses remained potentiated for the rest of the recording period (up to 40 min) after resetting the membrane potential to control level (221 ± 60%, n = 15 and 219 ± 61%, n = 11 for MF‐EPSP and MF‐EPSC, respectively). We shall refer to this effect as hyperpolarization‐induced LTP (HI‐LTP). In the absence of afferent stimulation, membrane hyperpolarization was unable to produce HI‐LTP. In contrast to MF‐EPSPs, the mean amplitude of CF‐EPSPs did not increase significantly after hyperpolarization relative to controls (138 ± 29%, n = 22). HI‐LTP was associated with modifications of classical indices of presynaptic release: paired‐pulse facilitation, failures rate, coefficient of variation of EPSP amplitudes and quantal content. The induction of HI‐LTP was NMDA independent but was dependent on metabotropic glutamate receptors (mGluRs) activation and calcium release from inositol 1,4,5‐triphosphate (IP 3 )‐sensitive intracellular stores: it was prevented by mGluR antagonist, intracellular heparin and BAPTA. We conclude that while the induction of HI‐LTP was postsynaptic, its expression was presynaptic.