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Long‐term potentiation of GABAergic synaptic transmission in neonatal rat hippocampus
Author(s) -
Caillard Olivier,
BenAri Yehezkel,
Gaiarsa JeanLuc
Publication year - 1999
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1999.0109r.x
Subject(s) - gabaa receptor , long term potentiation , postsynaptic potential , neurotransmission , neuroscience , depolarization , postsynaptic current , synaptic plasticity , gabaergic , chemistry , biophysics , inhibitory postsynaptic potential , biology , excitatory postsynaptic potential , receptor , biochemistry
1 The plasticity of GABAergic synapses was investigated in neonatal rat hippocampal slices obtained between postnatal days 3 and 6 using intracellular recording techniques. Ionotropic glutamate receptor antagonists were present throughout the experiments to isolate GABA A receptor‐mediated postsynaptic potentials (GABA A PSPs) or currents (GABA A PSCs). 2 Repetitive depolarizing pulses (20 pulses, 0·5 s duration, at 0·1 Hz, each pulse generating 4‐6 action potentials) induced a long‐term potentiation in the slope and amplitude of the evoked GABA A PSPs and GABA A PSCs. 3 Long‐term potentiation was prevented by intracellular injection of the calcium chelator BAPTA (50 mM), or when the voltage‐dependent calcium channels blockers Ni 2+ (50 μM) and nimodipine (10 μM) were bath applied. 4 Repetitive depolarizing pulses induced a persistent (over 1 h) increase in the frequency of spontaneous GABA A PSCs. 5 Repetitive depolarizing pulses induced a long‐lasting increase in the frequency of miniature GABA A PSCs, without altering their amplitude or decay‐time constant. 6 It is concluded that the postsynaptic activation of voltage‐dependent calcium channels leads to a long‐term potentiation of GABAergic synaptic transmission in neonatal rat hippocampus. This form of plasticity is expressed as an increase in the probability of GABA release or in the number of functional synapses, rather than as an upregulation of postsynaptic GABA A receptor numbers or conductance at functional synapses.