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Developmental Shift From Long‐term Depression to Long‐term Potentiation at the Mossy Fibre Synapses in the Rat Hippocampus
Author(s) -
Battistin Tiziana,
Cherubini Enrico
Publication year - 1994
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 - 10.1111/j.1460-9568.1994.tb00567.x
Subject(s) - long term potentiation , cnqx , excitatory postsynaptic potential , neuroscience , nmda receptor , long term depression , postsynaptic potential , neural facilitation , hippocampus , neurotransmission , synapse , chemistry , synaptic fatigue , ltp induction , ampa receptor , synaptic plasticity , biology , receptor , inhibitory postsynaptic potential , biochemistry
During development, in the CA1 hippocampal region, long‐term potentiation (LTP) starts appearing at postnatal (P) day 7 and reaches its maximal expression towards the end of the second postnatal week. However, LTP is often preceded by long‐term depression (LTD), an activity‐dependent and long‐lasting reduction of synaptic strength. LTD can be induced by sustained, low‐frequency stimulation of the afferent pathway and is dependent on activation of N ‐methyl‐D‐aspartate (NMDA) receptors. We report here that, in the CA3 hippocampal region, during a critical period of postnatal development, between P6 and P14, a high‐frequency stimulation train (100 Hz, 1 s) to the mossy fibres in the presence of the NMDA receptor antagonist (+)‐3‐(2‐carboxy‐piperazin‐4‐yl)‐propyl‐1‐phosphonic acid (CPP; 20 μM) induced LTD. The depression of the amplitude of the field excitatory postsynaptic potential (EPSP) was 28 ± 7% ( n = 21). This form of LTD was NMDA‐independent and synapse‐specific. When a tetanus was applied in the presence of CPP and 6‐cyano‐7‐nitroquinoxaline‐2, 3‐dione (CNQX; 50 μM), which blocked the field EPSP, it failed to induce LTD upon washout of CNQX. LTD was probably postsynaptic in origin since it did not affect paired‐pulse facilitation. A rise in extracellular calcium concentration (from 2 to 4 mM) produced LTP instead of LTD. At the end of the second postnatal week, the same high‐frequency stimulation train to the mossy fibres induced LTP as in adult neurons. Functional changes in synaptic connections during development may control membrane depolarization and the amount of intracellular calcium necessary to trigger either LTD or LTP.

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