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Calcium‐calmodulin signalling pathway up‐regulates glutamatergic synaptic function in non‐pyramidal, fast spiking rat hippocampal CA1 neurons
Author(s) -
Wang JinHui,
Kelly Paul
Publication year - 2001
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.1469-7793.2001.0407a.x
Subject(s) - long term potentiation , postsynaptic potential , ampa receptor , excitatory postsynaptic potential , neurotransmission , chemistry , neuroscience , bapta , glutamatergic , synaptic plasticity , schaffer collateral , nmda receptor , biophysics , glutamate receptor , inhibitory postsynaptic potential , biology , extracellular , receptor , biochemistry
The role of Ca 2+ ‐calmodulin (CaM) signalling cascades in modulating glutamatergic synaptic transmission on CA1 non‐pyramidal fast‐spiking neurons was investigated using whole‐cell recording and perfusion in rat hippocampal slices. Paired stimuli (PS), consisting of postsynaptic depolarization to 0 mV and presynaptic stimulation at 1 Hz for 30 s, enhanced excitatory postsynaptic currents (EPSCs) on non‐pyramidal neurons in the stratum pyramidale (SP). The potentiation was reduced by the extracellular application of d ‐amino‐5‐phosphonovaleric acid (DAP‐5, 40 μ m ), and blocked by the postsynaptic perfusion of 1,2‐bis(2‐aminophenoxy)‐ethane‐ N,N,N′,N′ ‐tetraacetic acid (BAPTA, 10 m m ), a CaM‐binding peptide (100 μ m ) or CaMKII (281–301) (an autoinhibitory peptide of CaM‐dependent protein kinases, 100 μ m ). The application of adenophostin, an agonist of inositol trisphosphate receptors (IP 3 Rs) that evokes Ca 2+ release, into SP non‐pyramidal neurons via the patch pipette (1 μ m ) enhanced EPSCs and occluded PS‐induced synaptic potentiation. The co‐application of BAPTA (10 m m ) with adenophostin blocked synaptic potentiation. In addition, Ca 2+ ‐CaM (40:10 μ m ) induced synaptic potentiation, which occluded PS‐induced potentiation and was attenuated by introducing CaMKII (281–301) (100 μ m ). EPSCs were sensitive to an antagonist of α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazole propionic acid receptor (AMPAR). Application of Ca 2+ ‐CaM into SP non‐pyramidal neurons induced the emergence of AMPAR‐mediated EPSCs that were not evoked by low stimulus intensity before perfusion. Ca 2+ ‐CaM also increased the amplitude and frequency of spontaneous EPSCs. A scavenger of nitric oxide, carboxy‐PTIO (30 μ m in slice‐perfusion solution), did not affect these increases in sEPSCs. The magnitude of PS‐, adenophostin‐ or Ca 2+ ‐CaM‐induced synaptic potentiation in SP non‐pyramidal neurons increased during postnatal development. These results indicate that Ca 2+ ‐CaM signalling pathways in CA1 SP non‐pyramidal neurons up‐regulate glutamatergic synaptic transmission probably through the conversion of inactive‐to‐active synapses.