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  • Title: Dendritic Ca2+ accumulations and metabotropic glutamate receptor activation associated with an N-methyl-D-aspartate receptor-independent long-term potentiation in hippocampal CA1 neurons.
    Author: Petrozzino JJ, Connor JA.
    Journal: Hippocampus; 1994 Oct; 4(5):546-58. PubMed ID: 7889125.
    Abstract:
    Bathing hippocampal slices in the potassium channel blocker tetraethylammonium (TEA), while stimulating the Schaffer collaterals at a low frequency, induces Ca(2+)-dependent, N-methyl-D-aspartate (NMDA) receptor-independent long-term potentiation of synaptic transmission (LTPk) in CA1 neurons. We have combined ratio imaging of fura-2 and mag-fura-5 in hippocampal CA1 neurons with intracellular and field recordings to evaluate postsynaptic Ca2+ changes that occur in the induction of LTPk. Test stimuli were applied at 0.05 Hz to stratum radiatum in the presence of the NMDA receptor antagonists D,L-2-amino-5-phosphonovaleric acid (100 microM) or MK-801 (10 microM). During TEA exposure (15-25 mM; 10 min), cells fired prolonged action potentials both spontaneously and in response to test stimuli resulting in transient, micromolar Ca2+ accumulations in both somata and dendrites. The initial EPSP slope, measured 60 min after TEA wash-out, was potentiated to approximately 200% of control. The Ca2+ channel blocker nimodipine (10 microM) greatly reduced Ca2+ transients in both magnitude and duration and prevented LTPk induction. Pretreatment of slices with compounds that block metabotropic glutamate receptor (mGluR)-stimulated phosphoinositide hydrolysis, L-2-amino-3-phosphonopropionic acid (L-AP3, 50-200 microM) or L-aspartate-beta-hydroxamate (50-100 microM), as well as protein kinase C (PKC) inhibitors (sphingosine, 20 microM; RO-31-8220, 0.2 microM; or calphostin C, 2 microM) also blocked LTPk. Ca2+ transients were unaffected by L-AP3 or RO-31-8220. These findings suggest that Ca2+ influx through voltage-gated channels and co-activation of PKC by mGluRs are both necessary for induction of LTPk. Activation of mGluRs must also occur in NMDA receptor-dependent induction paradigms, but is possibly of lesser importance owing to the much greater gating of Ca2+ directly into the dendritic spines.
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