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Removal of extracellular calcium after conditioning stimulation disrupts long-term potentiation in the CA1 region of rat hippocampal slices
| Content Provider | Semantic Scholar |
|---|---|
| Author | Katsuki, Hirohiko Izumi, Yukitoshi Zorumski, Charles F. |
| Copyright Year | 1997 |
| Abstract | During a conditioning stimulus, the influx of Ca2+ into neurons appears to be crucial for the induction of long-term potentiation at CA1 hippocampal synapses. We report here that extracellular Ca2+ is also required for full production of long-term potentiation during a critical period following the conditioning stimulus. In control slices, removal of extracellular Ca2+ (0 mM Ca2+/10 mM Mg2+) for 15 min eliminated synaptic transmission. Following reintroduction of normal extracellular solution, synaptic responses recovered fully within 15 min. However, removal of extracellular Ca2+ 15-30 min after theta burst stimulation significantly decreased the magnitude of long-term potentiation. A time window seems to exist for this effect, since either earlier or later Ca2+ removal was less effective. The effect of the 0 mM Ca2+/10 mM Mg2+ solution was observed in the absence of afferent stimulation, suggesting that evoked synaptic activity is not required. Perfusion with an extracellular solution containing Cd2+ (40 microM), a broad spectrum inhibitor of voltage-dependent Ca2+ channels, or a low concentration (50 microM) of Ni2+, which preferentially blocks T-type, low-voltage-activated Ca2+ channels, also caused a significant decrease in potentiation, whereas an inhibitor of L-type, high voltage-activated Ca2+ channel, nifedipine (20 microM), had no effect. These results suggest that the presence of extracellular Ca2+ during a specific period after high-frequency synaptic activity is necessary for the maintenance of long-term potentiation, and that voltage-gated Ca2+ channels play a role in the stabilization of synaptic plasticity. |
| Starting Page | 1113 |
| Ending Page | 1119 |
| Page Count | 7 |
| File Format | PDF HTM / HTML |
| DOI | 10.1016/S0306-4522(97)80003-6 |
| PubMed reference number | 9027871 |
| Journal | Medline |
| Volume Number | 76 |
| Alternate Webpage(s) | https://api.elsevier.com/content/article/pii/S0306452297800036 |
| Alternate Webpage(s) | https://www.sciencedirect.com/science/article/pii/S0306452297800036?dgcid=api_sd_search-api-endpoint |
| Alternate Webpage(s) | https://doi.org/10.1016/S0306-4522%2897%2980003-6 |
| Journal | Neuroscience |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
