QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

This Article Full Text Full Text (PDF) Submit an eLetter Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (76) Citing Articles via Google Scholar Google Scholar Articles by Nakamura, T. Articles by Ross, W. N. Search for Related Content PubMed PubMed Citation Articles by Nakamura, T. Articles by Ross, W. N. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB CAFFEINE CALCIUM COMPOUNDS CALCIUM, ELEMENTAL CYCLOLEUCINE

 Previous Article  |  Next Article 

The Journal of Neuroscience, November 15, 2000, 20(22):8365-8376

Inositol 1,4,5-Trisphosphate (IP₃)-Mediated Ca²⁺ Release Evoked by Metabotropic Agonists and Backpropagating Action Potentials in Hippocampal CA1 Pyramidal Neurons

Takeshi Nakamura, Kyoko Nakamura, Nechama Lasser-Ross, Jean-Gaël Barbara, Vladislav M. Sandler, and William N. Ross

Department of Physiology, New York Medical College, Valhalla, New York 10595

We examined the properties of [Ca²⁺]_i changes that were evoked by backpropagating action potentials in pyramidal neurons in hippocampal slices from the rat. In the presence of the metabotropic glutamate receptor (mGluR) agonists t-ACPD, DHPG, or CHPG, spikes caused Ca²⁺ waves that initiated in the proximal apical dendrites and spread over this region and in the soma. Consistent with previously described synaptic responses (Nakamura et al., 1999a), pharmacological experiments established that the waves were attributable to Ca²⁺ release from internal stores mediated by the synergistic effect of receptor-mobilized inositol 1,4,5-trisphosphate (IP₃) and spike-evoked Ca²⁺. The amplitude of the changes reached several micromoles per liter when detected with the low-affinity indicators fura-6F, fura-2-FF, or furaptra. Repetitive brief spike trains at 30-60 sec intervals generated increases of constant amplitude. However, trains at intervals of 10-20 sec evoked smaller increases, suggesting that the stores take 20-30 sec to refill. Release evoked by mGluR agonists was blocked by MCPG, AIDA, 4-CPG, MPEP, and LY367385, a profile consistent with the primacy of group I receptors. At threshold agonist concentrations the release was evoked only in the dendrites; threshold antagonist concentrations were effective only in the soma. Carbachol and 5-HT evoked release with the same spatial distribution as t-ACPD, suggesting that the distribution of neurotransmitter receptors was not responsible for the restricted range of regenerative release. Intracellular BAPTA and EGTA were approximately equally effective in blocking release. Extracellular Cd²⁺ blocked release, but no single selective Ca²⁺ channel blocker prevented release. These results suggest that IP₃ receptors are not associated closely with specific Ca²⁺ channels and are not close to each other.

Key words: pyramidal neuron; dendrite; IP₃ receptor; metabotropic receptor; BAPTA; EGTA; carbachol; bis-fura-2; furaptra; endoplasmic reticulum

---

Copyright © 2000 Society for Neuroscience  0270-6474/00/20228365-12$05.00/0

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help