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

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

The Journal of Neuroscience, August 6, 2008, 28(32):7945-7953; doi:10.1523/JNEUROSCI.2165-08.2008

This Article Full Text Full Text (PDF) Supplemental Data 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 Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Lee, J. S. Articles by Lee, S.-H. Search for Related Content PubMed PubMed Citation Articles by Lee, J. S. Articles by Lee, S.-H. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB CALCIUM COMPOUNDS CALCIUM, ELEMENTAL SODIUM

 Previous Article  |  Next Article 

Cellular/Molecular
Presynaptic Release Probability and Readily Releasable Pool Size Are Regulated by Two Independent Mechanisms during Posttetanic Potentiation at the Calyx of Held Synapse

Jae Sung Lee, Myoung-Hwan Kim, Won-Kyung Ho, and Suk-Ho Lee

National Research Laboratory for Cell Physiology, Department of Physiology, Seoul National University College of Medicine and Neuroscience Research Institute, Seoul National University Medical Research Center, Seoul 110-799, Korea

Correspondence should be addressed to Dr. Suk-Ho Lee, Department of Physiology, Seoul National University College of Medicine, Chongno-Ku, Yongon-Dong 28, Seoul 110-799, Korea. Email: leesukho{at}snu.ac.kr

At the immature calyx of Held, the fast decay phase of a Ca²⁺ transient induced by tetanic stimulation (TS) was followed by a period of elevated [Ca²⁺]_i for tens of seconds, referred to as posttetanic residual calcium (Ca_res). We investigated the source of Ca_res and its contribution to posttetanic potentiation (PTP). After TS (100 Hz for 4 s), posttetanic Ca_res at the calyx of Held was largely abolished by tetraphenylphosphonium (TPP⁺) or Ru360, which inhibit mitochondrial Na⁺-dependent Ca²⁺ efflux and Ca²⁺ uniporter, respectively. Whereas the control PTP lasted longer than Ca_res, inhibition of Ca_res by TPP⁺ resulted in preferential suppression of the early phase of PTP, the decay time course of which well matched with that of Ca_res. TS induced significant increases in release probability (P_r) and the size of the readily releasable pool (RRP), which were estimated from plots of cumulative EPSC amplitudes. TPP⁺ or Ru360 suppressed the posttetanic increase in P_r, whereas it had little effect on the increase in RRP size. Moreover, the posttetanic increase in P_r, but not in RRP size, showed a linear correlation with the amount of Ca_res. In contrast, myosin light chain kinase (MLCK) inhibitors and blebbistatin reduced the posttetanic increase in RRP size with no effect on the increase in P_r. Application of TPP⁺ in the presence of MLCK inhibitor peptide caused further suppression of PTP. These findings suggest that Ca_res released from mitochondria and activation of MLCK are primarily responsible for the increase in P_r and that in the RRP size, respectively.

Key words: posttetanic potentiation; residual calcium; mitochondria; myosin light chain kinase; readily releasable pool; calyx of Held

---

Received June 24, 2008; revised June 5, 2008; accepted June 13, 2008.

Correspondence should be addressed to Dr. Suk-Ho Lee, Department of Physiology, Seoul National University College of Medicine, Chongno-Ku, Yongon-Dong 28, Seoul 110-799, Korea. Email: leesukho{at}snu.ac.kr

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help