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

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

The Journal of Neuroscience, July 16, 2008, 28(29):7359-7369; doi:10.1523/JNEUROSCI.5618-07.2008

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 ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Keck, T. Articles by White, J. A. PubMed PubMed Citation Articles by Keck, T. Articles by White, J. A. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB GLYCINE STRYCHNINE

 Previous Article  |  Next Article 

Cellular/Molecular
Frequency-Dependent Glycinergic Inhibition Modulates Plasticity in Hippocampus

Tara Keck, Kyle P. Lillis, Yu-Dong Zhou, and John A. White

Department of Biomedical Engineering, Center for BioDynamics, Center for Memory and Brain, Boston University, Boston, Massachusetts 02215

Correspondence should be addressed to either of the following at their present address: Dr. Tara Keck, Department of Cellular and Systems Neurobiology, Max Planck Institute of Neurobiology, Am Klopferspitz 18, D-82152 Martinsried, Germany, Email: keck{at}neuro.mpg.de; or Dr. John A. White, Department of Bioengineering, University of Utah, 20 South 2030 East, 108 BPRB, Salt Lake City, UT 84112, Email: john.white{at}utah.edu

Previous studies have demonstrated the presence of functional glycine receptors (GlyRs) in hippocampus. In this work, we examine the baseline activity and activity-dependent modulation of GlyRs in region CA1. We find that strychnine-sensitive GlyRs are open in the resting CA1 pyramidal cell, creating a state of tonic inhibition that "shunts" the magnitude of EPSPs evoked by electrical stimulation of the Schaffer collateral inputs. This GlyR-mediated shunting conductance is independent of the presynaptic stimulation rate; however, pairs of presynaptic and postsynaptic action potentials, repeated at frequencies above 5 Hz, reduce the GlyR-mediated conductance and increase peak EPSP magnitudes to levels at least 20% larger than those seen with presynaptic stimulation alone. We refer to this phenomenon as rate-dependent efficacy (RDE). Exogenous GlyR agonists (glycine, taurine) block RDE by preventing the closure of postsynaptic GlyRs. The GlyR antagonist strychnine blocks postsynaptic GlyRs under all conditions, occluding RDE. During RDE, GlyRs are less responsive to local glycine application, suggesting that a reduction in the number or sensitivity of membrane-inserted GlyRs underlies RDE. By extending the RDE induction protocol to include 500 paired presynaptic and postsynaptic spikes, we can induce long-term synaptic depression (LTD). Manipulations that lead to reduced functionality of GlyRs, either pharmacologically or through RDE, also lead to increased LTD. This result suggests that RDE contributes to long-term synaptic plasticity in the hippocampus.

Key words: glycine; long-term depression; CA1; hippocampus; frequency; patch clamp

---

Received Sept. 27, 2006; revised April 10, 2008; accepted May 27, 2008.

Correspondence should be addressed to either of the following at their present address: Dr. Tara Keck, Department of Cellular and Systems Neurobiology, Max Planck Institute of Neurobiology, Am Klopferspitz 18, D-82152 Martinsried, Germany, Email: keck{at}neuro.mpg.de; or Dr. John A. White, Department of Bioengineering, University of Utah, 20 South 2030 East, 108 BPRB, Salt Lake City, UT 84112, Email: john.white{at}utah.edu

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help