| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1 Center for Neural Science, New York University, New York, New York 10003; 2 Department of Biology, New York University, New York, New York 10003
Submitted 17 April 2003; accepted in final form 15 May 2003
Inhibitory transmission is critically involved in the functional maturation of neural circuits within the brain. However, the mechanisms involved in its plasticity and development remain poorly understood. At an inhibitory synapse of the developing auditory brain stem, we used whole cell recordings to determine the site of induction and expression of long-term depression (LTD), a robust activity-dependent phenomenon that decreases inhibitory synaptic gain and is postulated to underlie synapse elimination. Recordings were obtained from lateral superior olivary (LSO) neurons, and hyperpolarizing inhibitory potentials were evoked by stimulation of the medial nucleus of the trapezoid body (MNTB). Both postsynaptic glycine and GABAA receptors could independently display LTD when isolated pharmacologically. Focal application of GABA, but not glycine, on the postsynaptic LSO neuron was sufficient to induce depression of the amino acid–evoked response, or MNTB-evoked inhibitory postsynaptic potentials. This GABA-mediated depression, in the absence of MNTB stimulation, was blocked by a GABAB receptor antagonist. To assess whether a change in neurotransmitter release is associated with the LTD, the polyvalent cation, ruthenium red, was used to increase the frequency of miniature inhibitory synaptic events. Consistent with a postsynaptic locus of expression, we found that the mean amplitude of miniature events decreased after LTD with no change in their frequency of occurrence. Furthermore, there was no change in the paired-pulse ratio or release kinetics of evoked inhibitory responses. Together, these results provide direct evidence that activity-dependent LTD of inhibition has a postsynaptic locus of induction and alteration, and that GABA but not glycine plays a pivotal role.
This article has been cited by other articles:
|
|
 |
|
  Y. Ben-Ari, J.-L. Gaiarsa, R. Tyzio, and R. Khazipov GABA: A Pioneer Transmitter That Excites Immature Neurons and Generates Primitive Oscillations Physiol Rev, October 1, 2007; 87(4): 1215 - 1284. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. A. Howard, R. M. Burger, and E. W Rubel A Developmental Switch to GABAergic Inhibition Dependent on Increases in Kv1-Type K+ Currents J. Neurosci., February 21, 2007; 27(8): 2112 - 2123. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. L. Pallas, P. Wenner, C. Gonzalez-Islas, M. Fagiolini, K. A. Razak, G. Kim, D. Sanes, and B. Roerig Developmental Plasticity of Inhibitory Circuitry J. Neurosci., October 11, 2006; 26(41): 10358 - 10361. [Full Text] [PDF]
|
|
|
|
 |
|
 A. H. Seidl and B. Grothe Development of Sound Localization Mechanisms in the Mongolian Gerbil Is Shaped by Early Acoustic Experience J Neurophysiol, August 1, 2005; 94(2): 1028 - 1036. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C.-Y. Chen and A. C. Bonham Glutamate suppresses GABA release via presynaptic metabotropic glutamate receptors at baroreceptor neurones in rats J. Physiol., January 15, 2005; 562(2): 535 - 551. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
