Recognition molecule associated carbohydrate inhibits postsynaptic GABA(B) receptors: a mechanism for homeostatic regulation of GABA release in perisomatic synapses

Mol Cell Neurosci. 2003 Oct;24(2):271-82. doi: 10.1016/s1044-7431(03)00163-5.


Extracellular matrix molecules are important cues in the shaping of nervous system structure and function. Here, we describe a novel mechanism by which the HNK-1 carbohydrate carried by recognition molecules regulates perisomatic inhibition in the hippocampus. Neutralization of HNK-1 activity by an HNK-1 antibody results in GABA(B) receptor-mediated activation of K(+) currents in CA1 pyramidal cells, which elevates extracellular K(+) concentration and reduces evoked GABA release in perisomatic inhibitory synapses. This mechanism is supported by pharmacological analysis in hippocampal slices and data showing that the HNK-1 carbohydrate binds to GABA(B) receptors and inhibits GABA(B) receptor-activated K(+) currents in a heterologous expression system. We suggest that the HNK-1 carbohydrate is involved in homeostatic regulation of GABA(A) receptor-mediated perisomatic inhibition by suppression of postsynaptic GABA(B) receptor activity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • CD57 Antigens / metabolism*
  • Cell Line
  • Hippocampus / metabolism
  • Homeostasis / physiology*
  • Humans
  • Mice
  • Mice, Inbred C57BL
  • Rats
  • Receptors, GABA-B / metabolism*
  • Synapses / drug effects*
  • Synapses / metabolism
  • gamma-Aminobutyric Acid / metabolism*


  • CD57 Antigens
  • Receptors, GABA-B
  • gamma-Aminobutyric Acid