Abstract
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.
Published Version
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