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Modulation of the glycine response by Ca²⁺-permeable AMPA receptors in rat spinal neurones

Tian-Le Xu * ¹, Ji-Shuo Li ¹, Young-Ho Jin * and Norio Akaike *

In acutely isolated rat sacral dorsal commisural nucleus (SDCN) neurones, application of kainate (KA) reversibly potentiated glycine-evoked Cl^- currents (I_Gly) in a concentration-dependent manner.

The cellular events underlying the interaction between non-NMDA receptors and glycine receptors were studied by using nystatin-perforated patch and cell-attached single-channel recording modes.

The action of KA was not accompanied by a shift in the reversal potential for I_Gly. In dose-response curves, KA potentiated I_Gly without significantly changing glycine binding affinity.

GYKI 52466 blocked while NS-102 had no effect on the KA-induced potentiation of I_Gly.

The potentiation was reduced when KA was applied in a Ca²⁺-free extracellular solution or in the presence of BAPTA AM, and was independent of the activation of voltage-dependent Ca²⁺ channels.

Pretreatment with KN-62, a selective Ca²⁺-calmodulin-dependent protein kinase II (CaMKII) inhibitor, abolished the action of KA. Inhibition of calcineurin converted the KA-induced potentiation to a sustained one.

Single-channel recordings revealed that KA decreased the mean closing time of glycine-gated single-channel activity, resulting in an increase in the probability of channel opening.

It is proposed that Ca²⁺ entry through AMPA receptors modulates the glycine receptor function via coactivation of CaMKII and calcineurin in SDCN neurones. This interaction may provide a new postsynaptic mechanism for control of inhibitory synaptic signalling and represent one of the important regulatory mechanisms of spinal nociception.

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