GABAA and strychnine-sensitive glycine receptors modulate N-methyl-d-aspartate-evoked acetylcholine release from rat spinal motoneurons: A possible role in neuroprotection

It is concluded that glutamate acts on the NMDA receptors situated on spinal motoneurons to evoke ACh release, which can be inhibited through the activation of GABAA and glycine receptors present on the same neurons. These data suggest that glutamatergic overload of receptors located onto spinal cord motoneurons might be decreased by activating GABAA and glycine receptors.