GABBR1 and Alzheimer disease: The authors proposed that the orthodromic potentials invading the Ia terminal and generated by the facilitation of sodium spikes via GABA-A receptors near Ranvier nodes, could reduce neurotransmitter release long enough to decrease the amplitude of subsequent H-reflexes and that postsynaptic inhibition mediated by GABA on GABA-A and GABA-B receptors on motoneurons may account for long depression during the P-AD.