Ketamine reduces synaptic transmission and DF2 enhances recovery from ketamine-induced synaptic depression at crayfish neuromuscular junctions

Abstract

Ketamine is a chemical that blocks N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-isoxazole propionic acid (AMPA) receptors and reduces excitatory postsynaptic potential (EPSP) amplitude. Due to this capability, ketamine is commonly used as an anesthetic; however, recent studies are showing its potential use as an antidepressant. DF2, an FMRFamide-related neuropeptide, creates a long-lasting enhancement of EPSPs, which may be able to counter the effects of ketamine. To see if DF2 enhances recovery from ketamine-induced EPSP depression, we induced EPSPs in crayfish tail extensor muscles. We stimulated the muscle in a normal physiological saline solution (Ringer’s solution), a ketamine solution, a Ringer’s solution with DF2 added, and finally, a ketamine solution with DF2 added. Our results show that ketamine reduced EPSP amplitude, and DF2 was not able to successfully recover the EPSP back to normal ranges after ketamine. Thus, although ketamine can decrease EPSP, DF2 was able to minimize ketamine’s effects.