L-2-Amino�3-phosphonopropionic acid modulates the release of glutamate by blocking presynaptic group II mGlu receptors at neuromuscular junction in <em>Procambarus clarkii</em>

Abstract

The non-selective antagonist DL-AP3, L-2-Amino-3-phosphonopropionic acid, was used to regulate the response of the Group II metabotroic glutamate receptors (mGlurs) on the presynaptic terminal in the common North American crayfish, Procambarus clarkii. The experiment was conducted to better understand the negative feedback mechanism of the Group II mGlurs, thereby furthering current research concerning the adverse effects of amyotrophic lateral sclerosis (ALS) and other degenerative neurological diseases caused by neurotoxicity within the synaptic cleft. Our results confirmed the hypothesis that the addition of the antagonist DL-AP3 to an extracellular fluid containing high concentrations of glutamate precipitated a subsequent increase in the stimulated excitatory postsynaptic potential (EPSP). Likewise, the difference in the addition of DL-AP3 to an extracellular fluid containing a high concentration of glutamate when compared to an extracellular fluid containing a low concentration of glutamate without the addition of DL-AP3 was not statistically significant. The modulation of frequencies between 0.5 Hz and 10 Hz provided further evidence to support our hypothesis by demonstrating that the Group II mGlurs were responsive to increased activity of synaptic transmission.