Functional Assessment of Peripheral Cholinergic Neurotransmission in Rats with Fetal Valproate Syndrome

One of the most widespread experimental models for studying the development of autism spectrum disorders (ASDs) and methods of their therapy is the valproic acid-induced rodent model. Individuals born to females who received injections of valproic acid during pregnancy demonstrate a number of ASD-specific impairments. It was previously found that valproic acid affects neuromuscular transmission and, moreover, alters the expression of a set of genes during the development of neuromuscular junction. However, until recently it was unknown whether neuromuscular transmission changes in animals with fetal valproate syndrome and, if so, how? Using the “rotating rod” functional test, we found that in rats with a developed valproate syndrome, the coordination of movements did not differ from control animals. Using the methods of microelectrode electrophysiology, we analyzed (i) the amplitude-time parameters of single postsynaptic signals; (ii) the frequency of spontaneous release of acetylcholine quanta, (iii) the number of acetylcholine quanta released in response to the stimulus, (iv) the amplitude of evoked responses during rhythmic stimulation. We did not reveal any changes in the processes of acetylcholine release from the nerve ending and its reception on the muscle fiber membrane, both at rest and during nerve stimulation. Thus, it can be concluded that in rats with a developed fetal valproate syndrome, peripheral cholinergic neurotransmission does not undergo any functionally significant changes.