THE EFFECTS OF DEVELOPMENTAL NICOTINE EXPOSURE ON MUSCLE FATIGABILITY IN NEONATAL RATS

Abstract

This study aimed to explore the effects of developmental nicotine exposure (DNE) on the fatigability of the diaphragm in neonatal rats ages postnatal day 0-14. We hypothesized that chronic perinatal nicotine exposure would desensitize or functionally alter nicotinic acetylcholine receptors (nAChRs) at the neuromuscular junction. Muscle fatigue can be defined as the point where the muscle, in this case the diaphragm, is no longer able to produce a target force. Muscles were fatigued either through direct stimulation of the muscle or through electrical transmission through the phrenic nerve. Fatigue was quantified as the percent change in force outputs after five minutes of intermittent stimulation (330 ms trains, 0.5 trains/sec, 40 Hz, 0.2 ms pulse width). Neuromuscular transmission failure, wherein transmission across the neuromuscular junction falters, was also measured by stimulation of the phrenic nerve, as above, but with superimposed direct muscle stimulation every two seconds9. The results showed that there was no significant difference in muscle fatigability or the integrity of the neuromuscular junction between control and DNE animals. These results may be explained by the high safety factor present at the neuromuscular junction.