Kinetics of neurotransmitter release in neuromuscular synapses of newborn and adult rats
Language English Country United States Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
24412779
DOI
10.1016/j.ijdevneu.2013.12.010
PII: S0736-5748(14)00003-3
Knihovny.cz E-resources
- Keywords
- Developing neuromuscular junction, Kinetics of quantum release, Ryanodine receptors, Synaptic latency,
- MeSH
- Bungarotoxins pharmacokinetics MeSH
- Electric Stimulation MeSH
- Rats MeSH
- Gallic Acid analogs & derivatives pharmacokinetics MeSH
- Neuromuscular Junction drug effects growth & development metabolism MeSH
- Neurotransmitter Agents metabolism MeSH
- Receptors, Nicotinic metabolism MeSH
- Animals, Newborn MeSH
- Reaction Time physiology MeSH
- Ryanodine pharmacokinetics MeSH
- Synaptic Potentials physiology MeSH
- Synaptophysin metabolism MeSH
- Age Factors MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate MeSH Browser
- Bungarotoxins MeSH
- Gallic Acid MeSH
- Neurotransmitter Agents MeSH
- Receptors, Nicotinic MeSH
- Ryanodine MeSH
- Synaptophysin MeSH
The kinetics of the phasic synchronous and delayed asynchronous release of acetylcholine quanta was studied at the neuromuscular junctions of aging rats from infant to mature animals at various frequencies of rhythmic stimulation of the motor nerve. We found that in infants 6 (P6) and 10 (P10) days after birth a strongly asynchronous phase of quantal release was observed, along with a reduced number of quanta compared to the synapses of adults. The rise time and decay of uni-quantal end-plate currents were significantly longer in infant synapses. The presynaptic immunostaining revealed that the area of the synapses in infants was significantly (up to six times) smaller than in mature junctions. The intensity of delayed asynchronous release in infants increased with the frequency of stimulation more than in adults. A blockade of the ryanodine receptors, which can contribute to the formation of delayed asynchronous release, had no effect on the kinetics of delayed secretion in the infants unlike synapses of adults. Therefore, high degree of asynchrony of quantal release in infants is not associated with the activity of ryanodine receptors and with the liberation of calcium ions from intracellular calcium stores.
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