Synaptic fatigue

[1] It is caused by a temporary depletion of synaptic vesicles that house neurotransmitters in the synapse, generally produced by persistent high frequency neuronal stimulation.

[citation needed] It has previously been shown that repeated short trains of action potentials causes an exponential decay of the synaptic response amplitudes in the neurons of many neural networks, specifically the caudal pontine reticular nucleus (PnC).

[5] It is important that the recycling of neurotransmitters take place at an effective and efficient rate in order to prevent synaptic fatigue from negatively affecting signal transmission.

[citation needed] Maintaining a readily releasable vesicle pool is important in allowing for the constant ability to pass physiological signals between neurons.

The timing it takes for neurotransmitter to be released into the synaptic cleft and then be recycled back to the presynaptic cell to be reused is not currently well understood.

[5] The existence and observations of synaptic fatigue are accepted universally, although the exact mechanisms underlying the phenomenon are not completely understood.

Perforant path–granule cells (PP-GC) in the dentate gyrus of the hippocampus in adult rats have been shown to experience fatigue at lower frequencies (0.05-0.2 Hz).

The second form of plasticity disappears with maturation of PP-GCs, although the reversible low frequency depression remains unchanged.

The results showed that fatigue was more significantly pronounced in the APP/PS1 mice, which indicates a decrease in the amount of readily releasable pools of vesicles in the presynaptic neuron.

The short-term effects are explained by a hypothesis that states that depression is acutely brought on by an immediate decrease in catecholamines in the brain.

Under stressed conditions, vesicle exocytosis is potentiated and a release of catecholamines causes depression of presynaptic cells because of depleted neurotransmitters.