Regulation of ACh release at neuromuscular junction

An interesting question was raised a few days ago by a couple of you regarding the neuromuscular junction (NMJ).
Is there any mechanism that regulates the amount of ACh released at the NMJ?
One of the most important factors that determine the amount of ACh release at the NMJ is off course the ECF Ca++ concentration. A fall in ECF [Ca++] will decrease ACh release as the Ca++ influx that occurs during a presynaptic potential is dependent on the out-to-in gradient for Ca++.
Other than that, in many of the central neural synapses there are additional presynaptic mechanisms that influnce neurotransmitter release. Receptors for the very neurotransmitter released at a synapse are often present on the presynaptic membrane. Such receptors are refered to as autoreceptors. The nerutransmitter released during synaptic transmission, in addition to its primary action on the postsynaptic side, also binds to these presynaptic autoreceptors and brings about changes in the presynaptic mechanisms thus influencing further release of neurotransmitters. For instance, consider the synapses in the sympathetic nervous system. Nor-adrenaline is a neurotransmitter employed by sympathetic nerve endings and acts upon different types of nor-adrenergic post synaptic receptors. A particular type of adrenergic receptor, the alpha2 adrenergic receptor, is found on the presynaptic membrane of these nerve terminals. The nor-adrenaline released during sympathetic activation acts on these presynaptic autoreceptors to reduce further release nor-adrenaline. Thus this is an example for a feed back regulation of neurotransmitter release. In some cases such feedback regulation may increase neurotransmitter release rather than decrease it. Such mechanisms are believed to be important in maintaining the sensitivity of the post-synaptic emmbrane to neurotransmitters and regulating the efficiency of synaptic transmission.
Coming back to the NMJ, it was traditionally believed that such feedback regulation of neurtransmitter release does not occur at the NMJ. But recent studies suggest that the release of ACh at NMJs may also be influenced by a feedback effect of ACh on presynaptic autoreceptors which belong to the muscarinic class of cholinergic receptors.It remains to be seen how important such regulation is and whether it has clinical significance.