An influx of calcium at the presynaptic terminal is absolutely required to activate fusion of vesicles with the membrane, and therefore release of their contents into the presynaptic cleft. Given that the specific deficit in these mutants is at the final stage of fusion, we know that the action potential propagated (so it's likely not sodium or potassium) and the presynaptic membrane is not responding to the voltage change to permit an influx of calcium. Therefore, voltage-gated calcium channels are the likely cause of this deficit. 

Neurotransmitters are found in the synaptic cleft; hormones travel through the bloodstream. Endocrine signaling is much slower than synaptic signaling, but hormone receptors have a much higher affinity for their ligand, than neurotransmitter receptors do. The highest speed of nerve cell electrical impulses is somewhere around . Neurotransmitters are localized around the synaptic cleft; hormones are dispersed in the blood.

The absolute refractory period during depolarization is the period in which it is impossible for another depolarization to occur.  The reason that another depolarization can not occur is that the voltage-gated sodium channels are inactivated.  This renders them unable to function, and also unable to receive any signal to activate again.  If the channels were closed rather than inactivated, they could still receive electrical input to open again.

After acetylcholine is excised from the presynaptic neuron to act on its receptors in the postsynaptic neuron, it is removed from the synaptic space by the enzyme, acetylcholinesterase.  Acetylcholinesterase breaks it down into acetate and choline which can then be removed.

Gap junctions serve as connections between cells for communication.  Molecules that are polar and small enough to fit through gap junctions will be able to move between the communicating cells.  Ions, sugars, amino acids, and nucleotides are all small enough to move through.  However, proteins will generally be too large to fit through the small (roughly 20 angstroms wide) gap junctions.

Chromaffin cells are located in the adrenal gland, and release epinephrine and norepinephrin.

Of the options given, only norepinephrine is synthesized in storage vesicles. The rest are synthesized in cytoplasm. 

Tyrosine hydroxylase is the rate-limiting enzyme for all catecholamine synthesis reactions. L-aromatic amino acid decarboxylase is needed to catalyze the step from DOPA to dopamine. Norepinephrine synthesis requires dopamine beta-hydroxylase and epinephrine synthesis requires dopamine beta-hydroxylase and phenylethanolamine N-methyltransferase (PNMT) in addition to the other enzymes mentioned.

Parkinson disease is associated with decreased dopamine concentration. It is commonly treated with L-DOPA, which can cross the blood brain barrier and be converted to dopamine.

Tryptophan is the original substrate for serotonin synthesis. All other answers are involved in the catecholamine synthesis pathway.