Ca2+
The cause of synaptic delay is attributed mainly to the time needed for the synaptic vesicles to release neurotransmitter into the synaptic cleft. While it can be considered a combination of binding to the presynaptic membrane (which is relatively a transient process) and subsequent exocytosis of the neurotransmitter, the main factor is release. Additionally, it does take a very short period of time for the neurotransmitter to diffuse across the synaptic cleft and bind to to its receptors on the post-synaptic membrane.
The ion needed to initiate the release of acetylcholine into the synaptic cleft is calcium (Ca2+). When an action potential reaches the presynaptic terminal, it causes voltage-gated calcium channels to open, allowing calcium to enter and trigger the release of acetylcholine-containing vesicles.
If there is leftover neurotransmitter in the synaptic gap, it can be taken back up into the presynaptic neuron through a process called reuptake or broken down by enzymes to clear the signal between neurons. This recycling process helps ensure that the signal is only transmitted when and where it is needed to prevent overstimulation of the postsynaptic neuron.
The molecule needed to initiate the process of glycolysis is glucose.
Firstly, we need the neurotransmitter at synaptic junctions to stimulate an action potential on the postsynaptic neurone. Continued amounts of neurotransmitter will keep Na+ diffusing in, and will keep the action potential resending when the period of refraction should be occurring.Therefore, if we do not destroy the neurotransmitter when it is not needed, a signal will keep being sent, and the effector muscle/gland will keep being stimulated.For example, touching a hot plate results may result in your bicep contracting to pull your arm away. If the neurotransmitter isn't destroyed, your bicep will keep contracting even after the event.
I believe varicosity in the context of your question refers to the enlarged and tortuous vein, artery, or lymphatic vessel in the area of the synapse. Therefore in the aplysia synaptic junctions between the sensory and motor neurons experience long term facilition in response to 5-HT and long term depression in response to RMRFamide. Research has shown macromolecules synthesis is needed for expression of the long lasting structural changes in the sensory cells and that this synthesis is porportional with long term functional modulation of sensorimotor synapses.
dopaime
Neurotransmitter binding are designed to be brief so that another one can be initiated if needed. Failure to break down neurotransmitters so that a signal is always activated can be disasterous to a biological organism. In fact, nerve gases, (e.g. sarin) work by inhibiting the enzyme cholinesterase, which breaks down acetylcholine in autonomic nerve synapses and neuromuscular junctions.
Radiant energy
It is possible that nothing is wrong with the first neuron and that the second neuron has been desensitized, or if it is the first neuron then vesicles are not fusing with the membrane and releasing neurotransmitters. This could be because a toxin has damaged the proteins that control vesicle integration, or because the calcium channels have been blocked, or in the lab setting the terminal may have run out of neurotransmitter.
true activation energy is the minimum amount of energy needed to start a chemical reaction
To initiate a chemical reaction an activation energy is necessary.