How can you measure neurotransmitter release from a presynaptic neuron by recording from a postsynaptic neuron
444030
Easy, by measuring from the postsynaptic neuron, you can see how many neurotransmitters were actually received.  Knowing the rate of neurotransmitter response, release can be determined.  Besides, its more practical to do it this way.  The derivative of the change in rise time is the slope.  In other words, the slope describes the rate at which the change in rise time occurs.  Finally, there are several factors which could contribute to both the change in rise time and the rate of change.  Namely, change in pH and introdution of various bacteria.
462432
The sympathetic nerves arise in the brain in the reticular formation, a diffuse set of nuclei (cell bodies in the brain or spinal cord) and send axons (bioelectrical transmission lines) the the lateral horn of the spinal cord.  The reticular formation receives incoming pain signals as well as higher input from the hypothalamus, cortex and elsewhere.  The axons descending to the lateral horn snynape (form chemical connections that communicate with the next neuron by chemicals known as neurotransmitters) with the cell bodies of motor neurons.  These motor neurons send myelinated (myelin is a biological insulator) axons to the ganglia (collections of cell bodies outside the brain and spinal cord) for the sympathetic nervous system.  These ganglia include a long chain that entends from the cervical to the lumbar regions, plus other ganglia in the head and adbominal cavity.  This synapse typically releases the neurotransmitter, acetylcholine, which acts on nicotinic type "N" receptors - nicotinic-ganglionic receptors.   Nicotinic "N' receptors are distinguished from nicotinic "M" receptors (the neuromuscular junction) that serve skeletal muscle by differing responsiveness to pharmacological agents.  The post-synaptic (cell that receives the chemical signal) neurons are not mylenated and project to the visceral organs, skin, and blood vessels where they release neurotransmitters (norepinephrine or, in the case of skin, acetylcholine) that act on the effector organs.
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Endorphin release in the brain.
459623
It is a neurotransmitter in the catecholamine family that mediates chemical communication in the sympathetic nervous system, a branch of the autonomic nervous system. Like other neurotransmitters, it is released at synaptic nerve endings to transmit the signal from a nerve cell to other cells. Norepinephrine is almost identical in structure to epinephrine, which is released into the bloodstream from the adrenal medulla under sympathetic activation. The sympathetic nervous system functions in response to short-term stress; hence norepinephrine and epinephrine increase the heart rate as well as blood pressure. Other actions of norepinephrine include increased glycogenolysis (the conversion of glycogen to glucose) in the liver, increased lipolysis (the conversion of fats to fatty acids; in adipose (fat) tissue, and relaxation of bronchial smooth muscle to open up the air passages to the lungs. All of these actions represent a mobilization of the body's resources in order to meet the stressful challenge–such a response is often termed the "flight or fight" syndrome.
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released from muscle stores as a form of energy
42599
There are many, many neurotransmitters, and I doubt that we've managed to identify them all.\n\nThe primary excitatory NT is glutamate, and the primary inhibitory NT is GABA (gamma-aminobutyric acid).  Other prominent and important NTs include acetylcholine, serotonin, dopamine,  and norepinephrine.\n\nIf you're mining for a research paper, that should help you get started.  Beyond that, I'm afraid your question doesn't make much sense.
237583
for skeletal muscle - nerve impulse depolarises muscle cell surface, calcium released, ATP driven actin-myosin contraction cycle.
696929
Neuronal activity is very complex, while influx of one molecule into the hilloc causes its depolarisation in one neuron it leads to hyperpolarisation in another.  With sufficient depolarisation and build up of Excitation K+ and Na+ activity beggins.  for every 2K+ brought into the cell 3Na+ are emitted from the cell.  This causes a cascade down the cell due to comple intracellular events of the depolarization being propagated down the axon.  This is electrical activity and so can be detected with electrodes.  There are many different types of proteins some of which are voltage sensitive along the length of the axon.  The local change in voltage activates these other channels leading to further depolarization and propogation moving along on.  This allows the depolarization to effectivley jump from one node of ranvier to the next (none insulated parts of neuron).  Talking of insulation, the mylin sheeth is made of schwan cells which promots signal propogation much like plastic covering copper.\n\nThe internal signals are very complex and would require a diagram, but involve Gproteins and Ca++.......
459299
Patch clamp experiments measure flux through an ion channel. A tiny piece of cell membrane containing the channels of interest is held in a solution at the tip of a pipet connected to a probe that meaures the concentration of ions in the pipet compared to the solution. You can look at how drugs and volatge and things like that affect the opening of ion channels.
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label the known protein with a radioactive isotope, or better yet, maybe you could label the protein with a flourescent dye (dont know how, its beyond my expertise) and where ever the protein binds on the receptive cell may be what you're looking for.  but i dont know of any assays per se for it.
408755
They are neurotransmitter inhibitors.
197575
Endocrine refers to all hormones, not just those of the pancreas.  They are made in one cell and released into the blood stream where they work on distant cells.\n\nNeurological transmissions are predominately electrical.  The neuron gets depolarized and sends an electric signal down its axon (long process of the cell) to where it will be going to  (a muscle for example).  When the electric signal reaches its destination (the end of the axon) it causes a release of a neurotransmitter from the axon (each axon only releases one type of neurotransmitter).  These transmitters diffuse to where they are going (a muscle for example) and cause a change in that cell.\n\nSome similarities are that both hormones and neurotransmitters have specific receptors for them and they both cause changes in the cells that they interact with.  Also, there are some neurotransmitters that are hormones, they are released from the end of the axon into the bloodstream and then go to distant cells to do their work.
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http://www.medtronic.com/neuro/ttp/ps_jerry.html\ntry this, it tells all about it.
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The placement of nerve endings, and stimulation of nerve endings
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There are a number of theories, but the short answer is "nobody knows".  Could be establishment of new synapses, could be changes in receptor sensitivity, could even be new neurons stimulated to develop, but at this point, we dont have any real idea.
209382
Both:\n\nNeurotransmitters bond to activation sites to stimulate gates to open to pass on a signal along a signal transdunction line. Then the neurotransmitters break apart and inhibit the signal from going past the synapse. However, they are mainly stimulatory, since the only way they inhibit a signal is by breaking apart. So i guess i would actually say they stimulate gates to open
135532
You can either look it up or determine it experimentally.\nI cant get much more specific without additional details.