Actually when you get to the more complex ion channels such as the NMDA ion channel you end up with multiple effects from multiple neurotransmitters. For instance NMDA is a voltage gated Ampa receptor that is locked open when a second Neurotransmitter is detected to allow the Long-Term Potentiation that makes certain CA3 neurons more effective at holding trains of signals.

You might want to look at Kandel's work on the NMDA ion channel to see how all this works, but if I misremember correctly, the ion channel has a bi-directional aspect where it pumps K ions out, and Ca Ions in at the same time. As a result of pumping K ions out, they tend to build up just outside the ion channel, and when it goes quiescent, block the Ca input. (Or was that Magnesium that blocked it, yep definitley a teflon memory) In order to blow all these ions out of the way, the voltage in the cell has to increase to a certain state, at which point the blocking ions are repelled, and the pore opens.

If I misremember correctly, the Ampa portion of the ion channel keeps the channel open, by using Ampa as a sort of repulsion gate keeping the blocking ions from concentrating in the pore. The other neurotransmitter that I currently do not remember the name of, modulates the Ca ion intake and the K ion output.

By both taking Ca in, and therefore reducing habitation, and pushing K out, and therefore limiting the recovery after a spike, a long chain of impulses that support retriggering the neuron easily (hence potentiation) becomes possible.

Sorry, I guess I have to review Kandels Nobel Prize article again the details are starting to get mulched together too much.

Nice question...........from mango tree we get only mangod not the grapes right......like that there are many types of neurons in the body........like......sympathetic,parasympathetic,domamine,seratonin.......so on......based on the time of neuron , neurotransmittor will relese.....impulse is nothing but....imbalance in electric potential inside the neuron.....see goodman gillman once.....

Our human body contain number of cell each cell contain 46 chromosomes.....but perticular chromosome (the too specific gene) is active in perticular cell ex:pancretic cell will secret insulin only that means the gene responsible for secretion of insulin is active and rmaining genes(chromosomes) is in inactive state.........like wise neurotrasmittion also.......based on the need for body for action........neurotramittor will release.......wheter it is adrenalin or na or dopamine or gaba...or histamin and so on............

If u not able to follow my answer or if u find any mistakes in my answer reply me.................thanq

hi... ill suggest you to read the book "Ganong's Review of Medical Physiology"

@ragu ram:i understood two things from ur answer but not clear, one is each neuron have only one type of neurotransmitters or each neuron synthesis particular neurotransmitter in a particular time and another kind of neurotransmitter for another reaction as a response................if they did, impulse is the same but the output is different...am i clear?...it's confusing.....

http://en.wikipedia.org/wiki/Neuron

Please check this article. Each neuron can use only one of the neurotransmitter as a "primary" transmitter throughout the life. In some neurons, in addition to the primary "neurotransmitter", sometimes a peptidergic transmitter is also used as a "secondary " transmitter. Capacity of the neurons to express one or the other neurotransmitter is dependent on the transcription factors (and the transcription factor modulators) expression in the given neuron.

Ss want u told is currect......impulse is same but output is defferent

the out put of any neurotransmitter or even a hormone depends upon the type of receptors on post synaptic membrane or motor end plate... the real mechanism actually begins after the receptor... e.g. Acetylcholine in case of skeletal muscles generates the impulse that opens the calcium gates at sarcoplasmic reticulum that results in contraction... this is because of NICOTINIC receptors that is ionotropic means premeable to sodium so impulse generated...

2.. but the type of receptor present in heart for acetylcholine is MUSCARINIC that is metabtropic that inhibit the contraction of heart muscles so parasympathetic stimulation that release acetylcholine results in slow heart rate...... it that helpful?????

of course Mr muhammad and thank you... but my doubt is if a neuron contains two or more type of neurotransmitters in synapse, then how the impulse stimulate particular neurotransmitter?...is there any link between impulse(specificity due to impulse rate or something) and specific neurotransmitters(due to it's property like ionic and non ionic or polar, non polarity or something )..... or Each neuron contains only one type of neurotransmitter?...

so many neurons contains more than one neurotransmitter, I think that the relase of one type depends also by the glia cells that you can find near neuron, in Italy we call "sinapsi tripartita hypothesis"

We knows that glia cells are able to use neurotransmitter to regulate neuron neurotransmision

got it Dhanasekaran... if one neuron release more more than one neurotransmitters then it depends upon its collateral branch.... the impulse is same but the axon terminal of each collateral branch is specialized to produce and release only one type of neurotransmitter, if one axon has 3 collateral branches then these three branches may produce same neurotransmitter or it may be all different...

what determine the specific cell response not only neurotransmitter but also specific receptors and/or channels on cell membrane and inside the cell such as cytoplasmic and nuclear receptors.So,one neurotransmitter can have affinity to several types of receptors on different types of cells in different tissues with subsequent response specific to each cell according to a certain intracellular cascade determined by the genetic make- up of the cell .thanks.

I think you could read somethings about epigenetics... I'm really sorry but I can't help you on this

For what I know, the correct question concern how many different type of neurotransmitters are in a synapse not in a neuron. And for what I know the answer is "only one neurotransmitter type is present in a given synapse". In some the release of a neurotransmitter can have a different effect on the postsynaptic cell depending on the receptor type. Two example are Glutamatergic and Cholinergic synapses. AMPA and NMDA receptors are involved in Glutamate synapses while Nicotinic and Muscarinic can be involved in Cholinergic synapses :)

Actually when you get to the more complex ion channels such as the NMDA ion channel you end up with multiple effects from multiple neurotransmitters. For instance NMDA is a voltage gated Ampa receptor that is locked open when a second Neurotransmitter is detected to allow the Long-Term Potentiation that makes certain CA3 neurons more effective at holding trains of signals.

You might want to look at Kandel's work on the NMDA ion channel to see how all this works, but if I misremember correctly, the ion channel has a bi-directional aspect where it pumps K ions out, and Ca Ions in at the same time. As a result of pumping K ions out, they tend to build up just outside the ion channel, and when it goes quiescent, block the Ca input. (Or was that Magnesium that blocked it, yep definitley a teflon memory) In order to blow all these ions out of the way, the voltage in the cell has to increase to a certain state, at which point the blocking ions are repelled, and the pore opens.

If I misremember correctly, the Ampa portion of the ion channel keeps the channel open, by using Ampa as a sort of repulsion gate keeping the blocking ions from concentrating in the pore. The other neurotransmitter that I currently do not remember the name of, modulates the Ca ion intake and the K ion output.

By both taking Ca in, and therefore reducing habitation, and pushing K out, and therefore limiting the recovery after a spike, a long chain of impulses that support retriggering the neuron easily (hence potentiation) becomes possible.

Sorry, I guess I have to review Kandels Nobel Prize article again the details are starting to get mulched together too much.

Yes, I agree with almost all, I tried only to summarise to answer the originally question asked that was not related to AMPA and NMDA (which I used only as example) structure and function. :)

Science. 1998 Jul 17;281(5375):419-24.

Corelease of two fast neurotransmitters at a central synapse.

Jonas P, Bischofberger J, Sandkühler J.

A very nice study on how two transmitters can originate from a single neuron.

Neurons work in circuits. The stimulus for neuron to works not only just just electrical stimulus as in a laboratory, but any idea can stimulate neuron to work. In a circuits, neurone associate many stimuli of many circuits that work together ont many ideas. Neurons work just to convey impuls that bring ideas. So there is no specificity of neurotransmitters.

I thought I would add my conservation of Neuro-transmitter theory to the mix, just to add confusion. In this theory Neuro-transmitters are conserved, and re-used, not just at the individual cell level, but systemically, to allow the body to have separate channels of information working in parallel at the local level. One of the reasons there are so many side effects of neuro-active drugs based on Neuro-Transmission, is that each neuro-transmitter is used in multiple cases throughout the body, and there are different ion channels that are sensitive to it, associated with different organs. Thus a neuro-transmitter associated with depression might also be associated with regulation of digestion, and might modulate the expression of another neurotransmitter needed for muscle tone.

Hi. Ya neurons do have more than one neurotransmitters. But do not mistake it for neurotransmitters of opposite natures like excitatory and inhibitory in same neuron. Actually, neurotransmitters in such situations are called co-transmitters. generally, pepetides are packed in vesicles with main neurotransmitters. It is the strength of presynaptic potential which decides the release of transmitter or you may relate it with calcium influx at presynaptic nerve endings. The transmitters need not to be released simultaneously. If the potential is less frequent, it releases small vesicles localized near membrane and if highly frequent (strong) then releases the larger vesicles containing neuropeptides.