Word of the Week: Neurotransmitter

Jan 22 2012 Published by under Word of the Week

Last week's word of the week was not a sciencey word, but a fun word, because why not? But this word of the week is one I use ALL the time, and one that I always worry people don't know about. And your brain is full of them, so it seems relatively important to know what they are.

Neurotransmitter
: These are chemicals that are present in your brain, and serve a chemical messengers between neurons. Neurons do not actually touch each other, instead there is a little gap between one neuron and the next (called a synapse), and neurotransmitters are released from one neuron to the next, to keep a signal going.

An important note: neurotransmitters are released from inside the first neuron (from little bubbles called vesicles which bleb on to the outer membrane of the neuron and release their chemicals out into the space), but they do NOT go into the next neuron. Instead they hit the next neuron and bind to receptors on the cell surface, which change the inside of the target neuron to pass the message on.

Neurotransmitters can cause the next neuron to have an action potential and an excitatory effect, or they can cause that neuron to shut down temporarily, acting in an inhibitory manner. It all depends both on the type of neurotransmitter, and particularly on the RECEPTOR the neurotransmitter binds to. Examples of neurotransmitters include things like acetylcholine, GABA, glutamate, dopamine, serotonin, and norepinephrine (among others). But the chemical itself is merely one molecule, which is released from one neuron and binds to receptors on another. It is then taken up by transporters or degraded by enzymes.

EDIT: I would like to include a note by Dr. Zen (included in a comment below) about the difference between a neurotransmitter and a neuromodulator, which is a very fine one and worth thinking about.

A chemical that has fast, short-lived effect on a neuron is acting as a neurotransmitter. Neurotransmitters bind to receptors that are doorways in the neuron to let electrical current flow.

A chemical that has a slow, long-lasting effect on a neuron is acting as a neuromodulator. Neuromodulators bind to receptors that trigger events inside the cell, but those receptors don’t act as doorways for currents themselves.

The same chemical can be a neurotransmitter in one location and a neuromodulator in another. The same chemical can be acting as both a neurotransmitter AND a neuromodulator on the same neuron, if that neuron has two different kinds of receptors for that chemical on it.

27 responses so far

  • anon says:

    Nice and nicely explained. Thanks Maestro Scicurious.

  • Glutamate is a neurotransmitter, not glutamine.

  • Zen Faulkes says:

    Everything you say is true. But pretty much everything you write here also applies to another category of chemicals in the brain.

    A chemical that has fast, short-lived effect on a neuron is acting as a neurotransmitter. Neurotransmitters bind to receptors that are doorways in the neuron to let electrical current flow.

    A chemical that has a slow, long-lasting effect on a neuron is acting as a neuromodulator. Neuromodulators bind to receptors that trigger events inside the cell, but those receptors don’t act as doorways for currents themselves.

    The same chemical can be a neurotransmitter in one location and a neuromodulator in another. The same chemical can be acting as both a neurotransmitter AND a neuromodulator on the same neuron, if that neuron has two different kinds of receptors for that chemical on it.

    I usually use the phrase "neuroactive chemical" to include the whole set of neurotransmitters, neuromodulators, and gasotransmitters.

  • O.R. Pagan says:

    Nice article! Just a couple of nerdy points, though. The properties that you talked about apply to chemical synapses. Some neurons are actually in close physical contact with each other through connexins, which form the so-called gap junctions in electrical synapses.

    The second point is about inhibitory neurotransmission. When this happens, it is not as much that the neurons shuts down temporarily. Rather, the neurons are less likely to fire, because they are hyperpolarized...

    There is more technical points about neurotransmitters being excitatory in one type of organism and inhibitory in another, but this is a topic for another day (:-)

    My two cents...

  • The second point is about inhibitory neurotransmission. When this happens, it is not as much that the neurons shuts down temporarily. Rather, the neurons are less likely to fire, because they are hyperpolarized...

    This is also an incomplete understanding of inhibitory neurotransmission, which can make a neuron less likely to fire without hyperpolarizing it.

    • O.R. Pagan says:

      @Comrade: You make a valid point, so let me clarify my statement. Please correct me if I am wrong.

      Inhibitory neurotransmission modulated by neurotransmitters deal with chloride ion conductance through GABA-A, GABA-C and glycine receptors (in vertebrates at least). The binding of GABA or glycine to their receptors activate the anion channels, indeed hyperpolarizing the neuron.

      It is possible, though, to make a neuron less likely to fire by blocking its sodium channels with TTX or something like that, but in this case, it would no be neurotransmitter-modulated inhibitory neurotransmission...

      • No, you are still missing something. GABA- or glycine-induced increase in chloride conductance can make a neuron less likely to fire without hyperpolarizing the neuron.

        • O.R. Pagan says:

          I fail to see why... How can chloride intake in an already polarized neuron not make the resting potential even more negative? Now I am curious, what am I missing? Thanks!

          • You are making assumptions about two parameters that might not be satisfied at the location of the ligand-gated chloride channels and which will determine whether increasing the open probability of those channels hyperolarizes the membrane.

  • O.R. Pagan says:

    You are talking about a different thing now, namely the probability of a channel to open in the presence of agonist binding. Once the chloride channel opens, allowing chloride flow into a cell, hyperpolarization occurs, period.

  • You are making an assumption that may or may not be warranted about the relationship between two key physiological parameters, and which determines whether net chloride flux is inward or outward when chloride channels open. Period.

    Hint: Life is not a whole-cell voltage-clamp experiment.

  • O.R. Pagan says:

    @Socal_Dendrite: good point, thanks!

    @Comrade: You changed the nature of the question again. Let's see if I am sufficiently explicit now:

    Under normal conditions, again, in vertebrate organisms, the concentration of chloride is higher in the extracellular side than at the intracellular side. Therefore, when chloride-conducting channels open, the negative ions flow in favor of its concentration gradient, namely, towards the cell's interior, which is already negative at rest, again, under normal conditions. When negative charges are added to an already negative environment something even more negative results.... Therefore hyper... Well, you know the rest.

  • You are still failing to consider the complete set of cellular parameters that determines whether there is net inward or outward (or none) flux of chloride when chloride channels open.

    Hint: A permeant ion does not necessarily flow down its concentration gradient when the membrane becomes permeable to it.

  • O.R. Pagan says:

    I sense yet another change of subject... Please educate me...

  • Dude, this is really, really basic membrane physiology, and the subject has never changed. I'm surprised I have to explain it.

    The driving force on a permeant ion--and hence the direction in which it flows when a conduction pathway for it opens--is determined *both* by its concentration gradient *and* by the voltage across the membrane (i.e., the electrical gradient). The membrane potential at which there is no net inward or outward flux for a permeant ion with a given internal and external concentration--i.e., where the chemical potential energy and and electical potential energy of the ion are equal and opposite--is the Nernst equilibrium potential.

    Whether an ion flows in or out of the cell depends on the relationship between the Nernst equilibrium potential for that ion and the membrane potential. Unlike sodium and potassium--which must be regulated with very narrow concentration ranges both inside and outside the cell or else shitte goes to hell in a handbasket--cells have the ability to regulate internal chloride concentration within a pretty wide range. Thus, depending on the neuron and its physiological state, the chloride reversal potential can vary for an adult neuron between -40 and -70 mV.

    If a neuron with a chloride reversal potential of -50mV is sitting at a membrane potential of -60mV when a chloride conductance is activated, chloride flows *out* of the cell and depolarizes the membrane. However, despite this channel opening event depolarizing the membrane, it can be inhibitory--i.e., it can make the cell less likely to fire an action potential.

    Now see if you can figure out why this depolarizing conductance can be inhibitory!

  • O.R. Pagan says:

    You are correct... thank you for a complete answer....

  • Namnezia says:

    I think Zen's distinction of a neurotransmitter and a neuromodulator is a little unusual. It seems like what he is distinguishing is between neurotransmitters that bind to ionotropic vs metabotropic receptors. The definition I've seen of neuromodulators refers to neurotransmitters that diffuse over a large area binding to (typically metabotropic) receptors in multiple cells, rather than being confined to the bit of dendrite directly across or nearby the release site.

    Thus neuromodulators alter the firing properties of neurons and affect how they transfer information, as opposed to directly mediate fast, cell-to-cell communication.

  • [...] idea here is that the neurotransmitter norepinephrine (noradrenaline to you Brits) has roles both in the brain and in your blood vessels. [...]

  • John says:

    It did not even explain how the neurotransmitters are created. The Sodium-Potassium pump is how the neurotransmitters are created. From the imbalance of charge inside and outside of the neuron a charge is created. Three sodiums leave the neuron and two potassiums go inside the neuron thus creating the charge. When the charge reaches the end of the neuron(Axon) it then tells what neurotransmitter to be sent across the synapse.

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