I picture a neuron as having multiple trees of dendrites attached to the cell body with a single axon leaving the cell body. I believe the cell body near the axon root makes the decision to fire or not fire an action potential.

  • If the neuron has both excitatory and inhibitory synapses in the dendrite trees, how do these communicate to the cell body?

  • Does something like an action potential get transmitted down the dendritic trees to the cell body?

  • What is the difference between the excitatory and inhibitory signals that are transmitted?


2 Answers 2


An inhibitory synapse works just like an excitatory one!

When a presynaptic neuron fires it will release a neurotransmitter at its terminal(s). This neurotransmitter can be excitatory or inhibitory, the main excitatory one in the central nervous system being glutamate and the main inhibitory one GABA.*

GABA and Glu are far from being the only neurotransmitters in the brain, they're just a classic example, so we'll stick with them. When the neurotransmitter is released it binds to receptors on the postsynaptic neuron (provided, of course, that the postsynaptic neuron expresses these receptors).

Various GABA and Glu receptors exist, both ionotropic (i.e. channel-receptors that let ions flow through the membrane upon binding of the ligand) and metabotropic (i.e. receptors which activate an intracellular pathway that does not per se start the flow of ions, but that can induce it or prevent it indirectly). For simplicity we'll stick to ionotropic receptors.

Glu binds to three types of ionotropic receptors: AMPA, NMDA and kainate receptors. These have different kinetics/properties, but the bottom line is that they let cations (positively charged ions, such as Na+ and Ca++) into the cell. When this happens a postsynaptic depolarization happens, which is named EPSP (excitatory post-synaptic potential).
So, if the resting membrane potential was, say, -57mV, it will become, for instance -52mV. This means that, if the threshold potential for firing an action potential were -43mV the cell, which first needed a 14mV depolarization to fire now will need a 9mV depolarization. If subsequent EPSP sum they can depolarize the cell sufficiently to reach threshold and let the cell fire.

This image from Wikipedia is quite self-explicatory: in this case 3 synaptic events generated 3 EPSPs that summed, making the cell depolarize enough to reach threshold potential, and generate an action potential, that will then propagate to the cell body.

Sum of EPSP

GABA, on the other hand, binds to the GABA-A receptor, which is a chloride channel. In most cases, upon binding of GABA, GABA-A lets Cl- in the cell, effectively hypopolarizing it and generating an IPSP (inhibitory post-synaptic potential). The situation is the same (but opposite) to Glu, this time, though, the potential becomes more negative.

EPSP and IPSP can and do happen at the same time: as they can vary in frequency and intensity depending on the firing frequency and firing pattern of the presynaptic neuron, a pretty much continuous range of voltages can be achieved in the postsynaptic neuron.

Other controls over this process come from metabotropic receptors that can, for instance [de]phosphorylate (add or remove a phosphate group) ion channels modulating their permeability to ions or from the different kinetics of the different channels (for instance certain channels stay open for longer or open in a delayed manner etc), allowing for fine-tuning of the system.

*I am making a gross generalization here. A neurotransmitter is not excitatory or inhibitory per se, it depends on the context. For instance excitatory GABA synapses do exist.

  • $\begingroup$ I had read about EPSPs and IPSPs before and I now see that the main difference is the sign of the delta voltage change - thanks. My question still remains about how these travel down to the cell body down the dendrite tree. These are not action potentials and I thought action potentials were required for signals to travel unchanged over any distance. Do these EPSPs and IPSPs travel unchanged down the dendrite tree to the cell body to get "summed"? The membrane potential near the synapse changes but how does that change travel down the dendrite? The dendrite is not an electrical conductor. $\endgroup$
    – FrankH
    Jan 30, 2012 at 10:46
  • $\begingroup$ I think the answer provided by @yamad answers your concern very well $\endgroup$
    – nico
    Jan 30, 2012 at 16:58
  • $\begingroup$ I wish I could "accept" both your answer and yamad's answer ;-). Thanks again for a great answer... $\endgroup$
    – FrankH
    Jan 31, 2012 at 20:10
  • $\begingroup$ A small linguistic side-note: the term "stimulatory synapse" is not used in neuroscience. A search in Google scholar gave me 183 results and they were almost all, if not all, from immunology studies. Perhaps @Nico you meant "excitatory"? I replaced the occurrences in this answer and my edits got accepted, but they were now reverted back. $\endgroup$
    – vkehayas
    Sep 14, 2017 at 12:55
  • $\begingroup$ @vkehayas I reverted the edit, since I have definitely heard "stimulatory synapse" and "excitatory synapse" used in an exchangeable manner. To be fair, I did not check Google Scholar, but if you feel strongly about that please change it back and I will not revert it. $\endgroup$
    – nico
    Sep 19, 2017 at 10:55

From your comment to nico's good answer, it seems that your question is really about how synaptic potentials propagate through dendrites.

Canonically, synaptic potentials travel passively along membranes and is described by cable theory. The cable equation describes how the voltage will change over time and space along a cable. The theory was originally developed for signal decay in trans-Atlantic telegraph cables, but the principle holds for a voltage-independent length of membrane like a dendrite.

A key point is that the potential change "seen" by the cell body is different from the potential change seen locally at the site of the synapse itself. In fact, the voltage decays exponentially with increasing distance from the synapse. The extent of the signal decay is governed by the axial resistance (influenced by dendritic diameter), the membrane resistance, and membrane capacitance, and the branching pattern. A common neuron modeling environment called NEURON is basically a fancy solver for the cable equation.

You'll note that a consequence of this signal decay is that synaptic location matters a lot. Given an identical synaptic potential, a very distal synapse will have much less of an effect on the soma than a more proximal dendrite. Sometimes, the synaptic strengths are scaled to compensate for this location issue (a distal synapse will have a much larger local potential change). Many inhibitory synapses capitalize on this location dependence and are located close to the soma to act as shunts for all signals coming from the dendritic tree. When activated, an inhibitory synapse will decrease the local membrane resistance thereby decreasing cell excitability.

Finally, I'll note that although we often talk about dendrites as being passive conductors, dendrites are actually quite active and have many voltage-dependent channels. The voltage-dependent phenomena in the dendrite complicates the use of pure cable theory to understand the dynamics of synaptic potentials. However, cable theory is still the essential foundation upon which our growing understanding of the active dendrite is built.


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