My rudimentary understanding of the neuronal firing rate is that it varies person to person, and neuron to neuron. So any specific number for a firing rate would be specific to the test subject and type of neuron etc. However aside from this I'm interested to find out if any medication or specific dietary constituents have been shown to increase neuronal firing rate in average test subjects. To be clear I understand that some medication has been shown to help suffers of diseases such as Alzheimer's, but I'm interested in the typical human brain.

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    $\begingroup$ Why would you want to increase neuronal firing rate? That wouldn't necessarily lead to an increase in processing capacity. $\endgroup$
    – honi
    Jun 24, 2014 at 19:19
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    $\begingroup$ "I would assume increase neuronal firing would allow for faster processing capability" <- Don't assume that. $\endgroup$
    – jona
    Jun 24, 2014 at 19:44
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    $\begingroup$ @jona that was more of a passing comment. I'm interested in both what may increase the speed and what the effect of increasing the speed would be. Two separate questions really, I didn't want to confuse the two. $\endgroup$ Jun 24, 2014 at 19:51
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    $\begingroup$ @FraserOfSmeg, yours is a bit of a tricky and ambiguous question. What are you calling "increase in firing rate"? Are you referring to a specific spectral band, or are you talking about every-damn-neuron in the CNS? If it's the later, then it's going to be very hard to measure. To further complicate the issue, certain neurons are inhibitory, so increasing their firing-rates will decrease the firing-rate of their neighbors. I strongly doubt that a medication can affect the global firing rate of the brain, but it's also damn hard to measure. $\endgroup$ Jun 25, 2014 at 14:41
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    $\begingroup$ As far as I remember, it's the conductance velocity of neurons, not firing speed, which is important. I can't get the reference now, but look for something by Cooper, or McCrorie, or some combination of the two. $\endgroup$
    – Eoin
    Jun 26, 2014 at 22:53

1 Answer 1


You've received a few great comments from our neuroscience-savvy users that indicate ways in which this question can be construed as particularly challenging or maybe even unanswerable. However, I think there's a much more basic and limited understanding of your question that takes into account your self-professed unfamiliarity with neuropharmacology and permits a perfectly good intro-level answer. I don't specialize in this – I'm a psychologist, but more of a dabbler in neuroscience – but I'll take a crack at it anyway.

Agonists activate cellular receptors. Excitatory receptors produce excitatory postsynaptic potentials (EPSPs); i.e., they encourage neurons (of which they are components) to "fire". Hence the simple answer: any agonist of a neuron's excitatory receptors increases its firing rate by definition.

Glutamate is an excitatory neurotransmitter. It binds to glutamate receptors, which increase the likelihood or frequency of action potentials (i.e., firing events) in their neurons when activated. NMDA receptors (a type of glutamate receptor) play a role in long-term potentiation (effectively increasing the probability of firing and other criteria of synaptic strength), so the effects of glutamate sometimes outlast its direct activity.

Wikipedia lists several NMDA agonists, some of which are prescribed as ingested drugs. D-Cycloserine has applications in anxiety and addiction treatments. However, there is a balance to maintain, and the objective of medication is generally to restore a normative balance given some abnormality or damage.

Excitotoxicity due to excessive glutamate release and impaired uptake occurs as part of the ischemic cascade and is associated with stroke,[4] autism, some forms of intellectual disability, and diseases like amyotrophic lateral sclerosis, lathyrism, and Alzheimer's disease.[4][14]

Evidently treating Alzheimer's isn't as simple as increasing EPSPs – that might even be a move in the wrong direction. Nicotine may help with Alzheimer's, but the mechanism is more complex:

While tobacco smoking is associated with an increased risk of Alzheimer's disease,[85] there is evidence that nicotine itself has the potential to prevent and treat Alzheimer's disease.[86]...A study has shown a protective effect of nicotine itself on neurons due to nicotine activation of α7-nAChR and the PI3K/Akt pathway which inhibits apoptosis-inducing factor release and mitochondrial translocation, cytochrome c release and caspase 3 activation.[90]

It would seem nicotine's direct action is agonistic, but its mediated effect is antagonistic, and that's the effect that matters for Alzheimer's outcomes. Another wrinkle to nicotine's pharmacology is its agonistic role with acetylcholine, a neurotransmitter that plays excitatory and inhibitory roles for different purposes. This demonstrates the practical complexity of action potentials' causes and consequences.

4. Sapolsky, R. (2005). Biology and human behavior: The neurological origins of individuality (2nd ed.) The Teaching Company. "see pages 19 and 20 of Guide Book"
14. Hynd, M., Scott, H. L., & Dodd, P. R. (2004). Glutamate-mediated excitotoxicity and neurodegeneration in Alzheimer's disease. Neurochemistry International, 45(5), 583–595. DOI:10.1016/j.neuint.2004.03.007. PMID 15234100.
85. Peters, R., Poulter, R., Warner, J., Beckett, N., Burch, L., & Bulpitt, C. (2008). Smoking, dementia and cognitive decline in the elderly, a systematic review. BMC Geriatr 8(36). DOI:10.1186/1471-2318-8-36. PMC 2642819.
86. Henningfield, J.E., & Zeller, M. (2009). Nicotine psychopharmacology: Policy and regulatory. Handbook of Experimental Pharmacology, 192, 511–34. DOI:10.1007/978-3-540-69248-5_18. ISBN 978-3-540-69246-1. PMID 19184661.
90. Yu, W., Mechawar, N., Krantic, S., & Quirion, R. (2011, November). α7 nicotinic receptor activation reduces β-amyloid-induced apoptosis by inhibiting caspase-independent death through phosphatidylinositol 3-kinase signaling. J. Neurochem. 119(4), 848–58. DOI:10.1111/j.1471-4159.2011.07466.x. PMID 21884524.


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