Someone finally dissects the role new neurons play in fear conditioning

Based on a true story – how progress is made in the field of adult neurogenesis*

  1. A group of scientists reduce neurogenesis and report a memory deficit.
  2. A second group repeats the experiment, with only a few minor differences in protocol, and fails to find a memory deficit.
  3. A third group, using the same species as the first group but a protocol more similar to the second group, replicates the original finding but only when the experiment is performed on Wednesdays.
  4. Faith is restored.
  5. Five groups report no such neurogenesis-dependent memory deficit.
  6. It is reported that developmental exposure to strontium reduces adult neurogenesis by 40% AND produces the much sought after memory deficit. In a technical tour de force follow-up experiment, artisanal cheeses restore neurogenesis and reverse the memory deficits. Causation is established.
  7. BDNF.
  8. Everyone proclaims the role of neurogenesis in memory and is totally confused at the same time.
  9. Someone systematically examines all of the variables in the memory test to determine whether or not the whole thing is a hoax and they should just change careers**.
  10. We have never gotten this far.

Even at level 8, the neurogenesis-fear conditioning story was one of the more convincing arguments of new neuron functionality. With this study by Drew et al. we may soon be jumping for joy as we appear to be graduating to level 9.

The contribution of adult neurogenesis to contextual fear conditioning was greatest when mice were only given a brief training experience – mice lacking adult neurogenesis showed reduced fear of a context where they previously received a single footshock during a brief (3 min) exploration session. With longer exposures to the context, or additional footshocks, neurogenesis-deficient mice showed normal memory. This finding could be explained by the fact that young neurons have a lower threshold for synaptic plasticity, allowing them to encode fleeting experiences that would be forgotten if left to mature neurons.

So, brief training protocols may now likely be my first choice, at least when using mice. In fact, the only times I have observed contextual fear memory deficits in mice has been after brief training protocols almost identical to those used by Drew et al. So we just might have taken a big step forward. If not, check back in 5 years for my revised “How progress is made” list.

*or any other field for that matter
**this is not entirely a joke because, in this case, it both 1) appears to not be a hoax, and 2) marks the launch of the next phase of Michael Drew’s career (congrats)

Drew MR, Denny CA, & Hen R (2010). Arrest of adult hippocampal neurogenesis in mice impairs single- but not multiple-trial contextual fear conditioning. Behavioral neuroscience, 124 (4), 446-54 PMID: 20695644

3 thoughts on “Someone finally dissects the role new neurons play in fear conditioning

  1. Interesting. I like the idea that new cells are required for the most rapid forms of learning.

    In the memory literature there’s a lot of interest in single-trial learning in rodents as a model of “episodic” memory in humans. See for example

    1. Henke, K., A model for memory systems based on processing modes rather than consciousness. Nat Rev Neurosci, 2010.
    2. Langston, R.F., et al., The role of hippocampal subregions in memory for stimulus associations. Behav Brain Res, 2010.

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