Denny et al. (2014) and Cazzulino et al. (in press)


Denny et al. (2014) Hippocampal memory traces are differentially modulated by experience, time, and neurogenesis. Neuron, 83(1): 189-201.

Cazzulino et al. (accepted for publication). Improved specificity of hippocampal memory trace labeling. Hippocampus.

Denny et al. used a different method of memory trace labeling as do the Garner et al. and Liu, Ramirez et al. studies. However, it’s the same principle. Here, instead of removing Dox from the diet to label memory traces, the authors inject ArcCreERT2 mice with an estrogen receptor antagonist (in this case, it was tamoxifen) which in turns induces DNA activation. This only happens, however, in those cells that are actively producing the protein in the promoter region of the transgene: Arc. Arc is an immediate early gene expressed in cells that have recently been highly active. Thus, the authors targeted these recently active cells using this system and were able to express in them a protein of interest, e.g. eYFP. After tagging hippocampal neurons involved in memory encoding with eYFP, (more…)


Pytte et al. (2008)

Citation: Pytte et al. (2008). Regulation and function of neuronal replacement in the avian song system. In: Zeigler HP, Marler P, editors. Neuroscience of Birdsong. Vol. 28. Cambridge University Press; 350–366.

Another brief review due to a presentation tomorrow.

Today’s paper is a book chapter co-authored by my doctoral advisor, Dr. Carolyn Pytte.

The authors review the literature about the possible causes and function of neurogenesis in the songbird system.

Yiu et al. addressed the question of how certain neurons in the amygdala will be recruited into memory traces while most other amygdala neurons won’t, the answer being their relative levels of excitation at the time of memory occurrence.

Dr. Pytte’s has focused on neurogenesis in the song system of the zebra finch. In addition to the avian song system, neurogenesis also occurs, of course, in the mammalian hippocampus, my main region of focus. In both systems, more neurons that are born in adulthood die than those that survive and integrate into the surrounding circuitry. So why do particular neurons survive while others die?

In this case, the authors suggest that it is those neurons who have won the audition:


More specifically, the authors write:

“Neurons with response properties consistent with optimal song structure are cast while those that do not fit the part are rejected, prompting more neurons to be auditioned.”

So what are these response properties? If the conclusions of Yiu et al. are to be extended to the hippocampus, and adult-born neurons, it would likely be that more excitable neurons, perhaps more specifically with shorter response latencies or reduced spike frequency adaptation, would survive and become incorporated into memory traces. Interestingly, all young, adult-born neurons are hyper-excitable. They’re even excited by GABA.

So, are certain adult-born neurons in either the avian song system or the hippocampus significantly more excitable than their peers? Or is the excitation described by Yiu et al. transient and probabilistic? Perhaps those cells incorporated into a trace were doing the right thing at the right time.