Gupta & Hasselmo (2014)


Gupta & Hasselmo (2014) Modulatory Influences on the Hippocampus and Entorhinal Cortex. In Space, Time, and Memory in the Hippocampal Formation. Ch7 (pg. 153-189)

This chapter focused on the function of neuromodulators on the hippocampal system. And it was packed with information. Acetylcholine, dopamine, norepinephrine, metabotropic glutamate receptors, GABA-B receptors, serotonin all have different effects on excitatory transmission, inhibitory transmission, spike frequency adaptation, resting membrane potential, and plasticity. By the way, all of these modulators may have different effects on each event depending on (more…)


Derdikman & Moser (2014)


Derdikman & Moser (2014) Spatial Maps in the Entorhinal Cortex and Adjacent Structures. In Space, Time, and Memory in the Hippocampus. Ch5 (pg. 107-126)

When the Cognitive Map Theory of the hippocampus was originally postulated, it was suggested that spatial representation was the job solely of the hippocampus. However, it has since been discovered that other structures, such as the entorhinal cortex, are integral for establishing spatial representations in the brain. Specifically, this chapter focuses on the medial entorhinal cortex, which, compared to the lateral entorhinal cortex, seems to be preferentially involved in spatial representation rather than object representation.

The entorhinal cortex is home to a particular cell type called grid cells. Grid cells are (more…)

Winter & Taube (2014)


Winter & Taube (2014). Head Direction Cells: From Formation to Integration. In Space, Time and Memory in the Hippocampus. Chapter 4 (pg 83-06)

This chapter focusing, on head direction cells, began the discussion on how the mammalian processes space and position in it.

Head directions (HD) cells fire most when (more…)

Ho & Burwell (2014)

Citation: Ho & Burwell (2014). Perirhinal and postrhinal functional inputs to the hippocampus. In Space, Time, and Memory in the Hippocampus. Ch. 2 (pg. 55-81)

This chapter gives an overview of the functions of two neighboring cortical areas involved in the hippocampal system: the perirhinal (PER) and postrhinal (POR) cortices. These areas are largely thought of as being important for object memory and visuospatial memory, respectively.

It has been demonstrated that (more…)

Ryan, Roy, Pignatelli et al. (2015)

Citation: Ryan, Roy, Pignatelli et al. (2015). Engram cells retain memory under retrograde amnesia. Science, 348(6238): 1007-1013

OK, so if I’ve learned one thing from the papers reviewed so far, it’s that the population of neurons active during the encoding of a new memory must be reactivated for that memory to be successfully remembered. But, does synaptic plasticity need to occur within the engram circuit for recall?


And no. (more…)

Tanaka et al. (2014)


Tanaka et al. (2014). Cortical representations are reinstated by the hippocampus during memory retrieval. Neuron, 84(2): 347-354

One of the most influential ideas in considering the function of the hippocampus is that reactivation of hippocampal memory traces drives the cortex back to the state it was in during the encoding, thus allowing for a re-experience of past events. However, until Tanaka et al.’s 2014 study, it appears that there was never direct evidence that this indeed occurs.

Tanaka et al. used a similar Tet-Off system used by Liu, Ramirez et al. to express GFP and ArchT in neurons of dorsal CA1 that were active in encoding. ArchT, by the way, inhibits (more…)

Schafe et al. (2005)


Schafe et al. (2005). Tracking the fear engram: The lateral amygdala is an essential locus of fear memory storage. The Journal of Neuroscience, 25(43): 10010-10015

This study is about localizing components of the fear memory engram. Although it was well established that the amygdala is involved in fear processing, it had not yet been shown that this was a site of fear memory storage. Specifically, it was debated whether or not the lateral amygdala (LA) stored memories.

To test this, the Schafe et al. injected the lateral amygdala with (more…)

Ramirez, Liu et al. (2013) and Liu, Ramirez et al. (2013)


Ramirez, Liu et al. (2013). Creating a false memory in the hippocampus. Science, 341(6144): 387-391.

Liu, Ramirez et al. (2013). Inception of a false memory by optogenetic manipulation of a hippocampal memory engram. Phil Trans R Soc B, 369(1633): 20130142

To be fair, one of these papers reviews the other as well as the Liu, Ramirez, et al. paper I’ve already reviewed. But A) I read both, and B) I need to make up ground in advance for the 6 months I’ll need to re-read, understand, and review Marr’s 1971 paper.

I highly recommend playing the theme music to Inception while reading this paper and/or blog post.


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…)

Garner et al. and Liu, Ramirez et al. (2012)


Garner et al. (2012). Generation of a synthetic memory trace. Science, 35(6075): 1513-1516

Liu, Ramirez et al. (2012). Optogenetic stimulation of a hippocampal engram activates fear memory recall. Nature, 484: 381-385

Two papers today because they’re relatively quick reads, were published at the same time, are very similar and are equally awesome (I’m also 5 behind on the whole 366 thing). First, a word about Dox. In 1992, a paper was published outlining how to drive or repress the transcription of certain genes with what’s called a tetracycline-controlled transactivator (tTA). In what’s called the Tet-Off version of this system, the presence of doxycycline will inhibit specific genes from being transcribed. However, without Dox, those same genes are free to be transcribed. Both of these papers used this system in combination with c-fos promoter to manipulate memory traces in a very interesting way. Without Dox, neurons that were actively transcribing c-fos, that is, highly active cells, would synthesize a certain protein of interest. (more…)