A related question is how fewer synapses and unique inhibitory connectivity affects their information processing capabilities. The verdict is out on whether new neurons are more or less involved in information processing than their mature counterparts. Currently, the best information we have is from studies looking at activity, measured by immediate early gene expression, in response to behavioral stimulation. The true measure of whether a neuron is involved in information processing / representation is if it spikes, i.e. fires action potentials, in response to a specific stimulus. Since new neurons have fewer synapses it’s very possible that they aren’t able to represent many different types of information, and therefore aren’t capable of associating information during memory formation. On the other hand, new neurons synapses are more plastic, perhaps making them better able to associate information even if they have fewer synapses.

And so I wasn’t surprised that the Schinder lab was the one to answer these questions at SFN. They were the ones who finally definitively showed that immature neurons are indeed more excitable than mature neurons. And on Saturday, Lucas Mongiat presented right next to me during the poster session and was kind enough, once 5 o’clock rolled around, to take a few extra minutes to tell me their new story (after traveling all night from Argentina and coming straight to his poster board from the airport!).

They first addressed the question of whether or not immature neurons are more likely to be “activated” than mature neurons. Activation was measured in retrovirally-labeled neurons in hippocampal slices by two methods: calcium imaging and spiking in response to perforant path stimulation. Input-output curves showed that immature neurons were more likely to be activated than mature neurons, regardless of the stimulus strength. Mature neurons could be made to behave like immature neurons if picrotoxin was added to the bath, blocking inhibitory connections.

So what’s going on with inhibition? At the time of spiking, inhibition and excitation were equivalent in the mature neurons, making it hard to become excited and fire an action potential. In contrast, inhibition occurred later in immature neurons, making it easier to fire in response to perforant path activity. Their next question was whether or not new neurons are more likely to associate inputs at a physiological level.

To answer this, they used two stimulating electrodes to activate different perforant path inputs onto granule neurons. Calcium responses were measured to identify activated neurons. The idea is that the two inputs will activate populations of neurons. Some neurons will be activated only by input 1 and others only by input 2. However, another population will be activated by both inputs and those neurons are the ones that are best suited for associating information as would happen during memory formation. Comparing immature (4w old) and mature (8w) adult-born cells as well as the overall population (which would be a mixed age, though mostly older than the adult-born cells) it was only the immature adult-born cells that were more likely to respond to both inputs. That the mature adult-born cells were similar to the general population suggests that adult-born cells eventually mature to become similar to perinatal-born cells.

While I’m no expert electrophysiologist, these data are exciting because they show for the first time that new neurons have the physiological potential to associate inputs better than mature neurons. Computational models and behavioral predictions needed this!

The different timecourse of inhibition makes me wonder how immature neurons handle timing of activity. For example, if input 1 is strongly activated and a subthreshold input 2 follows shortly thereafter, is input 2 potentiated and better able to activate the postsynaptic cell in the future? Does the delayed inhibition make them better at temporal summation? Does it alter the recruitment of immature neurons into cell assemblies, since this is dictated by the precise timing of neuronal firing?

DATA? MORE DATA? PLEASE?!?!

A: Development – Functional Neurogenesis – @jsnsndr

B: Neural Excitability, Synapses, and Glia: Cellular Mechanisms – Brainteresting – @brainteresting

C: Disorders of the Nervous System – Neurobytes – @neurobytes @rimrk

C: Disorders of the Nervous System – Scicurious: Scientific American Scicurious: Scientopia – @scicurious

D: Sensory and Motor Systems – Paula’s Piece of Mind – @Paulineddra

E: Homeostatic and Neuroendocrine Systems – Dormiviglia – @Beastlyvaulter (protected)

F: Cognition and Behavior – Future Dr. Science Lady – @Drsciencelady

G: Novel Methods and Technology Development – Guitchounts – @Guitchounts

H: History, Teaching, Public Awareness, and Societal Impacts in Neuroscience – Neuroflocks – @Scipleneuro

SUN: Student Undergrad Neurobloggers – SUN – @Astroglia

It’s surprising that it’s 2011 and there’s no regular meeting on adult neurogenesis. There have been neurogenesis sessions at other meetings and perhaps the occasional, sometimes closed, neurogenesis meeting here and there, but nothing regular for all to attend. This Keystone meeting on adult neurogenesis will hopefully mark the end of this. About 180 people attended this meeting organized by Jenny Hsieh, Fred Gage, Alejandro Schinder and Pierre-Marie Lledo. The attendees included a large proportion of old and new adult neurogenesis researchers from around the world. And from the scientific program you can see that the interests were diverse, spanning molecular and cellular regulation, anatomy and physiology of new neurons, behavioral functions, clinical relevance and cross-species comparative studies. Data aside, it was also a chance to meet people whose names you’ve seen for years in print but never encountered in the haystack that is SFN. For me, some of these people were long time giants in the field while others were newcomers. A number of people told me they read this blog. And even find it useful!

I didn’t take notes but a number of presentations and themes left an impression. I’ll summarize them in a way that is both brief and poor, so as to minimize any prepublication conflicts:

• Jonas Frisen had some new data using his carbon dating method for measuring adult neurogenesis in humans. From the 10 sec that the slide was up on the screen it looked like he had new data suggesting adult neurogenesis occurs in appreciable amounts in the human hippocampus.
• Grigori Enikolopov presented a novel, interesting (and therefore controversial) story where the radial glial stem cells of the hippocampus each divide rapidly several times and then differentiate into astrocytes, in contrast to the prevailing hypothesis that they are largely quiescent and divide infrequently (his confocal images were absolutely stunning too)
• Gerd Kempermann, using an ablation model, suggested that new neurons are important for reversal learning in the water maze
• Hans-Peter Lipp had a provocative talk on the significance of adult neurogenesis, based on his work in natural populations. He and Irmgard Amrein and collaborators are scouring the globe for the weirdest of mammals, to determine what types of geographical, territorial, social etc factors regulate neurogenesis. Plaguing the natural population field is the same problem found in the human literature (not surprising since humans are a natural population) – analyses only involve endogenous markers of neurogenesis (must it really be this way?) and therefore cannot examine long-term cell addition or fate (such as can be done with BrdU or retrovirus). Regardless, fascinating.
• Amar Sahay / Rene Hen has developed a novel mouse where neurogenesis can be upregulated genetically, apparently avoiding the nonspecific effects seen with usual models of increased neurogenesis (e.g. running, enriched environment).
• Alejandro Schinder’s work on the physiology of new neurons was impressive because it tackled key questions for understanding what new neurons are capable of doing during behavior. He is looking at the ability of new neurons to associate/integrate inputs (and therefore information) from the lateral and medial perforant paths. He also showed that new neurons in the ventral hippocampus mature more slowly than those in the dorsal hippocampus, which is relevant given the spatial/mnemonic vs. emotional dissociation between these two regions.
• Erno Vreugdenhil provided new evidence that glucocorticoids remain on of the strongest regulators of adult-generated neurons, with glucocorticoid receptor-deficient new neurons displaying profoundly accelerated maturation and abnormal migration
• Martin Wojtowicz presented data from two different hippocampal tasks showing that rats lacking new neurons are more prone to memory interference
• Nora Abrous‘ work reminded us that, while it’s simpler to say that learning enhances neurogenesis, it’s not nearly the whole story (learning also reduces neurogenesis and death of some cells may be required for the survival of others).
• Paul Frankland received too much attention from this blog during SFN so he can take a break here but you’ll notice his website is looking somewhat…blogish. Maybe he can be encouraged to develop it?
• Michael Bonaguidi / Hongjun Song developed an interesting mouse model where they could fluorescently label as few as 2 stem cells in the entire hippocampus, thereby creating an immunohistochemical nightmare. But also enabling a clean look at the asymmetric and symmetric division of these cells and their progeny that is difficult to see in other models where hundreds of cells are dividing in close proximity to one another.
• Adi Mizrahi’s lab has been monitoring the turnover of new olfactory bulb neurons and their activity in vivo, using 2-photon microscopy and optogenetic approaches. They’ve suggested that even when many months old and fully mature, adult-generated neurons are functionally relevant.
• Tsuyoshi Miyakawa presented some interesting data showing that a number of different mouse models of psychiatric disease share a common feature: an immature dentate gyrus (builds on this paper, which showed that antidepressants, in addition to increasing neurogenesis, “de-mature” mature granule neurons).

Are we spending too much effort studying adult neurogenesis? This was a question I couldn’t help but ask myself during the meeting. Probably a natural feeling when every single talk is on the same topic. But I think it’s valid in spite of this. There was a lot of technically-amazing work presented and it made me wonder if the neurogenesis work is being matched by efforts to understand similar processes in mature dentate gyrus neurons or mature neurons in other neuronal populations. Can we understand the significance of adult neurogenesis if we don’t understand the networks in which they reside? (It’s worth mentioning that some work, e.g. by Schinder’s group, often measures electrophysiological properties of adult-born and perinatal-born neurons, and compares the two. In this way we do learn about both new neuron and general dentate gyrus function)

Is neurogenesis really low in humans? Some presentations of human data and non-human (but long-lived) animals suggested that neurogenesis must be trivial in adult humans. I’m all for being skeptical but I’m not sure this is necessarily the case. The numbers in the Eriksson and Kempermann studies suggest to me that neurogenesis in humans might actually be much more robust than is commonly thought (a topic I’ll write more about soon). Furthermore, differences in neurogenesis across rodent strains and species are great enough that it seems premature to dismiss it in humans based on low numbers in non-human primates.

Where should the field go? The meeting had a great sense of community I thought. Perhaps the only thing missing was some general discussion or consultation about where to go next. Are there certain questions we need to address more than others? For example, one suggestion I heard was that maybe we should spend more time studying neurogenesis in primates, since our comparative knowledge of neurogenesis is weak, our knowledge of primate adult neurogenesis is laughable, and our knowledge of human neurogenesis needs all the help it can get.

Do we need a new diagram illustrating the stages of neurogenesis? Every speaker had their own variant of this image, which usually differed in the shade of grey used to fill the soma of mature granule neurons, or the number of quaternary processes present on radial glia. I therefore spent a few hours on Microsoft Paint and came up with this, which you’re all welcome to use if you ever want to spice things up.

Word has it that if this meeting was deemed successful, there may be another one in 2013. If so, and, barring any major catastrophes in my personal life — see you there.

Presentations. 1. Yet another poster from the Frankland lab. I’m not sure that it’s surprising but certainly elegant and essential work. It’s known that hippocampal lesions can more reliably produce retrograde memory deficits than anterograde memory deficits. This is because in the normal brain a hippocampal strategy often dominates and therefore damage occurring after learning will structurally destroy the memory. In contrast, post-damage learning can be relatively spared because other brain structures can compensate. This study tested whether adult-born neurons play a similar role in learning by using mice with diptheria toxin receptors specifically expressed in adult-born neurons. This allowed them to kill new neurons either before or after training in discriminative fear conditioning and water maze tasks. Consistent with the general hippocampal story described above it was only when the neurons were killed after learning that memory was degraded. 2. The environment-specific new neuron activation story was interesting but is still a work in progress. Basically, it appears that if enriched environment #1 enhances survival of new neurons during their immature stage then only that environment (and not a different enriched environment #2) is capable of activating those neurons when they’re mature. The problem was that the enriched environment #2 was not capable of enhancing new neuron survival (which is in itself kind of interesting – they speculated that because it was very open, with no hiding places, it may have been stressful) and so it also may not be as capable of activating new neurons. Apparently they’re testing different enriched environments to determine which types enhance neuronal survival. Once they get 2 environments that are equally capable of enhancing survival, it will be interesting to see the extent to which neuronal activation is specific to the environment that the new neurons experienced previously. 3. Lastly a bit of neuroendocrine anatomy was interesting to me – people have long wondered how the hippocampus could be modulating the endocrine stress response. The hippocampus has many glucocorticoid receptors and lesions of the hippocampus increase circulating glucocorticoids but the circuitry needed to regulate the HPA axis has never been clear. This poster used lesions, tracer experiments and immediate-early gene imaging and concludes that multiple higher-order regions of the brain (mPFC and hippocampus) converge on the Bed Nucleus of the Stria Terminalis, which then exerts inhibitory control over the HPA axis.

Blogosphere. Being selected as an official neuroblogger more than doubled the traffic to Functional Neurogenesis over the last couple weeks. Most of the SFN neurobloggers got a passing grade here (phew). Some interesting discussion there about whether writing about science could be a waste of time inasmuch as it takes away from experiments / papers / funding. Interesting in that I’m surprised it could be so frowned upon (fortunately, I’ve never been the victim of such frowning).

And now for the final day of Photos of Popular Posters!

Whereas I have previously focussed only on popular posters, here I found an aisle imbalance:

Many people were interested in Learning and Memory: Physiology (right) but Modulation of Fear/Aversive Learning and Memory (left) appears to be a topic that SFN could eliminate for SFN 2011. Zeroing in on the hotness of the above scene I found that:

Spaces within spaces: Rat posterior parietal cortex neurons register position across three spatial scales simultaneously by Doug Nitz was getting all the attention. More attention than any of the other PPP winners and so it gets dubbed the SFN2010 most popular poster. In fact, I might have put this presentation in my itinerary had I come across it in the online abstracts so, take home message: always be sure to crowd around the already-crowded posters.

Using POMC-Cre to drive expression of tetanus toxin in dentate granule neurons the authors were able to inhibit synaptic transmission in the mossy fiber output of the dentate gyrus and investigate its role in pattern separation (defined behaviorally as the ability to distinguish fine spatial/sensory details) and pattern completion (ability to recreate a fully memory from partial cues). Interestingly, the transgenic model did not block transmission in new neurons aged 4-6 weeks-old and younger. This was demonstrated with a viral strategy, where newborn granule neurons were made to express both mCherry-VAMP2 and synaptophysin-GFP. Examining puncta in mossy fiber boutons it was clear that immature neurons had both red- and green-labeled boutons and that, with age, tetanus toxin degraded the fluorescently-labeled VAMP leaving only green boutons (the immunohistochemistry images were beautiful in this poster by the way).

So, with the model established, they went on to perform discriminative contextual fear conditioning as a test of pattern separation: mice were required to learn that one context predicted shock and another context did not. Surprisingly, given the often-cited role of the dentate gyrus in pattern separation and context discrimination, mice lacking mossy fiber transmission were better at this task. The pattern completion task was also contextual fear conditioning-based but used the immediate shock deficit (aka context pre-exposure facilitation effect) paradigm. Here, mice failed to learn to fear a context paired with shock if they spend only short amount of time in the context (here it was 10s I believe). However, pre-exposing the mice to the context several weeks earlier enabled control mice to learn despite the brief training experience (i.e. training/shocking with only brief cue exposure, they were able to “pattern complete” and retrieve the full memory of the context). But the mice lacking mossy fiber transmission were impaired at this task.

What the heck does this mean? Well, one possibility is that mature granule neurons/mossy fibers impair behavioral pattern separation and, upon inhibiting them, a pattern separation function of immature neurons is uncovered. This is a bit of a stretch I think. I wonder whether such a population of immature neurons (4 week-old neurons are just becoming functional) could have a significant impact. But it’s possible and would be fascinating to test whether eliminating this additional population would change the behavioral phenotype. These findings also seem at odds with previous studies from the same group showing that NMDAR dysfunction in the dentate gyrus leads to impaired context discrimination rather than the improved context discrimination observed here. Then again, blocking NMDARs is a completely different type of lesion than blocking an entire output pathway…in any case, I think we can agree – great food for thought.

And now time for PPP!

Maybe I have no idea what’s interesting or important. To obviate this potential problem, here are Photos of Popular Posters. What everyone else found interesting. In the MMM/LLL area…

A computational model of the role of orbitofrontal cortex and ventral striatum in signalling reward expectancy in reinforcement learning. I walked by this poster twice – each walk separated by about and hour and both times PACKED! You will notice the high degree of chin-touching in the audience – an additional measure of popularity that I will include in SFN2011’s reporting (once I get the method down).

The human substantia nigra and ventral tegmental area compute experiential and fictive error learning signals. Congrats – big crowd especially considering that, as far as I know, there’s not even adult neurogenesis in these brain regions!

Corticostriatal and glutamatergic mediation of cognitive flexibility and habit, by Brigman et al. Congratulations – you were popular.

And, Optogenetic manipulation of locus coeruleus norepinephrine neurons: Effects on set-shifting, by Cope et al. Also popular.

Supplemental Methods & Results: Afternoon strolls in the development and in vivo-electrophysiology-during-behavior themes revealed a number of potentially far more popular posters. However, these posters were excluded from the experiment because many of the poster “viewers” were not actively engaged with a poster. Instead, they displayed dazed looks in other directions and appeared to actually be moving, perhaps suffering from SFN exhaustion and traffic jamming.

Brain Control

The other presentation was supposed to educate animal researchers about….what is done to animals during research.

I’ve been to a lot of Society for Neuroscience meetings and this was the first time I’ve seen these guys. Again, I didn’t have time to go over the data but usually when I read papers I just look at the pictures anyway, and theirs were pretty good. No, in all seriousness, experimenting on animals is not a light matter and I can understand that it’s not for everyone. But given the incredibly hard work being done to ease human suffering, and the amazing technological advances that are being made, it’s not clear to me that animal research is obviously flawed, wasteful, unethical, or fraudulent. Now that I look closer I also wouldn’t be surprised if these “representative images” don’t quite illustrate the full story either.

And on to lighter fare:

Maybe you’ll arrive at a talk only to find the room filled to capacity and you, unable to enter

Maybe (since I can’t find a ref) this is because there is (an insane) a fair number of attendees: (36,000)  30,654

Glenn Close is an actress though I can’t actually tell you what she’s been in. She gave a talk about mental illness and there was a post about it that clogged up the #sfn10 hashtag pipeline.

Theme H posters get a plug on the home page for this year’s meeting. Apparently people need to be reminded to visit them. They have to do with history, society, and maybe some other stuff.

1) 405.14/MMM34 – Mossy fiber input for pattern separation and pattern completion
*T. NAKASHIBA¹, J. CUSHMAN², K. A. PELKEY³, C. J. MCBAIN³, M. S. FANSELOW², S. TONEGAWA¹;
¹The RIKEN-MIT Ctr. For Neural Circuit Genetics, The Picower Inst. For Lear, CAMBRIDGE, MA; ²Dept. of Psychology, UCLA, Los Angeles, CA; ³NICHD, NIH, Bethesda, MD

So by inserting, like, 27 transgenes a mouse was created where the mossy fibers, the axons that connect the dentate gyrus to CA3, can be inducibly silenced. Since there are a number of pathways that connect the cortex to CA3 this looks like an effective way to determine the importance of this one pathway for behavior and physiology. It appears that the mossy fiber pathway promotes a pattern completion function rather than a pattern separation function. Using discriminative contextual fear paradigms, mice lacking mossy fiber functionality were better at discriminating related contexts, and worse at a task that required them to treat related contexts differently.

2) 709.24/MMM74 - Increased connectivity with inhibitory interneurons underlies functional integration of newborn neurons in the dentate gyrus of the hippocampus
*L. RESTIVO¹, M. SAKAGUCHI¹, P. W. FRANKLAND^1,2,3;
¹Program in Neurosciences & Mental Hlth., The Hosp. For Sick Children, Toronto, ON, Canada; ²Inst. of Med. Sci., ³Dept. of Physiol., Univ. of Toronto, Toronto, ON, Canada

Using a GFP retrovirus, this looks to be latest of only a few studies of the mossy fiber output of new neurons. And the only one that has looked at new neuron mossy fiber synaptogenesis in response to learning (recently it was shown that learning alters afferent synaptogenesis in new neurons). Basically, it appears that new neurons, after water maze training, have increased synaptogenesis onto inhibitory interneurons without any change in the number and size of synapses onto excitatory principal CA3 neurons. Neat-O.

3) 100.8/KKK24 - Encoding to consolidation: An optogenetic probe reveals continuous modulation of hippocampal information processing by behavioral state
*C. KEMERE¹, M. F. CARR¹, M. P. KARLSSON², F. ZHANG³, K. DEISSEROTH⁴, L. M. FRANK¹;
¹UCSF, San Francisco, CA; ²HHMI-Janelia Farm, Ashburn, VA; ³Society of Fellows, Harvard Univ., Cambridge, MA; ⁴Stanford Univ., Stanford, CA

The results are a little vague but the question and method are both pretty interesting here. Directing channelrhodopsin to dentate gyrus neurons and using a probe that can both light-activate those neurons and simultaneously record from downstream CA3 and CA1 these authors examined how dentate gyrus activation modulates activity in CA3/CA1 during different behavioral states. And they argue that information processing does not simply alternate between discrete states during locomotion vs. stillness/sleep, but rather that there is a continuum between these states that varies with how fast the animal is moving.

So you end up supplementing your name searches with some combinatorial keyword strategy.  You find some cool posters.  And then you discover that your blogging partner already found the same posters and posted about them two days ago.  So you ice your scrolling finger and post about a few cool abstracts he didn’t already mention.

JSS, our very own functional neurogenista (neurogenisto?) extraordinaire, has a doozy this year, implicating adult-born neurons in feedback regulation of the HPA axis stress response.  Glucocorticoids released by the adrenals in response to stress activate receptors in the hippocampus (and other regions), which, in turn, suppress further glucocorticoid release.  Jason shows that this hippocampal feedback regulation is impaired when adult hippocampal neurogenesis is blocked by either of two different methods.  The convergent results with two different methods constitutes strong evidence that the impairment was caused by the arrest of neurogenesis rather than side-effects of either method of arresting neurogenesis.  This is exciting because it may be the best evidence yet linking adult hippocampal neurogenesis to a specific physiologic function.  The finding could also provide important insights into the still-poorly-understood role of adult hippocampal neurogenesis in depression and in the therapeutic effects of antidepressant drugs.  For instance, previous work suggests that increased neurogenesis may mediate some anxiolytic effects of antidepressant drugs.  Jason’s result suggests a potential mechanism: the antidepressant-induced increase in neurogenesis moderates stress-induced HPA activity.

It sure would be nice to know more about the gene expression profiles of neural progenitors and immature neurons in the adult brain.  With this information, you could devise new, more precise strategies for targeting genetic manipulations to these populations.  You could potentially identify gene networks that make immature neurons more excitable and plastic than their mature counterparts.  You could identify genes that cause some neural stem cells to divide while others remain quiescent, or that cause some progenitors to produce neurons while others produce glia or another copy of themselves.  Looks like someone is onto this.

Contextual fear memories are initially stored in the hippocampus.  But over time, they appear to migrate elsewhere.  We believe this because of experiments demonstrating that lesions to the hippocampus shortly after acquisition of contextual fear conditioning impair recall of the memory, whereas lesions made several weeks after acquisition usually do not impair recall.  So, where do the memories go and how do they get there?  Using immediate early genes, Paul Frankland’s lab has analyzed brain activity in response to recall of recent versus remote memories.  According to the abstract, the remote memories evoke activity in a broad swath of cortical and subcortical space, suggesting that remote memories have a highly distributed neural representation. I am looking forward to visiting the poster and finding out what the recent memory representation looks like.  Is it exclusively hippocampal, meaning that memories migrate over time from the hippocampus to a highly distributed extrahippocampal network? (Doubt it.) Or is the recent memory also highly extrahippocampal?  Perhaps the extrahippocampal network is involved all along, with its strength increasing over time so that the hippocampus is eventually rendered superfluous.

1) 31.20/C37 - Dentate network activity modulates integration of newborn granule cells
*F. KLEINE BORGMANN¹, J. GRÄFF², N. TONI³, I. M. MANSUY^4,5, S. JESSBERGER¹;
¹Inst. of Cell Biology, Swiss Federal Inst. of Technol. (ETH), Zürich, Switzerland; ²Brain Res. Inst., Univ. of Zürich, Zürich, Switzerland; ³Univ. of Lausanne, Lausanne, Switzerland; ⁴Brain Res. Inst., Univ. of Zurich, Zürich, Switzerland; ⁵Swiss Federal Inst. of Technol. (ETH), Zürich, Switzerland

This looks interesting because there is so little known about how neuronal activity regulates neurogenesis. In 2007 Toni et al. suggested that dendritic filopodia on new neurons form synapses with presynaptic boutons that have already formed a synapse onto a different (presumably mature) neuron. The question addressed here is whether altering excitability/plasticity at those pre-existing synapses affects the subsequent formation of new neuron synapses. In other words, if you make old neurons more plastic, will they outcompete new neurons for synaptic space? Seems maybe they do.

2) 203.9/KKK52 - Coding of temporal context in the hippocampus: Do rate codes offer insight into a time-of-day signature?
F. T. SPARKS*¹, E. A. MANKIN*², B. SLAYYEH², R. J. SUTHERLAND¹, *J. K. LEUTGEB²;
¹Dept of Neurosci., Univ. of Lethbridge, Lethbridge, AB, Canada; ²Ctr. for Neural Circuits and Behavior, Neurobiol Section, Div. of Biol Sci., UCSD, LA JOLLA, CA

We all know the hippocampus is important for episodic (-like) memory yet activity in hippocampal neurons is usually only measured in relation to spatial information. Memories also often contain temporal information and Rob Sutherland (one of the authors) has shown that rats indeed integrate time-of-day information into their memories. Here, measuring electrophysiological activity in hippocampal neurons, it is reported that 1) hippocampal neurons fire when a rat is in a specific spatial location, as expected; 2) when nearby contextual features are altered (square vs circular exploration chamber) the same population of neurons are active in the same places but they fire at different rates (rate coding); 3) what is unique here: hippocampal neurons also used a rate code to differentiate between a given context explored in the morning vs the afternoon. Thus, time-of-day is a contextual feature that is encoded in the hippocampus. Interestingly, it is reported that the rate codes for spatial and temporal information are carried by different populations of neurons.

3) 330.6/A6 - Experience specific information encoding by newborn neurons of the adult dentate gyrus
*G. D. CLEMENSON, JR, F. H. GAGE;
Salk Inst., La Jolla, CA

This presentation builds on Kee 2007, who showed that 10-week-old neurons are only activated in the water maze if they were functional at the time of the original water maze training, and Tashiro 2006 who claimed that, when a mouse re-experiences something, it is new neurons that were in their critical period during the original experience that are activated. We still have a ways to go before we understand how faithful new neurons are in their responding to different experiences – their enhanced plasticity and unique physiology has caused some speculation that they could be promiscuous, participating in many different experiences. This study seems like it may have the best evidence that young neurons are in fact quite selective in what they encode.