The remarkable finding in the present study was the transient appearance of large numbers of EGFP-labeled multipolar cells in the SVZ and IMZ during E16-18. Their morphology has been described in the hippocampal primordium of the rabbit and monkey by the Golgi method, but their significance has not been adequately discussed. The presence of the multipolar cells in the SVZ and IMZ has also been reported in neocortical development. In our study, the multipolar cells accounted for 30.1% of the EGFP-labeled cells in the neocortical primordium of the mouse at E16. Their migratory pattern within the subcortical zone is nonradial and has been described as multipolar migration, as opposed to radial locomotion or somal translocation. The multipolar cells migrate slowly, at about one-fifth the rate of the bipolar cells in the neocortex. - nakahira and yuasa 2005
Thom Yorke remixed a classical piece for a release called ‘Cortical Songs’. The title is intriguing and apparently refers to an orchestra partially controlled by a ‘tiny computer brain’. You can sample the result at imeem, courtesy of pitchfork media. Also, check out the record label’s myspace. They are called nonclassical music and they are repeat offenders in the classical remix department. I might pick up a few things from these guys.
the entire timespan in this picture is two minutes
Our data agree with the prediction that cortical activity flows through chains of synchronized neurons (synfire chains), which are reactivated with high temporal precision. Moreover, we describe a higher order grammar (18), by which these chains themselves can be modules of larger temporal structures (cortical songs), defined by their sequential order of activation, and which can last for minutes. These songs resemble spiking correlates of sequential behavior, like bird songs (19, 20) or spatial navigation (21), and have compressing dynamics, as if the circuit was replaying and modifying previously learned sequences (21–23). The mechanisms that generate and propagate synfire chains and cortical songs must be intrinsic to the cortical circuit, because they are preserved in slices, and might reflect the faithful reactivation of specific circuits (24), mediated by stereotypical synaptic dynamics (25, 26 ) and driven by pacemaker cells (8, 27). Because the activity drifts with time, it is also possible that short-lived patterns, perhaps reflecting ongoing circuit memory, are generated de novo (6, 28).
Hippocampal pyramidal cells can be subcategorized based on several criteria besides anatomical location. For instance, distinct types have been described with relation to firing phase of gamma, change in firing rate during theta, tonic vs phasic firing patterns during theta, apical dendrite morphology, histological markers such as calbindin, and gene expression profiles.
I came across the calbindin distinction reading this recent review from Klausberger and Somogyi. They provided a few specimens in the supplementary info. It’s difficult to tell anything about their overall morphology though.
Not so for these beautiful babies from Spruston’s group. The apical dendrites are clearly either twinned or not. Unfortunately, the group wasn’t able to detect any clear functional difference between the two dendrite morphologies using whole cell recordings. I’m not terribly upset about that though. You might’ve even expected that dendrite morphology would have a lot more to do with network connectivity than intrinsic excitability.
There has been a lot of recent interest in the diversity of GABAergic interneurons throughout the cortex and including the hippocampus. Some folks recently characterized the most abundant (but relatively quiet) type of interneuron in the hippocampus, the Ivy Cell. PING came together and formed a new nomenclature for interneuron classification.
I dig that. We need to know about all the different types of interneurons and which parts of the circuit they act on and how they contribute to / are affected by system oscillations. OTOH, I’m into getting into a little more refined classification of pyramidal neurons. There is a lot less obvious diversity in this population. When we find differences, they are subtle. I think these are the types of neuronal properties that could be controlled by a manageable number of gene regulatory differences. What’s the difference between a phasic and a tonic Theta-ON cell? Is it perhaps expression of some small collection of ion channels or a GABA-A subunit? When we discover these precise single gene types of effects we can turn them back around on the system to allow investigation of the importance of a given physiological property. With combinatorial transgenic manipulations we should already have the capability to shut down firing of, say, Calbindin positive, CA1 pyramidal neurons. Then you can test for altered network properties, stimulus coding properties, and learning/navigation changes.
Anyway. I’m starting a collection of pyramidal pics on flickr. Gonna make me some mooooooo cards.
GABA-A receptors are found on neurons all over your brain. When other neurons send them some GABA they let chloride ions flow across the cell membrane. This typically has the effect of increasing negative ions inside the cell and quieting things down (in the general case, more positive = more active). GABA-A antagonists injected into most any part of the brain would have remove GABA-mediated inhibition to a large extent. Cells would start firing a lot. These chemicals give us a tool to crank up neural activity for a period, to see what happens downstream. They were initially discovered as convulsants (you can imagine how convulsions could arise from reduced neural inhibition). Whoa, I almost thought that second weakest one was called tuRbocurarine. The TigerLillies have a song called QRV that always makes me think of curare on their Gorey tribute album.
It really does fuel disgust for police officers when they blatantly break the law, and it lends plausibility to all other accusations of misconduct (brutality, discrimination, etc). Jimmy Justice tracks them down and takes them to task. I wonder how he avoids arrest on trumped up charges. That is def the scariest part about confronting the beast.
Faculty of 1000 let me know over the weekend that there isn’t enough thujone in vintage absinthe to have any psychotropic effects. Absinthe isn’t any more dangerous than liquor, showing yet again how far U.S. policy on controlled substances is from an empriical basis. From the abstract:
All things considered, nothing besides ethanol was found in the absinthes that was able to explain the syndrome “absinthism.
lots of new types of small RNAs to digest. also, technicolour tracing with the brain bow mouse. and a glutamate receptor review from dr. ehlers who has brought us some really nice vesicle trafficking videos in the past and careful studies of the half-lives of proteins in the post-synaptic density.
too lazy for links
http://www.sciencemag.org/cgi/content/summary/320/5879/1023
http://www.sciencemag.org/cgi/content/full/sci;320/5879/1077
Here’s a fine piece of work from Miwa et al. comparing the role of NR2B subunits in the lateral amygdala versus the CA1 region. NMDA receptors are glutamate receptors heavily implicated in the initiation of synaptic plasticity underlying learning and memory. They consist of NR1 subunits in complex with any of the subtypes of NR2 units (NR2A-NR2D). The story goes that NR2B subunits are prominent early in development but are replaced with NR2A subunits in adulthood. The “doogie mouse” was created by transgenically increasing the NR2B contribution in adult mice because NR2Bs allow a longer time window in which to initiate plasticity processes. SInce then, a story has emerged that NR2Bs are typically found outside the synapse and are only activated when the signal is so strong that glutamate spills over. Miwa et al take that apart by showing through electrophysiology and immunogold electron microscopy that NR2Bs are present in synapses in the LA and CA1. They then run down a whole list of differences between the two regions.
“The properties of NMDA receptors in the LA were distinct from those in the CA1 region: a greater contribution of the NR2B subunit to synaptic NMDA responses ; a higher NR2B/NR2A ratio and a higher ratio of NMDA to AMPA receptor-mediated synaptic transmission ; smaller synaptic currents in the I–V curve of NMDA receptors; and lower Mg2+ sensitivity.”
Ignoring all caveats for a minute, the amygdala is where fear memories are made and the hippocampus is where memories of space, context, and personal events are made. It’s interesting to consider how the different memory systems will respond to drugs that affect NMDA receptors and perhaps disorders such as epilepsy and schizophrenia that are sometimes associated with NMDA receptor malfunctions. Functional contributions of synaptically localized NR2B subunits of the NMDA receptor to synaptic transmission and long-term potentiation in the adult mouse CNS
Hideki Miwa, Masahiro Fukaya, Ayako M. Watabe, Masahiko Watanabe and Toshiya Manabe
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