kaleidoscopik

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.