Thanks Matt, great response.
Given some clinical evidence of frontal theta activity being indicative of
pathology (also noted recently that during interferon treatment for Hep C a
pronounced increase in theta power band), your comments re GABA regulation
of the same is very interesting.
Matt Jones <jonesmat at physiology.wisc.edu> wrote in message
news:b86268d4.0109110739.18d2031b at posting.google.com...
> "John H" <John at faraway.com.au> wrote in message
news:<C5Lm7.2370$iH4.174324 at ozemail.com.au>...
> > Matt,
>> > Inhibition.
> > Thanks for the evolution lesson. Reading today a basic neuro primer
> > reads journal articles while reading primers) the author stated that in
> > humans interneurons occur in very high numbers relative to other
> > believe Matt that you have done research into GABA(still are?) and
> > you can provide any insight into the idea of this high density of
> > interneurons. If true, why, what is so special about human brains that
> > would require so many interneurons?
> > No, I cannot make any sense of inhibition being first. What a mystery
> > John.
>>> I think Richard makes interesting points elsewhere in this thread
> about why humans would have more interneurons, and I haven't really
> thought much about -why- we should have a lot, and in fact wasn't even
> aware that we did. I think Richard is referring to "interneurons" in
> the broadest sense, i.e., any neuron that doesn't project outside of
> aits local circuit, but interconnects cells within the circuit. These
> can be either excitatory or inhibitory. Below, I am referring to the
> narrower meaning of GABAergic inhibitory interneurons.
>> Mostly, I wonder why we have so few! Here's what I mean: In cortex and
> hippocampus (and many other places), the projection neurons that send
> signals to other brain regions tend to be excitatory, often arranged
> in a regular sheet, and are very numerous, outnumbering inhibitory
> interneurons by about 10-to-1. Meanwhile, the inhibitory neurons are
> fewer, and scattered around without nearly as much obvious
> orientational regularity. Also, there are often just one or two kinds
> of excitatory neurons, but lots and lots of distinctly different kinds
> of interneurons. In hippocampus, there are about 3 main types of
> excitatory cells (granule cells and CA1 and CA3 pyramidal cells), but
> there are about 20 kinds of identifiable interneuron types (depending
> on who you read). These interneurons can be distinguished by the
> histochemical markers they express (i.e., calcium binding proteins,
> neurotransmitter receptors), by their location and shape, and by
> -where- onto the principle cells they form their inhibitory synapses
> (i.e., dendrites vs soma vs axon). Also, they tend to make thousands
> of synapses through axons that branch widely and contact many many
> principal cells at once.
>> Well, it's probably -not- just to stop principal cells from firing.
> You don't need anything like this much complexity to do such a
> pedestrian task. One of the more well-studied aspects of interneuron
> function appears to be that they control the periodicity of
> oscillations, for example theta and gamma oscillations. These
> oscillations have been proposed to act something like a clocking
> signal, that allows different circuits to synchronize the activity of
> many principal cells, thereby marking those cells as conveying
> information about a common object or percept. The evidence for this
> role of interneurons in dictating oscillation properties is now quite
> strong, though the "purpose" of the oscillations themselves is still
> very much in debate.
>> It turns out you can get fairly interesting behavior out of circuits
> that contain -nothing- but inhibitory neurons, because each cell has
> its own native excitability even without excitatory synaptic drive.
> Thus, two interneurons coupled to each other can produce either
> synchronous or alternating oscillations. Many interneurons wired up
> together can create a "pacemaker" circuit, even though none of the
> cells themselves are inherently periodic. Interneuron-interneuron
> connections are widespread in cortex, and this may be part of their
>> Aside from oscillations, interneurons probably contribute to
> information processing by deciding -exactly- when a target neuron is
> allowed to spike and when not. This is clearly important at the gross
> level, because if you block inhibition you get seizures, and if you
> enhance it, you get amnesia, anxiolysis, analgesia and unconsciousness
> (e.g., almost -all- general anesthetics potentiate GABA-A receptor
> function). However, on a finer level, it makes sense for information
> processing to be able to regulate spiking in a complex way. If you
> want to send a high amount of information over a channel, you need to
> be able to send an awful lot of different patterns, not just an
> oscillation with a fixed frequency. For example, a perfectly periodic
> pulse train contains literally only 1 bit of information (i.e.,
> whether the train is on or off). That is, it can be compressed into a
> single binary number (on or off). However, a string of pulses
> separated by random times cannot be compressed at all. Therefore it
> takes as many bits to describe it as there are time intervals in the
> pulse train (i.e., t contains a lot more information). Highly
> random-looking spiketrains are much more likely to be high in
> information content than regular ones (note that it can therefore be
> quite difficult to tell the difference between efficient signalling
> and noise).
>> Inhibition helps neurons to produce highly random-looking spiketrains
> (e.g., see papers by Dieter Jaeger), and thus increases the
> information capacity. It is not clear whether this capacity is actualy
> used, but it is there. And largely because of the complexity of
> inhibitory connectivity.