MJ: 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
Thus, two interneurons coupled to each other can
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
GS: Interesting.....I have believed for a long time
that spontaneous locomotion (spontaneous at the
level of behavior - i.e., no eliciting stimulus) is close
to the first kind of behavior in existence. I believe
that it is more fundamental than the unconditioned
reflex which almost certainly requires excitatory
synaptic drive. So, the notion that inhibitory
neurotransmission is, evloutionarily, the most
primitive, makes some sense to me, given what you
write about oscillations which are almost certainly
the backbone of most central pattern generators.
BTW, what is the evidence that inhibitory
connections are the first to arise?
"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.