To what degree is brain neurotransmission activity a balanced Gaba / Glutamate system ? EEG wave is now interpreted as being the summation of inhibitory gaba and excitatory glutamate neurons. (canonical cortical circuit hypothesized by Douglas and Martin (1990)) Some research says that Gaba lies in basket cells, others in Pyramidal, while other transmitters are small in number and are co-active with glutamate.

The synthesis of GABA is linked to the Kreb's cycle derived from Glutamate. Since Glutamate fires in all 100 billion brain neurons while Gaba is the main inhibitory neuron then does this imply that GABA is also present equally or in a large percentage of all neurons. Haven’t had any luck yet in finding papers on Such pervasiveness of GABA throughout every neuron. Would be glad to have any refs for data about this for a review on neurochemical distribution.

Thanks

FL

Sprinklehopper,
A straightforward answer to your question of balance between GABA and glutamate is difficult to give. I hope this explains why:
1. There is no controversy about GABA being the major inhibitory neurotransmitter in the brain; neurons manufacturing and releasing GABA can be found in great abundance, although they are perhaps less numerous than neurons manufacturing and releasing GABA.
2. It is not common for any given neuron to produce more than one neurotransmitter. In fact you will often see neurons classified based on the major type of neurotransmitter they produce and release (e.g gabaergic, glutamatergic, dopaminergic, etc. neurons).
3. You must know about synapses. So when a neurotransmitter is released into synaptic cleft it diffuses to the postsynaptic site, a neuron that has receptors for different kinds of neurotransmitters. Now, it is VERY common for any given neuron to have receptors to different neurotransmitters, it is extremely common for a neuron to have receptors to both GABA and glutamate. I must add that although these different neurotransmitter receptors are likely to be present in the same neuron, they may or may not be at the same synapse. So your question of balance depends essentially on how many gabaergic and glutamatergic inputs a given neuron receives and how many (and what kind) of GABA and glutamate receptors are available to respond to these inputs. While this may be a reasonable question to ask about a particular neuron it is unlikely that we'll be able to answer this question with any considerable accuracy about the whole of "brain neurotransmission". In fact, it is unlikely even that there is a definite excitation/inhibition ratio applicable to all the neurons in the brain.
You are right in noticing that GABA can be found in basket cells, pyramidal cells are usually excitatory (glutamatergic) although they do have GABA receptors. There is a great variety of other inhibitory neurons most of which inhibit by releasing GABA; some examples are Golgi cells of the cerebellum, stellate and other types of the so-called interneurons. For information of this sort you should probably look in any more or less detailed neuroscience textbook.

Thank you for that reply utnap. It is helpfull to re-remember that Gaba synapses are on glutamate neurons. Since Gaba is derived from glutamate i see them as being opposites of the same system. That is that Gaba puts the brakes on glutamate. So is Gaba brain wide ? When I last read about that the Gaba receptors they seemed to be more midbrain transcallosal. Perhaps that is the optimum point for whole brain regulation.

What i had thought is that Gaba or Glutamate are gates for ion energy. That we know anyway, but specifically that Gaba A and C receptors trigger chlorine for inhibition and glutamate receptors trigger sodium for excitation. They also trigger potassium and calcium respectively.

Sprinklehopper,
It is indeed an amazing fact that the major excitatory (glutamate) and the major inhibitory (GABA) neurotransmitter are part of the same biosynthetic pathway. You have to remember though, that it doesn't mean that both GABA and glutamate are synthesized in the same neuron. It takes a certain enzyme called glutamic acid decarboxylaze to convert glutamate to GABA and it is only neurons expressing this enzyme that can manufacture GABA. It is interesting to think, as you suggest, of GABA synthesis as means to curtail synthesis of glutamate (of course, certain enzymes must be present for glutamate synthesis to occur also).
I don't know what context you saw the "midbrain transcalossal" localization of GABA receptors, but while there probably are GABA receptors at both the targets of transcalossal neurons and targets of midbrain neurons, I assure you that these targets are by far not the only neurons in the nervous system to express GABA receptors. And, yes, in a loose sense, GABA is brainwide.
And you are once again making a keen observation that GABA and glutamate receptors exert their opposite actions by conducting different kinds of ions. I think you may be visualizing the process in a slightly incorrect way. If not, you should forgive me this short explanation: both GABA and glutamate receptors are proteins piercing the lipid bilayer of neuronal cell membrane. These proteins have the capacity to open, like a gate, whenever GABA binds to a GABA receptor or glutamate -- to a glutamate receptor. When this happens a receptor opens and creates a pathway into the inside of the cell. In case of GABA receptors this patway/opening is selective for chloride ions, in case of glutamate the patway is selective to sodium, potassium, and sometimes calcium ions. As you probably know chloride ions are negatively charged so when they are allowed into the cell they hyperpolarize it (make it more negative) and therefore harder to depolarize (excite). When sodium or calcium ions (which are are positive) are allowed into the cell through glutamate-gated receptors the cell is on the opposite depolarized (excited).
The interplay between excitation and inhibition in the nervous system is truly something extraordinarily interesting when you think about single neurons (themselves ignorant of you as a person). The outcome of this interplay is absolutely mind-boggling when you imagine that it creates a self-organizing dynamic system that defines our perceptions, memories, plans, our entire personalities.

Yes, GABA and Glutamate are distributed throughout the brain, though my understanding is that primary and secondary sensory areas have relatively more GABA than 'higher' association areas, which may suggest a relatively greater role for GABA in the initial stages of sensory processing versus later stages. I'm not sure offhand whether Glutamate exhibits a similar pattern or not.

Dear Meta-Brain Neuroscientists,

I am curious to know if anyone is aware that there is fairly/relatively new information on the relationship between the GABA & GLUTAMATE and OCD?

I found this post very interesting (that which I could follow - LOL), since I am currently trying to understand the GABA & GLUTAMATE and the relationship between the two. I suffer from OCD and understand Namenda is providing relief for this mental disorder. Namenda is a re-uptake inhibitor for Glutamate and is currently approved by the FDA for Alzheimer's.

One question I have, if you would please -
I do not understand which is the "precursor" to which - GABA or GLUTAMATE (if there is such a relationship). The reason for my question is I am not sure if I need to focus my research on GABA or GLUTAMATE in my search for an augmentor for my current medications. I'm curious to know which raises/lowers which, if at all.

Thanks!


Best regards,

Kurt Grossman

(This is for my personal information and any medications or OTC herbs... I might try will come with the supvision and approval of my physicians.)

glutamate is a precursor of GABA