Glutamate Hypothesis of Schizophrenia - The Role of Inhibitory Transmission

The Role of Inhibitory Transmission

The cortico-striatal-thalamic loop, is the source of the ordered input necessary for a higher level upper cortical loop. Feedback is controlled by the inhibitory potential of the cortices. Through 5-HT2A efferents from layer V, transmission, processed, from layer III through the interneuron layer reaches the basal ganglia and brain stem. The core thalamic input to layer I is combined with the ordered matrix input to VI. A process happens with layer III/I and II/III efferents: these circuits are where our self/other perception, and the mechanisms for logic lie.(anteriorly) Also, it is how, through the entorhinal cortex, which almost completely lacks layer IV, can control orbitofrontal and thalamic output from the hippocampus, as well as (indirectly) provide a pathway for hippocampal communication to the other cortices. This is opposed by the frontal lobes, which have much larger granular areas, thus inhibitory potential,from input to the striatum.

Another modulatory factor is the corpus callosum, providing a direct inhibitory connection, interhemispherical, to the cortical layer VI, thus indirectly to layer V. As such, the halves of the brain exert some control over basal input of the other side, but can only inhibit due to the GABAergic nature of the corpus callosum. The root of this control is an extraordinarily complex dihemispherical beat frequency in layer IV between layer V and layers II/III. One might say qualia happens here. How the other side can (indirectly) inhibit the 5-HT2A signal cascade, is crucial for the development of language. It requires highly structured left side structures allowing for the imagination of the formants, and the mouth movements that correspond to them. It also needs a more distributed, contextual, reality based side, to integrate the naturally nonsensical medium of language back to intuitive sensory/spatial analogies.

Dopamine hypothesis of schizophrenia elaborates upon the nature of abnormal lateral structures found in someone with a high risk for psychosis.

Read more about this topic:  Glutamate Hypothesis Of Schizophrenia

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