Neuropharmacological profile of selected areas responsible for the inhibition of P50 wave: from the P50 wave to off-label treatment of schizophrenia
Abstrakt
Patients suffering from schizophrenia have been shown to ex- hibit impaired P50 ERP amplitude-reduction to the second (S2) relative to the first (S1) of identical brief auditory stimuli. This reduction is often mentioned in connection with the inability to filter redundant sensory stimuli typically manifested as in- ability to gate neuronal responses related to the P50 wave [1, 2].
The key neuronal structure responsible for the sensory gating process is the hippocampus. Inhibition of redundant stimuli in the hippocampus is affected via the release of glutamate from excitatory pathways, which is controlled by GABAB receptors.
It is closely connected with a physiological deficit of hippocampal GABAergic interneurons, which demonstrates neuropathological changes in schizophrenia. Several drugs are able to improve sensory gating, the effect of which is explained by their ability to disinhibit GABAergic neurons in the hippocampus.
The effect of setrons may be an example of such effective gabaergic interneurons disinhibition. This antagonist of 5-HT 3 receptors increased (by disinhibition of gabaergic interneurons) release of acetylcholine, which by agonism of alpha7 nicotinic receptors improved auditory gating [3].
Some of the P50 source analysis leads to the conclusion that while the temporal cortices are the main generator of the P50 component, the prefrontal cortex seems to be a main contributor to the process of sensory gat- ing (P50 amplitude reduction) [4]. The aim of our poster is to interlink a pharmacological profile of neuronal areas that are involved in the inhibition of P50 wave with clinical treat- ment of schizophrenia.
We believe that the neuropharmacological aspects of P50 wave offer an interesting hypothesis relating mainly to the pharmacological augmentation strategies. Some of them are suggested and explained further in our poster communication.