Mechanism action of Butethal
Butethal binds at a distinct binding site associated with a Cl- ionopore at the GABAA receptor, increasing the duration of time for which the Cl-
ionopore is open. The post-synaptic inhibitory effect of GABA in the
thalamus is, therefore, prolonged. All of these effects are associated
with marked decreases in GABA-sensitive neuronal calcium conductance
(gCa). The net result of barbiturate action is acute potentiation of
inhibitory GABAergic tone. Barbiturates also act through potent (if less
well characterized) and direct inhibition of excitatory AMPA-type
glutamate receptors, resulting in a profound suppression of
glutamatergic neurotransmission.
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