Neurochemical and Behavioral Features in Genetic Absence Epilepsy and in Acutely Induced Absence Seizures
Figure 11
A tentative model of intraneuronal integration triggered by transduction signal. GLU-R: glutamatergic receptors; GABA(A), GABAA receptor; DA-R: dopamine receptor; E: second messenger synthesizing enzyme; SF: phosphorilation substrate; G: G-protein, PK: different type of protein kinases; CaMK: calcium/calmodulin-dependent protein kinase. Metabolic reactions mediated by glutamatergic receptors are shown as solid lines. Metabolic reactions mediated by GABAA receptor are shown as dashed lines. Metabolic reactions mediated by dopamine receptors are shown as dotted lines. Intracellular metabolic feedback loops (autoregulation) are shown as the respective thick lines. For other details, see text.
