Figure 7.

Hypothetic representation of the glutamatergic modulation of neurovascular coupling in the cerebellum. Activation of NMDA receptors (NMDA-R) on stellate cells by glutamate (Glu) induces NO synthesis and release (inhibited by L-NAME) and subsequent vasodilation of neighboring blood vessels through activation of sGC (inhibited by ODQ). In contrast, activation of glutamate receptors (GluR) on Purkinje cells induces endothelin 1 and arachidonic acid (AA) release from membrane phospholipids (MPL). Endothelin 1-induced vasoconstriction is blocked by the selective ETA receptor antagonist BQ-123. In glia, arachidonic acid is successively metabolized into prostaglandin H2 (PGH₂) by cyclooxygenase (COX; inhibited by aspirin) and into thomboxane A₂ (TxA₂) by thomboxane synthase (TxS; inhibited by ozagrel). Release of TxA₂ constricts neighboring blood vessels via thromboxane A₂ receptors (TP). Although some of these pathways can also occur in Purkinje cells, they were omitted from the figure for clarity. Arg, Arginin.