hippocampal neurons, and they are thought to target and stabilize AMPARs to synapses
(Meng et al., 2003). Moreover, in 2006 Satake et al. ascribed a role for GluR2/GluR3containing
AMPARs in modulation of presynaptic function. They found such AMPARs
in presynaptic membranes of GABAergic interneurons, and by activating them they
managed to inhibit GABA-release into corresponding synapses. Speculatively, a lowering
of GluR3a in anoxic crucian carp may serve to lower the presence of GluR2/GluR3a
AMPARs in presynaptic membranes. Eventually this may lead to increased GABAergic
activity, which in turn will have inhibitory effects on the electric activity of the brain.
Increased levels of extracellular GABA is seen in the anoxic crucian carp brain, and is
thought to function as a metabolic depressant by reducing electric activity (Hylland and
Nilsson, 1999).