Parvalbumin and GABA Microcircuits in the Mouse Superior Colliculus.

The mammalian superior colliculus (SC) is a sensorimotor midbrain structure responsible for orienting behaviors. Although many SC features are known, details of its intrinsic microcircuits are lacking. We used transgenic mice expressing reporter genes in parvalbumin-positive (PV) and gamma aminobutyric acid-positive (GABA) neurons to test the hypothesis that PV neurons co-localize GABA and form inhibitory circuits within the SC.

A circuit model for saccadic suppression in the superior colliculus.

Attenuation of visual activity in the superficial layers (SLs), stratum griseum superficiale and stratum opticum, of the superior colliculus during saccades may contribute to reducing perceptual blur during saccades and also may help prevent subsequent unwanted saccades. GABAergic neurons in the intermediate, premotor, layer (SGI), stratum griseum intermedium, send an inhibitory input to SL. This pathway provided the basis for a model proposing that the SGI premotor cells that project to brainstem gaze centers and discharge before saccades also activate neighboring GABAergic neurons that suppress saccade-induced visual activity in SL.

Identity of a pathway for saccadic suppression.

Neurons in the superficial gray layer (SGS) of the superior colliculus receive visual input and excite intermediate layer (SGI) neurons that play a critical role in initiating rapid orienting movements of the eyes, called saccades. In the present study, two types of experiments demonstrate that a population of SGI neurons gives rise to a reciprocal pathway that inhibits neurons in SGS. First, in GAD67-GFP knockin mice, GABAergic SGI neurons that expressed GFP fluorescence were injected with the tracer biocytin to reveal their axonal projections.

Neurogranin expression in stably transfected N2A cell line affects cytosolic calcium level by nitric oxide stimulation.

To test a cellular effect of rodent neurogranin (Ng) oxidation as compared to Ng phosphorylation, we develop a cell model capable of stable expression of Ng using the Tet-On system, and determine whether Ng oxidation regulates intracellular calcium level. Our results show that Ng oxidation by nitric oxide donor induces an increase of [Ca(2+)](i) in Ng-expressed cells as compared to the control cells without expressing Ng. These results suggest that Ng oxidation plays a significant role in intracellular Ca(2+) homeostasis, essential for the activated signaling networks in learning and memory.