Stellate neurons mediate functional hyperemia in the cerebellar molecular layer.

Mice lacking cyclin D2 have a profound reduction in the number of stellate neurons in the cerebellar molecular layer. We used cyclin D2-null mice to study the contribution of stellate neurons in the increase of cerebellar blood flow (BFcrb) produced by neural activation. Crus II, a region of the cerebellar cortex that receives trigeminal sensory afferents, was activated by stimulation of the upper lip (5-30 V; 10 Hz), and BFcrb was recorded at the activated site by the use of a laser-Doppler flow probe. In wild-type mice, upper lip stimulation increased BFcrb in crus II by 32 +/- 2%. The rise in BFcrb was attenuated by 19% in heterozygous mice and by 69% in homozygous mice. In contrast to the cerebellum, the increases in somatosensory cortex blood flow produced by upper lip stimulation was not attenuated in D2-null mice. The field potentials evoked in crus II by upper lip stimulation did not differ between wild-type and D2-null mice. Stellate neurons are a major source of nitric oxide (NO) in the cerebellar molecular layer. The neuronal NO synthase inhibitor 7-nitroindazole attenuated the vascular response to crus II activation in wild-type mice but not in D2-null mice, suggesting that stellate neurons are the major source of NO mediating the vascular response. The data provide evidence that stellate neurons are a critical link between neural activity and blood flow in the activated cerebellum and that NO is the principal effector of their vascular actions.