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 s
tudy the contribution of stellate neurons in the increase of cerebellar blo
od flow (BFcrb) produced by neural activation. Crus II, a region of the cer
ebellar cortex that receives trigeminal sensory afferents, was activated by
stimulation of the upper lip (5-30 V; 10 Hz), and BFcrb was recorded at th
e activated site by the use of a laser-Doppler flow probe. In wild-type mic
e, 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 homozygou
s mice. In contrast to the cerebellum, the increases in somatosensory corte
x blood flow produced by upper lip stimulation was not attenuated in D2-nul
l 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 majo
r source of nitric oxide (NO) in the cerebellar molecular layer. The neuron
al NO synthase inhibitor 7-nitroindazole attenuated the vascular response t
o 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 res
ponse. 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.