Vibrissal stimulation raises cerebral blood flow (CBF) in the ipsilateral s
pinal and principal sensory trigeminal nuclei and contralateral ventroposte
romedial (VPM) thalamic nucleus and barrel cortex. To investigate possible
roles of adenosine and nitric oxide (NO) in these increases, local CBF was
determined during unilateral vibrissal stimulation in unanesthetized rats a
fter adenosine receptor blockade with caffeine or NO synthase inhibition wi
th N-G-nitro-L-arginine methyl ester (L-NAME) or 7-nitroindazole (7-NI). Ca
ffeine lowered baseline CBF in all structures but reduced the percent incre
ase during stimulation only in the two trigeminal nuclei. L-NAME and 7-NI l
owered baseline CBF but reduced the percent increase during stimulation onl
y in the higher stations of this sensory pathway, i.e., L-NAME in the VPM n
ucleus and 7-NI in both the VPM nucleus and barrel cortex. Combinations of
caffeine with 7-NI or L-NAME did not have additive effects, and none alone
or in combination completely eliminated functional activation of CBF. These
results suggest that caffeine-sensitive and NO-dependent mechanisms are in
volved but with different regional distributions, and neither fully account
s for the functional activation of CBF.