We have previously shown that exposure of rats to constant light (LL)
induced a decrease in NO synthase (NOS) activity in the pineal gland.
We present here the evidence that chronic (5 days) norepinephrine (NE)
or isoproterenol treatment prevents the effect of LL and enhances pin
eal NOS activity in LL animals. This effect of NE appears to be mediat
ed by beta-adrenoceptors, because it was not mimicked by the alpha-ago
nist phenylephrine. Pineal NOS activity was reduced in 16-h light/8-h
dark animals treated for 4 days with the beta-adrenergic antagonist pr
opranolol but not with the alpha(1)-antagonist prazosin, indicating ag
ain an involvement of beta-adrenergic receptor in the control of NOS.
Treatment with adrenergic antagonists did not affect cortical NOS acti
vity, suggesting that the control of NOS is different in these two tis
sues or that the pineal expresses a specific isoform of the enzyme. Ta
ken together, these data suggest that NE controls NOS in the pineal gl
and through beta-adrenergic receptors. To our knowledge, this represen
t the first demonstration of a regulation of NOS by a neurotransmitter
in the CNS, as assayed under V-max conditions.