The C1 neurons, located in the rostral ventrolateral medulla (VLM), are 
activated by pain, hypotension, hypoglycemia, hypoxia, and infection, as well as 
by psychological stress. Prior work has highlighted the ability of these neurons 
to increase sympathetic tone, hence peripheral catecholamine release, probably 
via their direct excitatory projections to sympathetic preganglionic neurons. In 
this study, we use channelrhodopsin-2 (ChR2) optogenetics to test whether the C1 
cells are also capable of broadly activating the brain's noradrenergic system. 
We selectively expressed ChR2(H134R) in rostral VLM catecholaminergic neurons by 
injecting Cre-dependent adeno-associated viral vectors into the brain of adult 
dopamine-β-hydroxylase (DβH)(Cre/0) mice. Most ChR2-expressing VLM neurons (75%) 
were immunoreactive for phenylethanolamine N-methyl transferease, thus were C1 
cells, and most of the ChR2-positive axonal varicosities were immunoreactive for 
vesicular glutamate transporter-2 (78%). We produced light microscopic evidence 
that the axons of rostral VLM (RVLM) catecholaminergic neurons contact locus 
coeruleus, A1, and A2 noradrenergic neurons, and ultrastructural evidence that 
these contacts represent asymmetric synapses. Using optogenetics in tissue 
slices, we show that RVLM catecholaminergic neurons activate the locus coeruleus 
as well as A1 and A2 noradrenergic neurons monosynaptically by releasing 
glutamate. In conclusion, activation of RVLM catecholaminergic neurons, 
predominantly C1 cells, by somatic or psychological stresses has the potential 
to increase the firing of both peripheral and central noradrenergic neurons.