Identification of C1 and nonadrenergic presympathetic neurons (PSNS) of rostral ventrolateral medulla (RVLM) by juxtacellular label of single recorded cells "in vivo" in rat

Vasomotor sympathetic preganglionic neurons receive their main excitatory drive from PSNs located in the RVLM. It has been speculated that a slowly firing, slowly conducting subgroup of RVLM PSNs may be C1 cells whereas fast firing, faster conducting PSNs may be noncatecholaminergic. The first aim of the present study was to test this hypothesis using a method which allows for extracellular recording and labeling of single neurons. The second aim was to determine whether i.v. administration of the hypotensive α2-adrenergic agonist clonidine selectively inhibits C1 PSNs. In chloralose-anesthetized, artificially ventilated rats, 18 barosensitive PSNs were recorded, labeled with neurobiotin, and processed by immunocytochemistry for tyrosine hydroxylase (TH). PSNs were divided into 2 groups: slowly conducting cells [<1 m/s, firing rate 4.8±1.1 spikes/s (sp/s), n=9] and fast conducting cells (>1 m/s; firing rate 24.0±3.0 sp/s, n=9). All 9 slowly conducting cells were TH+, but only 4 out of the 9 fast cells were TH+. Clonidine (10 μg/kg, iv) lowered splanchnic nerve activity by 85% (n=8). Slowly conducting TH+ cells were 30% inhibited by 10 μg/kg clonidine (from 5.0±1.6 to 3.5±1.3 sp/s; n=7, P <0.05). Both TH+ and nonTH fast cells were inhibited by clonidine (from 19.8±3.7 to 10.4±2.1 sp/s, n=6, P < 0.05). These data demonstrate that the slowly conducting, barosensitive RVLM PSNs are C1 cells. We also confirm that a proportion of barosensitive, fast conducting RVLM PSNs are not C1 cells. Finally, both C1 and non-C1 PSNs can be inhibited by clonidine given iv, and both cell types may contribute to the sympatholytic effect of the drug.