Do Non‐C1 Cells In The Rostral Ventrolateral Medulla Increase Blood Pressure?

Abstract

C1 cells are a major group of neurons located in the rostral ventrolateral medulla (RVLM) that are glutamatergic and contain catecholamine synthetic enzymes such as tyrosine‐hydroxylase (TH), dopamine‐beta hydroxylase (DBH), and phenylethanolamine N‐methlytransferase (PNMT) (DePuy et al., 2013; Stornetta et al., 2002). Limited amount of information is available that suggests these neurons are the exclusive influence on blood pressure. Non‐C1 catechominergic cells also express vesicular glutamate transporter‐2 (VGLUT2) and are barosensitive and thus may have an impact on blood pressure (Stornetta et al., 2002). Optogenetic activation of C1 cells increases blood pressure specifically targeted in TH‐Cre rats by using a Cre‐dependent vector that drives channelrodopsin‐2 (ChR2) tagged with mCherry (Burke and Guyenet, 2014). However, in the mouse model when C1 cells are stimulated the results indicate a decrease in blood pressure. This difference is perhaps due to the close proximity of different types of C1 cells that are separated in the rat model. When C1 and non‐C1 neurons are stimulated in mice with the use of a CAMKII vector, there is a large increase in blood pressure. One unanswered question is whether CAMKII transduces glutamatergic neurons in the brainstem. This present study uses a CAMKII vector to express ChR2 in combination with mCherry. Oligonucleotide probes were used to label cells positive for VGLUT2. By using light microscopy we will ask if the non‐C1 cells transduced by CAMKII are glutamatergic. We found that on average, 90% (N=3) of CAMKII transduced cells within the RVLM contain VGLUT2.Support or Funding InformationUniversity of Virginia Summer Research Internship Program