C1 neurons in the rat rostral ventrolateral medulla differentially express vesicular monoamine transporter 2 in soma and axonal compartments

C. P. Sevigny, J. Bassi, A. G. Teschemacher, K. S. Kim, D. A. Williams, C. R. Anderson and A. M. Allen

European Journal of Neuroscience, Vol. 28 pp. 1536-1544, 2008

C1 neurons of the RVLM are defined as producing adrenaline, but the effect that adrenaline is used to is still not quite worked out; they are generally accepted as using glutamate as their major neurotransmitter.  To this end, they express a vesicular glutamate transmitter.  They also express a vesicular adrenaline transporter: VMAT2.  The authors of this paper looked at the differential expression of VMAT2 in the cell soma and axon terminals to determine if rostrally-located, bulbospinal C1 neurons release adrenaline somatodendritically (which requires cell body expression of VMAT2), synaptically, or both.

A lentivirus was used to identify the C1 neurons in one group of rats, rhodamine fluorescent microspheres were injected into the T3/T4 level of the spinal cord to identify spinally projecting neurons in a second group of rats, and anti-PMNT and anti-VMAT2 antibodies were used to identify PMNT (again, to identify C1 neurons) and VMAT2 in tissue sections.  Both brainstem sections and spinal cord sections were examined, to compare cell soma expression of VMAT2 in spinally projecting C1 nuerons to axonal expression in the same neurons.  Additionally, spinally projecting C1 neurons were compared to rostrally projecting C1 neurons.

Rostrally projecting C1 neurons did have VMAT2 present in their cell bodies, but bulbospinal C1 neurons, which were identified by the presence of the rhodamine fluorescent microspheres, rarely did.  VMAT2 was present in the axon varicosities in the spinal cord, though, suggesting that the bulbospinal C1 neurons do release adrenaline as a neurotransmitter.  While bulbospinal C1 neurons may not release adrenaline somatodendritically, though, some C1 neurons are thought to, and bulbospinal neurons seem to be excited to alpha-2-adrenoceptor blockade, suggesting that adrenaline may have a role in regulating the tonic activity of the RVLM.  In short, some C1 neurons, but not the bulbospinal C1 neurons, likely release adrenaline within the RVLM (which has an effect on tonic activity in the RVLM) while C1 bulbospinal neurons release adrenaline along with glutamate at their axon terminals.