Modulation of Bulbospinal Rostral Ventral Lateral Medulla Neurons by Hypoxia/Hypercapnia but Not Medullary Respiratory Activity

Carie R. Boychuk, Amanda L. Woerman, David Mendelowitz. Hypertension. 2012; 60:1491-1497 Published online before print October 29, 2012, doi: 10.1161/HYPERTENSIONAHA.112.197954. There is respiratory modulation of sympathetic nerve activity but the sites that are a responsible for this are unknown. The rvlm is located near respiratory neurons. The purpose of this study was to determine whether respiratory network pathways can drive rvlm activity. Also they tested whether hypoxia/ hypercapnia can modulate RVLM activity in brainstem slices. They injected CTB into the spinal cord and allowed the rats to recover for 3 to 5 days. They then euthanized the rats and they used bulbospinal neurons that were TH and CTB positive. They then recorded rhythmic inspiratory- related hypoglossal activity and spontaneous synaptic events in the RVLM bulbospinal neurons for 2 to 4 minutes. Then slices were infused with hypoxic /hypercapnic acsf for 10 minutes and then switched back to the control bath for 20 minutes. They showed that none of the bulbospinal rvlm had changes in glycinergic, GABAergic and glutamatergic events. However, in response to hypoxia/hypercapnia the slow firing increased their rate of firing and stayed elevated during the control period. The fast firing had a reduction in their firing rate after the hypoxic/hypercapnic event and returned to baseline firing during the control time period. In order to determine whether hypoxia/hypercapnic changes in rvlm neuronal activity were dependent on GABAergic and glycinergic neurotransmission, gabazine and strychnine were applied to slices. Applying gabazine and strychnine did not alter the neuronal activity alone. However, hypoxic/ hypercapnic events where blocked in the slow firing cells. From this study they concluded that inspiratory events do not affect RVLM neuronal activity in young rats. Also they showed that hypoxic /hypercapnic events can reverse gabaergic and glycinergic neurotransmission leading to increases in firing rate in C1 bulbospinal neurons slow firing in the RVLM. Finally, that fast firing c1 neurons in the rvlm response to hypoxia/hypercapnia are not due to modulation of gabaergic and glycinergic neurotransmission.-MD