Borella TL, Takakura AC, Moreira TS (2014) C1 neurons excite A5 noradrenergic neurons during hypoxia condition. Neuroscience 2014 Abstracts 168.07. Society for Neuroscience, Washington, DC.
Summary: C1 neurons activate sympathetic tone and stimulate the hypothalamic-pituitary-adrenal axis in circumstances such as pain, hypoxia or hypotension. They also innervate pontine noradrenergic cells group, including the locus coeruleus (LC) and the ventrolateral pontine catecholaminergic region (A5). Activation of C1 neurons reportedly inhibits pontine neurons; however, because these neurons are glutamatergic and have excitatory effects elsewhere, we re-examined the effect of C1 activation on pontine noradrenergic neurons (A5) using a more selective method. We examined the neuronal effects of destroying C1 catecholaminergic neurons with unilateral injection of the immunotoxin anti-dopamine beta-hydroxylase-saporin (anti-DβH-Sap) into the A5 region during hypoxic condition. Bilateral injections of anti-DβH-Sap into A5 destroyed tyrosine hydroxylase (TH) neurons but spared facial motoneurons and serotonergic neurons within the ventrolateral medulla. Hypoxia (8% O2 – 3 hours) induced a robust increase in Fos expression within the catecholaminergic C1 region of the ventrolateral medulla. On the lesioned side, Fos expression was significantly reduced (53.4 ± 17.6 vs. control: 129.8 ± 22.3 neurons) within the C1 region after hypoxia challenge. Residual Fos expression seen in lesioned side in response to hypoxia provides a basis for probing additional circuits that may be recruited in hierarchical manner in response to hypoxia. In conclusion, the C1 neurons activate the ventrolateral pontine noradrenergic neurons (A5 region) possibly via the release of glutamate from monosynaptic C1 inputs.
Related Products: Anti-DBH-SAP (Cat. #IT-03)