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Spinally‐projecting C1 neurons are not responsible for increased arterial pressure after nasal stimulation
Author(s) -
McCulloch Paul,
DiNovo Karyn
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.808.14
Subject(s) - rostral ventrolateral medulla , stimulation , neuroscience , chemistry , catecholaminergic cell groups , neuron , catecholaminergic , medulla oblongata , biology , central nervous system , catecholamine
Nasal stimulation (NS) can produce a sympathetically‐mediated increase in arterial blood pressure (BPa). Our objective was to determine if the increased BPa seen after NS occurs through activation of spinally‐projecting C1 RVLM neurons. Using Fos (a marker for activated neurons) and PNMT (a marker for C1 neurons), we found that NS activates both C1 and non‐C1 RVLM neurons. Only 7–24% of activated RVLM neurons were C1 neurons. Next we used Fos and PNMT immunohistochemistry with Fluorogold injections into the T3 IML to identify spinally‐projecting neurons activated by NS. Of all spinally‐projecting RVLM neurons, 10% were activated non‐C1 neurons, while 4% were activated C1 neurons. Of all activated RVLM neurons, 12% were non‐C1 spinally‐projecting neurons, while 4% were C1 spinally‐projecting neurons. Of all C1 neurons, 9% were activated and spinally‐projecting. Only 2% of all RVLM neurons were spinally‐projecting C1 neurons activated by NS. Finally, anti‐DβH‐saporin was injected into the T3 IML to selectively kill spinally‐projecting catecholaminergic neurons. In 3 of 12 rats, 77% of the spinally‐projecting C1 neurons within the RVLM were selectively killed. We found that successful ablation of spinally‐projecting C1 neurons did not eliminate the cardiovascular responses to NS. We therefore conclude that spinally‐projecting C1 neurons are not responsible for the increased BPa seen after NS.