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H-saporin
Department of Pharmacology, University of Virginia, Charlottesville, Virginia 22908
We examined the effects of
destroying bulbospinal catecholaminergic neurons with the immunotoxin
anti-dopamine 
-hydroxylase-saporin (anti-DH-Sap) on splanchnic
nerve activity (SNA) and selected sympathetic reflexes in rats.
Anti-DH-Sap was administered into the thoracic spinal cord with the
retrograde tracer fast blue. After 3-5 wk, anti-DH-Sap
eliminated most bulbospinal C1 (>74%), C3 (~84%), A5 (~98%),
and A6 cells. Noncatecholaminergic bulbospinal neurons of the rostral
ventrolateral medulla and serotonergic neurons were spared. Under
chloralose anesthesia, mean arterial pressure and heart rate of
anti-DH-Sap-treated rats (3-5 wk) were normal. Resting SNA was
not detectably altered, but the baroreflex range and gain were reduced
~40% (P < 0.05). Phenyl biguanide-induced decreases
in mean arterial pressure, heart rate, and SNA were unchanged by
anti-DH-Sap, but the sympathoexcitatory response to intravenous
cyanide was virtually abolished (P < 0.05). Rats that
received spinal injections of saporin conjugated to an anti-mouse IgG
had intact bulbospinal C1 and A5 cells and normal physiological responses. These data suggest that C1 and A5 neurons contribute modestly to resting SNA and cardiopulmonary reflexes. However, bulbospinal catecholaminergic neurons appear to play a prominent sympathoexcitatory role during stimulation of chemoreceptors.
cyanide; phenyl biguanide; tyrosine hydroxylase; phenylethanolamine-N-methyltransferase; tryptophan hydroxylase; splanchnic nerve activity
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