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Abolition of cyanide-induced sympathoexcitation by selective lesion of bulbospinal catecholaminergic neurons
Schreihofer AM, Guyenet PG (1999) Abolition of cyanide-induced sympathoexcitation by selective lesion of bulbospinal catecholaminergic neurons. Neuroscience 1999 Abstracts 474.6. Society for Neuroscience, MIami, FL.
Summary: The rostral ventrolateral medulla (RVLM) contains BS C1 adrenergic cells and non-CA neurons whose relative importance for the production of sympathetic vasomotor tone and cardiovascular reflexes remains unknown. In the present study we evaluate 2 sympathetic reflexes after selective lesions of BS CA neurons with the neurotoxin saporin-anti-dopamine beta hydroxylase (SAP-DBH). Rats received bilateral microinjections of SAP-DBH (42 ng/200nl/site) into the spinal cord centered at the intermediolateral cell column at T2 & T4 & T6 and were allowed to recover for 3-5 weeks. Arterial pressure (AP), heart rate (HR), and splanchnic nerve activity (SNA) were measured while the rats were chloralose-anesthetized, artificially ventilated, and paralyzed. Baseline AP and HR were comparable between control rats (n-7, 113 +/- 7 mmHg, 426 +/- 12 bpm) and lesioned rats (n=7, 123 +/- 4 mmHg, 448 +/- 7 bpm). In control rats stimulation of the carotid chemoreflex (100 micrograms/kg sodium cyanide, iv) produced a burst in SNA (266 +/- 26%) followed by inhibition (to 18 +/- 3% of base). In contrast, in the SAP-DBH-treated animals cyanide produced only an inhibition of SNA (to 33 +/- 7% of base). Mean AP responses mirrored the SNA responses. In contrast, the Bezold-Jarisch reflex was not diminished in the SAP-DBH-treated rats. Phenyl biguanide (5 micrograms/kg, iv) decreased AP (22 +/- 3 vs. 42 +/- 5 mmHg), SNA (85 +/- 4 vs. 67 +/- 6%), and HR (28 +/- 6 vs. 56 +/- 7 bpm) in control rats and lesioned rats respectively. Histological examination revealed that SAP-DBH depleted the vast majority of BS C1 cells (>70% of the rostral third of the C1 cell group), and >80% of the A5 cell group. These results indicate that sympathetic vasomotor tone persists and rats have a normal mean AP in the absence of most of BS C1 and A5 cells. Although the BS C1 cells may not be required for the Bezold-Jarisch reflex, BS CA cells are essential for the sympathoexcitatory response to cyanide. Work supported by NIH 28785.
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Lesions of the C1 catecholaminergic neurons of the ventrolateral medulla in rats using anti-DBH-saporin.
Madden CJ, Ito S, Rinaman L, Wiley RG, Sved AF (1999) Lesions of the C1 catecholaminergic neurons of the ventrolateral medulla in rats using anti-DBH-saporin. Am J Physiol 46:R1063-R1075. doi: 10.1152/ajpregu.1999.277.4.R1063
Summary: The authors review the use of anti-DBH-SAP (Cat. #IT-03) to study the role of C1 neurons within the rostral ventromedial medulla in cardiovascular regulation. This immunotoxin specifically removes C1 neurons containing dopamine beta-hydroxylase.
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Differential effects of neurotoxic destruction of descending noradrenergic pathways on acute and persistent nociceptive processing.
Martin WJ, Gupta NK, Loo CM, Rohde DS, Basbaum AI (1999) Differential effects of neurotoxic destruction of descending noradrenergic pathways on acute and persistent nociceptive processing. Pain 80:57-65. doi: 10.1016/s0304-3959(98)00194-8
Summary: The authors used Anti-DBH-SAP to re-examine the contribution of noradrenergic pathways to nociception and to morphine analgesia. They also evaluated morphine analgesia in the formalin test and found that toxin-treated animals exhibited enhanced morphine analgesia. These results establish the utility of using this immunotoxin to selectively destroy subpopulations of noradrenergic cell groups and provide evidence that acute and persistent nociception are differentially regulated by descending noradrenergic pathways.
Usage: Intrathecal treatment with Anti-DBH-SAP attenuates formalin pain (5.0 µg/20 µl).
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Activation of coeruleospinal noradrenergic inhibitory controls during withdrawal from morphine in the rat.
Rohde DS, Basbaum AI (1998) Activation of coeruleospinal noradrenergic inhibitory controls during withdrawal from morphine in the rat. J Neurosci 18(11):4393-4402. doi: 10.1523/JNEUROSCI.18-11-04393.1998
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Destruction of locus coeruleus neuronal perikarya after injection of anti-dopamine-beta-hydroxylase immunotoxin into the olfactory bulb of the rat.
Blessing WW, Lappi DA, Wiley RG (1998) Destruction of locus coeruleus neuronal perikarya after injection of anti-dopamine-beta-hydroxylase immunotoxin into the olfactory bulb of the rat. Neurosci Lett 243:85-88. doi: 10.1016/s0304-3940(98)00090-1
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Methods of sympathetic degeneration and alteration.
Picklo MJ (1997) Methods of sympathetic degeneration and alteration. J Auton Nerv Syst 62:111-125. doi: 10.1016/s0165-1838(96)00121-x
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Central noradrenergic lesioning using anti-DBH-saporin: anatomical findings.
Wrenn CC, Picklo MJ, Lappi DA, Robertson DR, Wiley RG (1996) Central noradrenergic lesioning using anti-DBH-saporin: anatomical findings. Brain Res 740:175-186. doi: 10.1016/s0006-8993(96)00855-4
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Lesioning of medullary noradrenergic and adrenergic neurons using the immunotoxin anti-DBH-saporin.
Wrenn CC, Picklo MJ, Lappi DA, Robertson D, Wiley RG (1996) Lesioning of medullary noradrenergic and adrenergic neurons using the immunotoxin anti-DBH-saporin. Neuroscience 1996 Abstracts 749.15. Society for Neuroscience, Washington, DC.
Summary: Anti-DBH-saporin (α-DBH-sap) is an anti-neuronal immunotoxin comprised of an antibody against the noradrenaline synthesizing enzyme dopamine β-hydroxylase (DBH) coupled by a disulfide bond to the ribosome inactivating toxin saporin. This immunotoxin was injected into the left lateral ventricle of rats at doses of 5, 10, and 20 μg. After a two week survival time, the rats were sacrificed and the ability of the immunotoxin to lesion noradrenergic and adrenergic neurons was assessed by immunohistochemical staining for tyrosine hydroxylase (TH), DBH, and phenylethanolamine n-methyl transferase (PNMT). The locus coeruleus was completely lesioned at all three doses. The A5 and A7 cell groups were completely lesioned at the two higher doses. In the medulla, lesioning of the ventrolateral Al/Cl cell group and the dorsomedial A2/C2/C3 cell group was qualitatively observed to be incomplete at all three doses. Cell counts of TH+, DBH+, and PNMT+ neurons revealed that the number of neurons staining for each enzyme was reduced by the immunotoxin dose dependently. The ventrolateral population was lesioned more closely to completeness than the dorsomedial population. These data show that α-DBH-sap can be used to produce lesions of brainstem noradrenergic and adrenergic neurons. Supported by the Department of Veterans Affairs.
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Anti-dopamine beta-hydroxylase immunotoxin-induced sympathectomy in adult rats.
Picklo MJ, Wiley RG, Lonce S, Lappi DA, Robertson D (1995) Anti-dopamine beta-hydroxylase immunotoxin-induced sympathectomy in adult rats. J Pharmacol Exp Therap 275(2):1003-1010.
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Noradrenergic lesioning with an anti-dopamine beta-hydroxylase immunotoxin.
Picklo MJ, Wiley RG, Lappi DA, Robertson D (1994) Noradrenergic lesioning with an anti-dopamine beta-hydroxylase immunotoxin. Brain Res 666:195-200. doi: 10.1016/0006-8993(94)90772-2
Related Products: Anti-DBH-SAP (Cat. #IT-03)