Experimental Biology 2018
Posters using ATS Products
Brainstem pre-sympathetic neuron controls oscillatory breathing in heart failure. Del Rio R, Andrade D, Toledo C, Diaz H, Lucero C, Arce-Alvarez A. Sunday, Apr. 22, 8:30 AM; 885.13 / A480
Summary: The authors hypothesized that selective elimination of catecholaminergic neurons from RVLM (C1 cells) delay cardiac deterioration in HFpEF rats. The selective ablation of C1 RVLM neurons was performed by Anti-DBH-SAP (Cat. #IT-03) injected stereotaxically into the RVLM (7.5 ng/150nl, bilateral).
Inflammation Differentially Impacts Phrenic Long-term Facilitation (pLTF) in Rats with Motor Neuron Death Induced by Intrapleural CTB-saporin Injections. Nichols N, Tanner M. Sunday, Apr. 22, 10:00 AM; 625.17 / A540
Summary: Because inflammation is a hallmark of all neurodegenerative diseases, and is known to prevent development of acute intermittent hypoxia-induced phrenic long-term facilitation (pLTF), the authors predicted that inflammation would impair pLTF in lesioned rats (CTB-SAP, Cat. #IT-14) and thus, anti-inflammatory drugs would enhance pLTF.
Ablation of neuromedin B (NMB)-expressing neurons located within retrotrapezoid nucleus (RTN) reduces the central respiratory chemoreflex (CRC) selectively in conscious rats. Souza G, Kanbar R, Stornetta D, Stornetta R, Guyene P. Monday, Apr. 23, 4:00 PM; 894.10 / A548
Summary: Lesions produced by microinjecting a substance-P analog conjugated with saporin (SSP-SAP, Cat. #IT-11) elicit small and/or transient CRC reductions in rats.
5-HT2B Receptor Expression in the Phrenic Motor Nucleus of Rats with Intrapleural CTB-Saporin-Induced Phrenic Motor Neuron Death. Borkowsk L. and Nichols N. Monday, Apr. 23, 10:00 AM; 743.8 / A458
Summary: Intrapleural injection of cholera toxin B fragment conjugated to saporin (CTB-SAP, Cat. #IT-14) selectively kills respiratory motor neurons. The authors tested the hypothesis that 5-HT2B receptor expression in the phrenic motor nucleus is decreased in 7d CTB-SAP treated rats, but is not different in 28d CTB-SAP treated rats when compared to controls.
BDNF Downregulates Adrenergic b-Receptor-Mediated Hypotensive Mechanisms in the Paraventricular Nucleus of the Hypothalamus (PVN). Thorsdottir D, Cruickshank N, Einwag Z, Dutko R, Erdos B. Monday, Apr. 23, 10:00 AM; 732.15 / A382
Summary: The authors tested the hypothesis that increased BDNF expression in the PVN elevates BP in part by diminishing the inhibitory input from NTS CA-ergic neurons projecting to the PVN by downregulating b-receptors in the PVN. Sprague-Dawley (SD) rats received bilateral PVN injections of AAV2 viral vectors expressing either green fluorescent protein (GFP) or BDNF and bilateral NTS injections of phosphate-buffered saline (PBS) or Anti-DBH-SAP (Cat. #IT-03), a neurotoxin selective to noradrenaline- and adrenaline-synthesizing neurons.
The Role of Patch Compartment Neurons in Methamphetamine-Mediated Reward. Kendrick T, Robinson H, Barker N, Patel B, Logue J, Horner A. Monday, Apr. 23, 12:30 PM; 681.2 / C7
Summary: The basis of this experiment was to investigate the role of the patch compartment neurons in METH-induced reward behavior. This goal was attained by determining if the ablation of the mu opioid receptor-containing neurons of the patch compartment would alter METH-mediated condition place reference (CPP), which is an indicator of drug reward, by using Dermorphin-Saporin (Cat. #IT-12) which is a neurotoxin used to accurately target and eliminate mu opiate receptor-containing neurons.
Anti-DBH-SAP (Cat. #IT-03)
A tool for eliminating cells that express dopamine beta-hydroxylase in rat; targeted via the antibody to dopamine beta-hydroxylase (DBH), eliminated via saporin
Dermorphin-Saporin (Cat. #IT-12)
A tool for eliminating cells that express the mu-opioid receptor (MOR); targeted via dermorphin, eliminated via saporin
CTB-SAP (Cat. #IT-14)
A tool for eliminating cells that express the GM1 receptor; targeted via cholera toxin B-subunit, eliminated via saporin
SSP-SAP (Cat. #IT-11)
A tool for eliminating cells that express substance P receptor (NK-1); targeted via Substance P, eliminated via saporin