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Medullary noradrenergic neurons mediate hemodynamic responses to osmotic and volume challenges
Marques SM, Naves LM, Silva TME, Cavalcante KVN, Alves JM, Ferreira-Neto ML, de Castro CH, Freiria-Oliveira AH, Fajemiroye JO, Gomes RM, Colombari E, Xavier CH, Pedrino GR (2021) Medullary noradrenergic neurons mediate hemodynamic responses to osmotic and volume challenges. Front Physiol 12:649535. doi: 10.3389/fphys.2021.649535
Summary: The study sought to determine the role of noradrenergic neurons in hypertonic saline infusion (HSI)-induced hemodynamic recovery. Findings show that together the A1 and A2 neurons are essential to HSI-induced cardiovascular recovery in hypovolemia.
Usage: Medullary catecholaminergic neurons were lesioned by nanoinjection of Anti-DBH-SAP (0.105 ng·nl−1) into A1, A2, or both (LES A1; LES A2; or LES A1+A2, respectively). Sham rats received nanoinjections of unconjugated saporin in the same regions.
Related Products: Anti-DBH-SAP (Cat. #IT-03), Saporin (Cat. #PR-01)
Developments in understanding diffuse noxious inhibitory controls: pharmacological evidence from pre-clinical research
Kucharczyk MW, Valiente D, Bannister K (2021) Developments in understanding diffuse noxious inhibitory controls: pharmacological evidence from pre-clinical research. J Pain Res 14:1083-1095. doi: 10.2147/JPR.S258602
Summary: This review discusses the pharmacological manipulation interrogation strategies that have been used to examine the functionality of diffuse noxious inhibitory controls (DNIC) and descending control of nociception (DCN).
Usage: Anti-DBH-SAP is one of the drugs tested to influence DNIC expression. They reference a publication that reported that icv injection of Anti-DBH-SAP abolished DCN expression. Anti-DBH-SAP (5 μg/5 μl) was injected in the left ventricle. Lesion of the LC resulted in failure of DNIC, an effect that mimics what is observed behaviorally after chronic TBI.
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Depletion of C1 neurons attenuates the salt-induced hypertension in unanesthetized rats.
Ribeiro N, Martins Sá RW, Antunes VR (2020) Depletion of C1 neurons attenuates the salt-induced hypertension in unanesthetized rats. Brain Res 1748:147107. doi: 10.1016/j.brainres.2020.147107
Objective: To determine if the ablation of C1 neurons mitigates high blood pressure induced by high-salt intake.
Summary: Data show that hypertension induced by high-salt intake is dependent on C1 neurons.
Usage: Bilateral injections of 2.4 ng/100 nl of Anti-DBH-SAP. The total number of TH+ neurons in the AS region was reduced by 37 ± 13% in the anti-DBH-SAP group when compared to control.
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Noradrenaline signaling in the LPBN mediates amylin’s and salmon calcitonin’s hypophagic effect in male rats.
Boccia L, Le Foll C, Lutz TA (2020) Noradrenaline signaling in the LPBN mediates amylin’s and salmon calcitonin’s hypophagic effect in male rats. FASEB J 34(11):15448-15461. doi: 10.1096/fj.202001456RRR
Objective: To assess the phenotype of amylin activated LPBN (lateral parabrachial nucleus) neurons, especially to confirm the CGRPergic phenotype and to uncover the specific role of NA (noradrenaline) signaling from the AP to the LPBN.
Summary: The present study confirmed the central role of the LPBN in propagating amylin’s and sCT’s hypophagic action, and particularly the importance of AP → LPBN NA signaling in the mediation of this process, through the activation of LPBN (CGRP and non-CGRP) neurons.
Usage: The neuronal pathways used to process the physiological response to amylin were investigated using 50-ng injections of Anti-DBH-SAP (Cat. #IT-03) into the area postrema (AP) or 25 ng into the lateral parabrachial nucleus (Potes et al., 2010).
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Loss of diffuse noxious inhibitory control after traumatic brain injury in rats: A chronic issue
Irvine KA, Sahbaie P, Ferguson AR, Clark JD (2020) Loss of diffuse noxious inhibitory control after traumatic brain injury in rats: A chronic issue. Exp Neurol 333:113428. doi: 10.1016/j.expneurol.2020.113428
Objective: To confirm hypothesis that dysfunctional descending noradrenergic and serotonergic pain control circuits may contribute to the loss of diffuse noxious inhibitory control (DNIC), a critical endogenous pain control mechanism, weeks to months after traumatic brain injury (TBI).
Summary: Results suggest that TBI causes maladaptation of descending nociceptive signaling mechanisms and changes in the function of both adrenergic and serotonergic circuits. Such changes could predispose those with TBI to chronic pain.
Usage: Anti-DBH-SAP (5 μg/5 μl) was injected in the left ventricle. Lesion of the LC resulted in failure of DNIC, an effect that mimics what is observed behaviorally after chronic TBI.
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Adrenergic supersensitivity and impaired neural control of cardiac electrophysiology following regional cardiac sympathetic nerve loss
Tapa S, Wang L, Francis Stuart SD, Wang Z, Jiang Y, Habecker BA, Ripplinger CM (2020) Adrenergic supersensitivity and impaired neural control of cardiac electrophysiology following regional cardiac sympathetic nerve loss. Sci Rep 10:18801. doi: 10.1038/s41598-020-75903-y
Summary: The authors present a novel mouse model of regional cardiac sympathetic hypo-innervation utilizing Anti-DBH-SAP.
Usage: Either 5μL of 40 ng/μL Anti-DBH-SAP or Mouse IgG-SAP (control) was applied three times directly to the exposed apical/anterior surface of the heart.
Related Products: Anti-DBH-SAP (Cat. #IT-03), Mouse IgG-SAP (Cat. #IT-18)
Integration of peripheral and central systems in control of ingestive and reproductive behavior
Schneider J (2020) Integration of peripheral and central systems in control of ingestive and reproductive behavior. Oxford Research Encyclopedia of Neuroscience . Oxford University Press doi: 10.1093/acrefore/9780190264086.013.23
Summary: Highly glucose-sensitive cells in the ventrolateral medulla send catecholaminergic projections to the PVH. These projections can be selectively destroyed by Anti-DBH-SAP “DSAP” experiments show that catecholaminergic projections from glucose-sensitive cells in the ventrolateral medulla are necessary for all responses to glucoprivation, including increases in epinephrine secretion, glucocorticoid secretion, sex behavior, and food intake.
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Neuroendocrine and behavioral consequences of hyperglycemia in cancer
Vasquez JH, Borniger JC (2020) Neuroendocrine and behavioral consequences of hyperglycemia in cancer. Endocrinology 161(5):bqaa047. doi: 10.1210/endocr/bqaa047
Summary: Ablation of norepinephrine containing projections to the arcuate (via Anti-DBH-SAP injections) alters AgRP and neuropeptide (NPY) concentrations, leading to impairments in hypoglycemic (glucoprivic) or ghrelin-induced feeding.
Usage: Anti-DBH-SAP (bilateral 42-ng intracranial injections) was used in rats to investigate the role of hindbrain catecholamine afferents in increased ARC NPY and AgRP gene expression.
Related Products: Anti-DBH-SAP (Cat. #IT-03)
An age- and sex-dependent role of catecholaminergic neurons in the control of breathing and hypoxic chemoreflex during postnatal development.
Patrone LGA, Capalbo AC, Marques DA, Bícego KC, Gargaglioni LH (2020) An age- and sex-dependent role of catecholaminergic neurons in the control of breathing and hypoxic chemoreflex during postnatal development. Brain Res 1726:146508. doi: 10.1016/j.brainres.2019.146508
Objective: To discover the role of brainstem catecholaminergic (CA) neurons in the hypoxic ventilatory response (HVR).
Summary: Brainstem CA neurons modulate the HVR during the postnatal phase, and possibly thermoregulation during hypoxia.
Usage: Evaluation of brainstem CA neurons in the HVR during postnatal development in male and female rats through specific cell depletion with Anti-DBH-SAP (420 ng/nL) injected in the fourth ventricle.
Related Products: Anti-DBH-SAP (Cat. #IT-03)
BDNF downregulates β-adrenergic receptor-mediated hypotensive mechanisms in the paraventricular nucleus of the hypothalamus.
Thorsdottir D, Cruickshank NC, Einwag Z, Hennig GW, Erdos B (2019) BDNF downregulates β-adrenergic receptor-mediated hypotensive mechanisms in the paraventricular nucleus of the hypothalamus. Am J Physiol Heart Circ Physiol 317(6):H1258-H1271. doi: 10.1152/ajpheart.00478.2019
Objective: To determine whether BDNF increases blood pressure in part by diminishing inhibitory hypotensive input from nucleus of the solitary tract (NTS) catecholaminergic neurons projecting to the PVN.
Summary: BDNF, a key hypothalamic regulator of blood pressure, disrupts catecholaminergic signaling between the NTS and the PVN by reducing the responsiveness of PVN neurons to inhibitory hypotensive β-adrenergic input from the NTS.
Usage: Bilateral NTS injections of sterile PBS (for control) or Anti-DBH-SAP (22 ng).
Related Products: Anti-DBH-SAP (Cat. #IT-03)