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Immunotoxin lesion of spinally projecting catecholamine neurons impairs the adrenal medullary response to glucoprivation and the sympathetic response to forced swim
Dinh TT, Duffy P, Ritter S (2002) Immunotoxin lesion of spinally projecting catecholamine neurons impairs the adrenal medullary response to glucoprivation and the sympathetic response to forced swim. Neuroscience 2002 Abstracts 76.5. Society for Neuroscience, Orlando, FL.
Summary: Distinct populations of hindbrain catecholamine neurons project spinally to innervate sympathetic and adrenal medullary preganglionic neurons. Previously we injected the immunotoxin, saporin conjugated to anti-dopamine beta hydroxylase (DSAP), into the spinal cord to selectively lesion these neurons. DSAP lesions abolished adrenal medullary Fos expression following insulin-induced hypoglycemia or 2-deoxy-D-glucose (2DG) and eliminated the hyperglycemic response to 2DG, which is mediated by adrenal medullary epinephrine (E) secretion. Here we examine the plasma E and norepinephrine (NE) responses to 2DG (250 mg/kg, s.c.) and to 5 min of forced swim in rats injected at T2-T4 with DSAP or unconjugated saporin (SAP) control solution. Blood was sampled remotely via jugular catheters between 0 and 240 min after 2DG or swim. Immunohistochemistry confirmed loss of dopamine B-hydroxylase throughout the spinal cord of DSAP rats. In DSAPs, both plasma E and hyperglycemic responses to 2DG were abolished or severely impaired compared to SAPs. 2DG did not elevate plasma NE in either group. Swim stress increased NE in both SAPs and DSAPs, but the DSAP response was only 60% of the SAP response. Results show for the first time that the selective activation of the adrenal medulla by glucoprivation, described previously, is mediated by spinally projecting catecholamine neurons. Results also demonstrate that spinal catecholamine terminals, presumeably arising from different hindbrain neurons, contribute to, but are not entirely responsible for, sympathetic neuronal responses to swim stress.
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Selective lesioning of the developing cholinergic and noradrenergic systems: Anatomical, neurochemical and functional effects
Leanza G, Cataudella T (2002) Selective lesioning of the developing cholinergic and noradrenergic systems: Anatomical, neurochemical and functional effects. FENS 2002 Abstracts 151.12. Federation of European Neuroscience Societies, Paris, France.
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Immunotoxic catecholamine lesions attenuate 2DG-induced increase of AGRP mRNA.
Fraley GS, Dinh TT, Ritter S (2002) Immunotoxic catecholamine lesions attenuate 2DG-induced increase of AGRP mRNA. Peptides 23(6):1093-1099. doi: 10.1016/s0196-9781(02)00044-x
Summary: The authors investigated mRNA levels of both agouti gene-related protein (AGRP) and neuropeptide Y (NPY) in rats after lesioning the PVH with anti-DBH-SAP (42 ng in 200 nl, Cat. #IT-03). The results show that the increase in AGRP mRNA levels due to 2DG administration was completely blocked.
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Alpha-7 nicotinic receptor expression by two distinct cell types in the dorsal raphe nucleus and locus coeruleus of rat.
Bitner RS, Nikkel AL (2002) Alpha-7 nicotinic receptor expression by two distinct cell types in the dorsal raphe nucleus and locus coeruleus of rat. Brain Res 938:45-54. doi: 10.1016/s0006-8993(02)02485-x
Summary: Neuronal nicotinic acetylcholine receptors (nAChRs) are suspected to play a role in neurophysiological disorders such as schizophrenia, Alzheimer’s disease, and epilepsy. Whereas the molecular and cellular properties of these receptors have been well characterized, the role of nAChRs in the nervous system is as yet unclear. The authors injected rats intracerebroventricularly with 5 µg/5 µl of anti-DBH-SAP (Cat. #IT-03) to eliminate the noradrenergic nuclei. Using these data along with data acquired by elimination of serotonergic nuclei with 5,7-DHT, the authors showed that both noradrenergic nuclei in the locus coeruleus and serotonergic nuclei in the dorsal raphe nucleus express the alpha-7 nAChR subunit.
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Spinal noradrenergic activation mediates allodynia reduction from an allosteric adenosine modulator in a rat model of neuropathic pain.
Li X, Conklin D, Ma W, Zhu X, Eisenach JC (2002) Spinal noradrenergic activation mediates allodynia reduction from an allosteric adenosine modulator in a rat model of neuropathic pain. Pain 97:117-125. doi: 10.1016/s0304-3959(02)00011-8
Summary: T62 is a thiobene compound that enhances adenosine agonist binding to the A1 receptor. Activation of the adenosine receptor has been effective in several different pain models. The authors used a spinal nerve ligation model for mechanical allodynia to assess T62 efficacy and mode of action. Rats treated with anti-DBH-SAP (4 µg in 5 µl, Cat. #IT-03) experienced no anti-allodynia effects from T62 administration, indicating that modulation of mechanical allodynia by T62 utilizes the spinal noradrenergic system.
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Featured Article: HCRT-SAP lesion produces sleepiness while anti-DBH-SAP lesion does not
Blanco-Centurion C (2002) Featured Article: HCRT-SAP lesion produces sleepiness while anti-DBH-SAP lesion does not. Targeting Trends 3(2)
Related Products: Anti-DBH-SAP (Cat. #IT-03), Orexin-B-SAP (Cat. #IT-20)
Read the featured article in Targeting Trends.
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Isoflurane and nociception: Spinal alpha2A adrenoceptors mediate antinociception while supraspinal alpha1 adrenoceptors mediate pronociception.
Kingery WS, Agashe GS, Guo TZ, Sawamura S, Davies MF, Clark JD, Kobilka BK, Maze M (2002) Isoflurane and nociception: Spinal alpha2A adrenoceptors mediate antinociception while supraspinal alpha1 adrenoceptors mediate pronociception. Anesthesiol 96:367-374. doi: 10.1097/00000542-200202000-00023
Summary: The authors injected 3 µg/3 µl of anti-DBH-SAP (Cat. #IT-03) into the lateral ventricle of rats to determine whether noradrenergic brainstem nuclei and descending spinal pathways are responsible for the antinociceptive actions of isoflurane. The results indicate that isoflurane modulates nociception by as many as three mechanisms, utilizing various combinations of noradrenergic neurons, adrenoceptors, and descending spinal pathways.
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Colocalization of mu-opioid receptors and activated G-proteins in rat cingulate cortex.
Vogt LJ, Sim-Selley LJ, Childers SR, Wiley RG, Vogt BA (2001) Colocalization of mu-opioid receptors and activated G-proteins in rat cingulate cortex. J Pharmacol Exper Ther 299:840-848.
Summary: The anterior cingulate cortex (ACC) is a primary site of opiate drug action, and much of this activity is associated with the m-opioid receptor (MOR). The mechanisms by which MOR regulates pain in the ACC are not well understood. Using anti-DBH-SAP (7 µg into left lateral ventricle in rat; Cat. #IT-03) the authors mapped MOR activity in the ACC and evaluated the histochemical and behavioral relationships between MOR binding and mu-receptor-activated G-proteins after lesioning.
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Novel method for localized, functional sympathetic nervous system denervation of peripheral tissue using guanethidine.
Demas GE, Bartness TJ (2001) Novel method for localized, functional sympathetic nervous system denervation of peripheral tissue using guanethidine. J Neurosci Methods 112:21-28. doi: 10.1016/s0165-0270(01)00452-6
Summary: Sympathectomy, or surgical interruption of sympathetic nerve pathways, is an important technique in the analysis of the sympathetic nervous system. The authors investigate and compare several different methods of performing a sympathectomy in hamsters, including surgery, chemical, and immunotoxic lesions using anti-DBH-SAP (ten 2-µl injections, at either 0.65 µg/µl or 0.325 µg/µl, into inguinal white adipose tissue; Cat. #IT-03).
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Selective immunotoxin lesion of spinally projecting norepineprhine and epinephrine (NE/E) neurons impairs the glucagon response to 2-deoxy-d-glucose (2DG).
Dinh TT, Sanders NM, Pedrow C, Ritter S (2001) Selective immunotoxin lesion of spinally projecting norepineprhine and epinephrine (NE/E) neurons impairs the glucagon response to 2-deoxy-d-glucose (2DG). Neuroscience 2001 Abstracts 947.1. Society for Neuroscience, San Diego, CA.
Summary: Previous work has shown that the targeted immunotoxin, anti-dopamine ß-hydroxylase conjugated to saporin (DSAP), can be used to selectively destroy subpopulations of hindbrain NE/E neurons projecting to or through a particular DSAP injection site. Using this approach, we have shown that NE/E neurons projecting to the hypothalamus are required for feeding and glucocorticoid responses to 2DG-induced glucoprivation and those projecting spinally are required for the adrenal medullary response. In this study, we injected DSAP or unconjugated saporin (SAP) control solution into the spinal cord at T2-T4 to investigate the role of the spinally projecting NE/E neurons in glucagon secretion induced by 2DG (250 mg/kg). Controls injected spinally with unconjugated saporin (SAP) had a glucagon response that peaked at 308% of pre-2DG levels, while DSAP-injected rats had a significantly blunted response to 2DG, peaking at 197% of pre-2DG levels. 2DG-induced hyperglycemia also was impaired in the DSAP rats, but not in the SAP rats. Both SAP and DSAP rats had normal feeding and glucocorticoid responses to 2DG. Results suggest that spinally-projecting NE/E neurons participate in the neural control of glucagon secretion under conditions of glucose deficit. In combination with other findings, these results indicate that hindbrain NE/E neurons contribute to four major glucoregulatory responses (increased feeding, and increased secretion of glucagon, glucocorticoids and adrenal medullary epinephrine) through their projections to hypothalamic or spinal cord effector sites.
Related Products: Anti-DBH-SAP (Cat. #IT-03)