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Role of paraventricular nucleus-projecting norepinephrine/epinephrine neurons in acute and chronic stress.
Flak J, Myers B, Solomon M, McKlveen J, Krause E, Herman J (2014) Role of paraventricular nucleus-projecting norepinephrine/epinephrine neurons in acute and chronic stress. Eur J Neurosci 39:1903-1911. doi: 10.1111/ejn.12587
Summary: Chronic stress can cause dysregulation of the paraventricular nucleus (PVN) of the hypothalamus, resulting in structural and function changes in the neurons involved. There are data indicating that post-stress enhancement of norepinephrine is involved in the processing of chronic stress. In this work the authors investigated the hypothesis that PVN-projecting norepinephrine/epinephrine (NE/E) neurons are necessary for chronic stress-induced drive of the hypothalamic-pituitary-adrenocortical (HPA) axis. Rats received bilateral 8.82 ng injections of anti-DBH-SAP (Cat. #IT-03) into the PVN. Saporin (Cat. #PR-01) was used as a control. Lesioned animals displayed attenuated peak ACTH, indicating that NE/E neurons are required for ACTH release in the HPA axis during chronic stress.
Related Products: Anti-DBH-SAP (Cat. #IT-03), Saporin (Cat. #PR-01)
Noradrenaline neuron degeneration contributes to motor impairments and development of L-DOPA-induced dyskinesia in a rat model of Parkinson’s disease.
Shin E, Rogers J, Devoto P, Björklund A, Carta M (2014) Noradrenaline neuron degeneration contributes to motor impairments and development of L-DOPA-induced dyskinesia in a rat model of Parkinson’s disease. Exp Neurol 257:25-38. doi: 10.1016/j.expneurol.2014.04.011
Summary: Although Parkinson’s disease is usually associated with loss of dopaminergic neurons in the substantia nigra, post-mortem studies have shown that noradrenergic neurons in the locus coeruleus also degenerate. In this work the authors develop a new Parkinson’s disease model by double lesioning with both 6-OHDA into the striatum and 2.5 μg bilateral injections of anti-DBH-SAP (Cat. #IT-03) into the lateral ventricles of rats. Double-lesioned animals performed worse on tests evaluating Parkinson’s disease symptoms than those lesioned only with 6-OHDA. The data suggest that Parkinson’s disease symptoms reflect the loss of both dopaminergic and noradrenergic neurons in the midbrain.
Related Products: Anti-DBH-SAP (Cat. #IT-03)
The rate of fall of blood glucose determines the necessity of forebrain-projecting catecholaminergic neurons for male rat sympathoadrenal responses.
Jokiaho A, Donovan C, Watts A (2014) The rate of fall of blood glucose determines the necessity of forebrain-projecting catecholaminergic neurons for male rat sympathoadrenal responses. Diabetes 63:2854-2865. doi: 10.2337/db13-1753
Summary: Different sets of glucosensors detect insulin-induced hypoglycemia depending on the onset rate. This detection controls the activation of sympathoadrenal counterregulatory responses (CRRs). Slow onset hypoglycemia, common with insulin therapy, is detected by glucosensors in the portal-mesenteric veins. Fast onset is detected by brain elements. The authors lesioned hindbrain catecholaminergic neurons to determine which set of responses-they interact with. Rats received 42 ng bilateral injections of Anti-DBH-SAP (Cat. #IT-03) into the paraventricular nucleus of the hypothalamus. Mouse IgG-SAP (Cat. #IT-18) was used as a control. The data indicate that these neurons are critical for detection of slow-onset insulin-induced hypoglycemia.
Related Products: Anti-DBH-SAP (Cat. #IT-03), Mouse IgG-SAP (Cat. #IT-18)
Stimulation of feeding by three different glucose-sensing mechanisms requires hindbrain catecholamine neurons.
Li AJ, Wang Q, Dinh TT, Powers BR, Ritter S (2014) Stimulation of feeding by three different glucose-sensing mechanisms requires hindbrain catecholamine neurons. Am J Physiol Regul Integr Comp Physiol 306(4):R257-R264. doi: 10.1152/ajpregu.00451.2013
Summary: The glucoregulatory system of the brain requires catecholamine neurons in the hindbrain. he sensory mechanisms and connected circuitry controlling the response to glucose deficit are not well understood. In order to investigate different drugs that stimulate food intake but interfere with cellular glucose metabolism and transport the authors administered 82 ng of anti-DBH-SAP (Cat. #IT-03) into the paraventricular nucleus as bilateral injections. Saporin (Cat. #PR-01) was used as a control. Lesioned animals did not increase food intake in response to any of the drugs, indicating that stimulation of food intake is activated through a catecholamine-dependent pathway.
Related Products: Anti-DBH-SAP (Cat. #IT-03), Saporin (Cat. #PR-01)
Gabapentin increases extracellular glutamatergic level in the locus coeruleus via astroglial glutamate transporter-dependent mechanisms.
Suto T, Severino AL, Eisenach JC, Hayashida KI (2014) Gabapentin increases extracellular glutamatergic level in the locus coeruleus via astroglial glutamate transporter-dependent mechanisms. Neuropharmacology 81C:95-100. doi: 10.1016/j.neuropharm.2014.01.040
Summary: Gabapentin is effective in reducing acute and chronic pain, but the mechanisms by which it works are not well understood. The authors assessed extracellular glutamate levels and glutamate interaction with several different cellular membrane proteins. Rats received a 0.25 μg injection of anti-DBH-SAP (Cat. #IT-03) into the locus coeruleus (LC) in order to deplete noradreline levels. Mouse IgG-SAP (Cat. #IT-18) was used as a control. The gabapentin-induced glutamate increase in the LC was not affected by the lesion, supporting data indicating that gabapentin induces glutamate release from astrocytes to stimulate descending inhibition.
Related Products: Anti-DBH-SAP (Cat. #IT-03), Mouse IgG-SAP (Cat. #IT-18)
Lesion of the commissural nucleus of the solitary tract/A2 noradrenergic neurons facilitates the activation of angiotensinergic mechanisms in response to hemorrhage.
Freiria-Oliveira AH, Blanch GT, De Paula PM, Menani JV, Colombari DS (2013) Lesion of the commissural nucleus of the solitary tract/A2 noradrenergic neurons facilitates the activation of angiotensinergic mechanisms in response to hemorrhage. Neuroscience 254:196-204. doi: 10.1016/j.neuroscience.2013.09.017
Summary: Previous work has generated conflicting data on the role of catecholaminergic A2 neurons in the nucleus of the solitary tract (NTS) in control of arterial pressure lability. The authors used Anti-DBH-SAP (Cat. #IT-03) to lesion these neurons in a hypotensive hemorrhage model. Rats received two injections of 12.6 ng into the commissural NTS. Mouse IgG-SAP (Cat. #IT-18) was used as a control. The lesioned animals quickly recovered from hypotension, but were impaired by the icv administration of losartan.
Related Products: Anti-DBH-SAP (Cat. #IT-03), Mouse IgG-SAP (Cat. #IT-18)
C1 neurons: the body’s EMTs.
Guyenet PG, Stornetta RL, Bochorishvili G, Depuy SD, Burke PG, Abbott SB (2013) C1 neurons: the body’s EMTs. Am J Physiol Regul Integr Comp Physiol 305(3):R187-204 . doi: 10.1152/ajpregu.00054.2013
Summary: Although mainly known for their involvement in the control of arterial pressure, C1 neurons are also suspected to participate in numerous other physiological processes such as neuroendocrine response, glucose homeostasis, food consumption, and others. This review discusses the role of these neurons as ’emergency medical technicians’ – cells that produce and modulate physiological survival responses to acute physical stress. The use of Anti-DBH-SAP (Cat. #IT-03) to delineate C1 neurons in the rostral ventrolateral aspect of the medulla oblongata is discussed.
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Hindbrain noradrenergic input to the hypothalamic PVN mediates the activation of oxytocinergic neurons induced by the satiety factor oleoylethanolamide.
Romano A, Potes CS, Tempesta B, Cassano T, Cuomo V, Lutz T, Gaetani S (2013) Hindbrain noradrenergic input to the hypothalamic PVN mediates the activation of oxytocinergic neurons induced by the satiety factor oleoylethanolamide. Am J Physiol Endocrinol Metab 305(10):E1266-73. doi: 10.1152/ajpendo.00411.2013
Summary: Feeding behavior and energy balance are in part controlled by signals from the gut. Oleoylethanolamide (OEA) is an acylethanolamide that is thought to play a role in this network. Since peripheral administration of OEA has effects on the nucleus of the solitary tract (NTS) and paraventricular nucleus (PVN) the authors investigated the role of noradrenergic afferent input to these areas. Rats received bilateral 84-ng injections of Anti-DBH-SAP (Cat. #IT-03) into the PVN. Mouse IgG-SAP (Cat. #IT-18) was used as a control.
Related Products: Anti-DBH-SAP (Cat. #IT-03), Mouse IgG-SAP (Cat. #IT-18)
Compensatory feeding after reversing dehydration-anorexia: Is it analogous to glucoprivic or food deprivation-induced feeding?
Vargas SL, Watts AG (2013) Compensatory feeding after reversing dehydration-anorexia: Is it analogous to glucoprivic or food deprivation-induced feeding?. Neuroscience 2013 Abstracts 757.04. Society for Neuroscience, San Diego, CA.
Summary: We use dehydration (DE)-anorexia to identify the neural networks associated with feeding behavior. How these networks are organized and interact to control ingestive behavior in both the normal and anorexic states allows us to determine how they function in health and disease. DE-anorexia involves replacing drinking water with hypertonic saline (HS) for up to 5 days. This leads to cellular dehydration, and a reduction in food and body weight. Reversing DE-anorexia by removing HS and reinstating drinking water leads to a robust feeding episode. Here we used two experiments to determine whether this water-activated compensatory feeding is functionally related to 2-deoxyglucose (2DG)-activated (glucoprivic) or to food deprivation-induced feeding. First, we determined whether forebrain-projection catecholamine (CA) neurons in the hindbrain are required for water-activated compensatory feeding. These neurons project to the paraventricular nucleus of the hypothalamus (PVH) and are required for 2DG feeding. To do this we lesioned this pathway with the retrogradely-transported immunotoxin, anti-dopamine beta-hydroxylase (DBH) Saporin (DSAP). Anesthetized adult male Sprague-Dawley rats (300g) were injected into the PVH with either a control SAP (MIgSAP) or DSAP. Three weeks later animals were housed in BioDaq monitoring cages to record their feeding behavior. All animals were given HS for 5 days. They were then given drinking water back on the 5th day, and euthanized 75 minutes later. Lack of immunohistochemical staining (IHC) for DBH in the PVH confirmed complete lesions. DSAP lesions had no significant effect on the amount eaten or the latency to begin feeding. Forebrain-projecting CA neurons are therefore not required for water-activated compensatory feeding. Second, we compared the feeding behavior of DE-rats given back water to that of food-deprived rats given food. We also examined the neuronal activity in the hindbrain of these animals using Fos. Meal pattern analysis showed little difference between groups, once feeding was initiated. Dual IHC labeling for Fos and DBH showed no colocalization following drinking water and deficit induced feeding. This contrasts with 2DG stimulated feeding. Furthermore, we show that the Fos expression in particular parts of the nucleus of the solitary tract and the parabrachial nucleus is consistent their roles in projecting visceral and gustatory information to the hypothalamus to coordinate feeding. Thus water-activated compensatory feeding engages mechanisms similar to those used during food deprivation-induced feeding rather than glucoprivic feeding.
Related Products: Anti-DBH-SAP (Cat. #IT-03)
The effect of noradrenaline depletion on motor impairment and dopamine cell loss in a rat model of Parkinson’s disease.
Shin EJ, Rogers, J, Björklund A, Carta M (2013) The effect of noradrenaline depletion on motor impairment and dopamine cell loss in a rat model of Parkinson’s disease. Neuroscience 2013 Abstracts 623.12. Society for Neuroscience, San Diego, CA.
Summary: Objective: Parkinson’s disease (PD) has been mainly known as a neurodegenerative disease with loss of dopaminergic (DA) neurons in the substantia nigra. However, studies of post mortem PD brains have shown that not only DA neurons but also the noradrenergic (NA) neurons in the locus coeruleus degenerate, and that the NA neurodegeneration may be as profound, and also precedes degeneration of the midbrain DA neurons. The early involvement of the NA system is also in line with the caudal-to-rostral disease progression predicted by the model proposed by Braak et al. Hence, we have investigated the effect of NA depletion on motor deficits and DA cell loss in a rat PD model. Methods: To generate two lesion paradigms, rats were injected with a dopamine toxin, 6-OHDA in striatum and/or a NA toxin, DBH-saporin in lateral ventricles. Animals have been tested in a battery of behavioural tests to check the degree of motor impairment. Perfused tissues were then subjected to immunohistochemistry to assess the amount of degeneration in striatal DA fiber and nigral DA neurons. Results: In three motor tests (cylinder, amphetamine-induced rotation, and corridor tests) there was no significant difference in motor deficit between groups. However, the DA- and NA-lesioned animals showed more severe motor deficits than the DA-lesioned animals in stepping, staircase, and rotarod tests. Post mortem analysis revealed that NA depletion did not affect the degree of DA loss in striatum and substantia nigra determined by optical densitometry with tyrosine hydroxylase staining and stereological cell estimation with vesicular monoamine transporter staining, respectively. These results suggest that Parkinsonian-like motor symptoms could be worsened by NA degeneration but it is not due to more profound DA cell degeneration upon NA removal but maybe by dysregulated DA cell function.
Related Products: Anti-DBH-SAP (Cat. #IT-03)