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Catecholaminergic neurons projecting to the paraventricular nucleus of the hypothalamus are essential for cardiorespiratory adjustments to hypoxia.
King T, Ruyle B, Kline D, Heesch C, Hasser E (2015) Catecholaminergic neurons projecting to the paraventricular nucleus of the hypothalamus are essential for cardiorespiratory adjustments to hypoxia. Am J Physiol Regul Integr Comp Physiol 309:R721-731. doi: 10.1152/ajpregu.00540.2014
Summary: Catecholaminergic neurons in the brainstem are known to be involved in cardiorespiratory control and to modulate sensory function. Some of the projections from these neurons are to the paraventricular nucleus (PVN), and are involved in cardiorespiratory and neuroendocrine responses to hypoxia. While data have shown the PVN-projecting neurons are activated by hypoxia, their function in this context is not known. In this work the authors bilaterally injected 42 ng of Anti-DBH-SAP (Cat. #IT-03) into the PVN of rats. Mouse IgG-SAP (Cat. #IT-18) was used as control. Respiratory measurements of the lesioned animals indicates that PVN-projecting catecholaminergic neurons are involved in peripheral and central chemoreflex and arterial oxygen levels during exposure to hypoxic stimuli.
Related Products: Anti-DBH-SAP (Cat. #IT-03), Mouse IgG-SAP (Cat. #IT-18)
Selective C1 lesioning slightly decreases angiotensin II type I receptor expression in the rat rostral ventrolateral medulla (RVLM).
Bourassa E, Stedenfeld K, Sved A, Speth R (2015) Selective C1 lesioning slightly decreases angiotensin II type I receptor expression in the rat rostral ventrolateral medulla (RVLM). Neurochem Res 40:2113-2120. doi: 10.1007/s11064-015-1649-3
Summary: Exogenous angiotensin II administered to the RVLM produces a significant pressor response that can be countered by angiotensin II type I receptor antagonists. In this work the authors examined the relative contribution of C1 and non-C1 neurons in the RVLM to this angiotensin II response. Rats received 10 or 15 ng of Anti-DBH-SAP (Cat. #IT-03) as unilateral injections into the RVLM. Mouse IgG-SAP (Cat. #IT-18) was used as control. The data indicate that the majority of angiotensin II type 1 receptors are expressed on non-C1 neurons or glia.
Related Products: Anti-DBH-SAP (Cat. #IT-03), Mouse IgG-SAP (Cat. #IT-18)
Selective optogenetic stimulation of the retrotrapezoid nucleus in sleeping rats activates breathing without changing blood pressure or causing arousal or sighs.
Burke P, Kanbar R, Viar K, Stornetta R, Guyenet P (2015) Selective optogenetic stimulation of the retrotrapezoid nucleus in sleeping rats activates breathing without changing blood pressure or causing arousal or sighs. J Appl Physiol (1985) 118:1491-1501. doi: 10.1152/japplphysiol.00164.2015
Summary: Hypoxia and hypercapnia both play roles in the activation of normal breathing. If either one is severe enough, arousal will also occur. The authors looked to better define the CNS pathways utilized by hypoxia and hypercapnia, as well as the pathways responsible for activation of arousal due to these conditions. The authors used optogenetic activation of the retrotrapezoid nucleus and C1 and A5 catecholaminergic neurons, as well as selective C1 neuron stimulation in rats. Some rats also received bilateral injections of Anti-DBH-SAP (Cat. #IT-03) totaling 0.88 μg into the region of the lateral horn of the second thoracic segment.
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Hindbrain catecholamine neurons activate orexin neurons during systemic glucoprivation in male rats.
Li A, Wang Q, Elsarelli M, Brown R, Ritter S (2015) Hindbrain catecholamine neurons activate orexin neurons during systemic glucoprivation in male rats. Endocrinology 156:2807-2820. doi: 10.1210/en.2015-1138
Summary: Norepinephrine and epinephrine-secreting catecholamine neurons are strong stimulators of food intake. The authors investigated the interaction between these catecholamine neurons and orexin neurons in the perifornical lateral hypothalamus (PeFLH), which are known to be involved with the stimulation of food intake, increased arousal, and behavioral activation. Rats received 82-ng injections of Anti-DBH-SAP (Cat. #IT-03) into the PeFLH terminal field in order to lesion catecholamine neurons. Saporin (Cat. #PR-01) was used as a control. Assessment of food intake in response to 2-deoxy-D-glucose, as well as selective catecholamine activation, indicated that orexin neuron activation may be involved in glucoprivic appetite responses.
Related Products: Anti-DBH-SAP (Cat. #IT-03), Saporin (Cat. #PR-01)
Individual differences in acute pain-induced endogenous analgesia predict time to resolution of postoperative pain in the rat.
Peters C, Hayashida K, Suto T, Houle T, Aschenbrenner C, Martin T, Eisenach J (2015) Individual differences in acute pain-induced endogenous analgesia predict time to resolution of postoperative pain in the rat. Anesthesiology 122:895-907. doi: 10.1097/ALN.0000000000000593
Summary: The authors investigated the relationship between preoperative Conditioned Pain Modulation (CPM) and the time course of recovery from surgery. CPM was evaluated using forepaw capsaicin injections into rats. During the study, lesioned rats received 5-μg intrathecal injections of anti-DBH-SAP (Cat. #IT-03), followed 14 days later by a partial L5 spinal nerve ligation surgery. Mouse-IgG-SAP (Cat. #IT-18) was used as a control. CPM was partially blocked in the lesioned animals, suggesting descending noradrenergic signaling is important in the time course of recovery from surgery.
Related Products: Anti-DBH-SAP (Cat. #IT-03), Mouse IgG-SAP (Cat. #IT-18)
Contribution of hindbrain catecholamine neurons to orexin-induced feeding
Li A-J, Wang Q, Davis H, Ritter S (2014) Contribution of hindbrain catecholamine neurons to orexin-induced feeding. Neuroscience 2014 Abstracts 834.08. Society for Neuroscience, Washington, DC.
Summary: Both lateral hypothalamic orexinergic neurons and hindbrain catecholaminergic neurons contribute to feeding behavior. In addition, both phenotypes are widely distributed in the brain and their terminal sites are in many cases overlapping. In the hindbrain, both orexin receptor subtypes (OX1R and OX2R) have been found in close proximity to dopamine-β-hydroxylase (DBH)-expressing cell bodies, raising the question of whether orexin stimulates feeding by activating catecholamine neurons. We tested this hypothesis in the present study. First, we implanted rats with fourth ventricular (4V) cannulas and tested feeding in response to 4V injection of orexin (0.5 nmol). Orexin stimulated feeding in rats, and this stimulation was abolished in rats given paraventricular hypothalamic injections of the retrogradely-transported immunotoxin, anti-DBH-saporin, which targets and destroys DBH-expressing neurons. We then examined hindbrain c-Fos expression in normal rats in response to 4V injection of the same orexin dose that stimulated food intake. Using multiple immunofluorescent labels and confocal microscopy we found that most of the orexin-induced c-Fos-immunoreactive (-ir) neurons in the dorsomedial and ventrolateral medulla were DBH-ir and, moreover, that orexin-ir varicosities were situated in close proximity to the Fos-expressing DBH-ir soma. Together these results suggest that orexin stimulates feeding, at least in part, by activating hindbrain catecholamine neurons.
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Hindbrain catecholaminergic projections to the paraventricular nucleus are required for activation of glutamatergic terminals by glycemic challenges
Johnson CS, Watts AG (2014) Hindbrain catecholaminergic projections to the paraventricular nucleus are required for activation of glutamatergic terminals by glycemic challenges. Neuroscience 2014 Abstracts 452.13. Society for Neuroscience, Washington, DC.
Summary: Hindbrain catecholaminergic inputs to the paraventricular nucleus of the hypothalamus (PVH) are necessary for the full response of neuroendocrine neurons to glycemic challenges. The drive provided to the neuroendocrine neurons by ascending catecholaminergic afferents also appears to require a glutamatergic component, as direct norepinephrine stimulation of the peri-PVH region results in a significant increase in glutamatergic excitatory postsynaptic potentials. To determine if these hindbrain catecholaminergic afferents are required to increase the excitatory synaptic drive to neuroendocrine neurons in the medial parvocellular region (mp) of the PVH, we have developed an immunocytochemical (ICC) method to assess if appositions alter their activity in response to a stimulus. This method relies on detecting the increased phosphorylation states of two key intracellular signaling intermediaries, ERK and synapsin I (Syn I), that occur as terminals become activated. Adult male Sprague-Dawley rats received central injections of the immunotoxin saporin conjugated with a dopamine-β-hydroxylase antibody, aimed at the PVH, to ablate catecholaminergic projections from the hindbrain. Rats were then fitted with jugular catheters and administered 2U/kg/ml insulin or 250 mg/kg 2-deoxy-glucose. Following perfusion, coronal sections were cut through the PVH and run for ICC using antibodies against Vesicular Glutamate Transporter 2 (VGluT2), phospho-ERK, and phospho-Syn I. Confocal Z-stacked images through the PVH were acquired, and analysis of 3D images was performed using Volocity software to assess colocalization of VGluT2 with phospho-ERK & phospho-Syn I in terminals within the PVHmp. The mean Pearson’s Colocalization Coefficient was compared across groups. With a glycemic challenge, animals with intact catecholaminergic projections showed an increased numbers of appositions exhibiting colocalization of VGluT2 with the phosphorylated signaling molecules compared to controls. Animals without hindbrain catecholaminergic projections, however, had significantly fewer colocalized appositions. This suggests that catecholaminergic inputs from the hindbrain to the PVH are necessary for the glutamatergic excitation to the neuroendocrine neurons in the medial parvocellular region of the PVH in response to a glycemic stressor, as demonstrated through changes in appositional activity levels.
Related Products: Anti-DBH-SAP (Cat. #IT-03)
C1 neurons excite A5 noradrenergic neurons during hypoxia condition
Borella TL, Takakura AC, Moreira TS (2014) C1 neurons excite A5 noradrenergic neurons during hypoxia condition. Neuroscience 2014 Abstracts 168.07. Society for Neuroscience, Washington, DC.
Summary: C1 neurons activate sympathetic tone and stimulate the hypothalamic-pituitary-adrenal axis in circumstances such as pain, hypoxia or hypotension. They also innervate pontine noradrenergic cells group, including the locus coeruleus (LC) and the ventrolateral pontine catecholaminergic region (A5). Activation of C1 neurons reportedly inhibits pontine neurons; however, because these neurons are glutamatergic and have excitatory effects elsewhere, we re-examined the effect of C1 activation on pontine noradrenergic neurons (A5) using a more selective method. We examined the neuronal effects of destroying C1 catecholaminergic neurons with unilateral injection of the immunotoxin anti-dopamine beta-hydroxylase-saporin (anti-DβH-Sap) into the A5 region during hypoxic condition. Bilateral injections of anti-DβH-Sap into A5 destroyed tyrosine hydroxylase (TH) neurons but spared facial motoneurons and serotonergic neurons within the ventrolateral medulla. Hypoxia (8% O2 – 3 hours) induced a robust increase in Fos expression within the catecholaminergic C1 region of the ventrolateral medulla. On the lesioned side, Fos expression was significantly reduced (53.4 ± 17.6 vs. control: 129.8 ± 22.3 neurons) within the C1 region after hypoxia challenge. Residual Fos expression seen in lesioned side in response to hypoxia provides a basis for probing additional circuits that may be recruited in hierarchical manner in response to hypoxia. In conclusion, the C1 neurons activate the ventrolateral pontine noradrenergic neurons (A5 region) possibly via the release of glutamate from monosynaptic C1 inputs.
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Lesions of hindbrain catecholaminergic projections to nucleus accumbens, bed nucleus of the stria terminalis, lateral parabrachial nucleus or locus coeruleus do not impair glucoprivic feeding
Dinh TT, Huston N, Ritter S (2014) Lesions of hindbrain catecholaminergic projections to nucleus accumbens, bed nucleus of the stria terminalis, lateral parabrachial nucleus or locus coeruleus do not impair glucoprivic feeding. Neuroscience 2014 Abstracts 256.05. Society for Neuroscience, Washington, DC.
Summary: We have shown previously that injection of the retrogradely transported immunotoxin, anti-dopamine beta-hydroxylase (DBH) saporin (DSAP), into the paraventricular nucleus of the hypothalamus (PVH) or arcuate nucleus, abolishes feeding in response to central or systemic glucoprivation. Since DSAP injection destroys DBH-expressing neurons with projections to the injection site, these results strongly implicate hindbrain catecholamine neurons as major mediators of glucoprivic feeding. In order to further define the essential circuitry underlying glucoprivic feeding, we injected DSAP into these additional sites: locus coeruleus (LC), accumbens shell (AcbSh), ventrolatersal bed nucleus of the stria terminalis (vlBNST) and lateral parabrachial nucleus (LPBN). These sites are innervated by hindbrain catecholamine neurons and some sites receive collateral innervation from PVH-projecting catecholamine neurons. Appropriate placement and volume for DSAP administration was determined by co-labeling of DBH-ir neurons with retrograde tracer injected into target sites. Lesions were confirmed by postmortem evaluation of DSAP injection site and by hindbrain catecholamine cell and terminal loss. We found that the feeding response to systemic glucoprivation was not significantly or permanently impaired by injection of DSAP into any of these sites. Based on our results to date, we tentatively conclude that direct projections from hindbrain catecholamine neurons to the LC, AcbSh, vlBNST and LPBN are not required for glucoprivic feeding. The hypothalamus appears to be the major recipient of direct innervation from catecholamine neurons required for glucoprivic feeding
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Effects of noradrenergic denervation by anti-DBH-saporin on behavioral responsivity to L-DOPA in the hemi-parkinsonian rat.
Ostock C, Lindenbach D, Goldenberg A, Kampton E, Bishop C (2014) Effects of noradrenergic denervation by anti-DBH-saporin on behavioral responsivity to L-DOPA in the hemi-parkinsonian rat. Behav Brain Res 270:75-85. doi: 10.1016/j.bbr.2014.05.009
Summary: Dopamine loss is central to Parkinson’s disease and is often accompanied by noradrenergic denervation of the locus coeruleus. In this work the authors examined the role this loss plays in L-DOPA therapy using a rat Parkinson’s disease model. The rats received 10 μg of anti-DBH-SAP (Cat. #IT-03) into the left lateral ventricle. Loss of norepinephrine (NE) neurons did not affect behavior, but lesioned animals were less responsive to the pro-motor therapeutic effects of L-DOPA.
Related Products: Anti-DBH-SAP (Cat. #IT-03)