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Raphe Magnus Nucleus is involved in ventilatory but not hypothermic response to CO2.
Dias MB, Nucci TB, Margatho LO, Antunes-Rodrigues J, Gargaglioni LH, Branco LG (2007) Raphe Magnus Nucleus is involved in ventilatory but not hypothermic response to CO2. J Appl Physiol 103(5):1780-1788. doi: 10.1152/japplphysiol.00424.2007
Summary: In this work the authors investigated the role that serotonergic neurons in the Raphe Magnus Nucleus (RMg) play in ventilatory and thermal responses to hypercapnia. 0.1 µl of 1 µM anti-SERT-SAP (Cat. #IT-23) was injected into the RMg of rats. Mouse IgG-SAP (Cat. #IT-18) was used as a control. Lesioned animals had a decreased ventilatory response to CO2, but hypercapnia-induced hypothermia was not affected. The data indicate that RMg serotonergic neurons contribute to CO2 ventilatory response but not to maintenance of ventilation.
Related Products: Anti-SERT-SAP (Cat. #IT-23), Mouse IgG-SAP (Cat. #IT-18)
Amyloid beta protein modulates glutamate-mediated neurotransmission in the rat basal forebrain: involvement of presynaptic neuronal nicotinic acetylcholine and metabotropic glutamate receptors.
Chin JH, Ma L, MacTavish D, Jhamandas JH (2007) Amyloid beta protein modulates glutamate-mediated neurotransmission in the rat basal forebrain: involvement of presynaptic neuronal nicotinic acetylcholine and metabotropic glutamate receptors. J Neurosci 27:9262-9269. doi: 10.1523/JNEUROSCI.1843-07.2007 PMID: 17728440
Summary: This work focused on the effect of amyloid beta on glutamate-mediated neurotransmission in the diagonal band of Broca. Using neurons identified by staining with Cy3-labeled 192-IgG (Cat. #FL-01, 5 µl of 1:1 diluted antibody injected into the left and right ventricle) the authors monitored the response to amyloid beta by measuring excitatory postsynaptic currents via whole-cell patch-clamp recordings. The results suggest that glutamate neurotransmission might be vulnerable to Alzheimer’s disease, and may also be a therapeutic target.
Related Products: 192-IgG Mouse Monoclonal, Cy3-labeled (Cat. #AB-N43FL3)
Expression and role of the corticotropin-releasing hormone/urocortin-receptor-binding protein system in the primate corpus luteum during the menstrual cycle.
Xu J, Xu F, Hennebold JD, Molskness TA, Stouffer RL (2007) Expression and role of the corticotropin-releasing hormone/urocortin-receptor-binding protein system in the primate corpus luteum during the menstrual cycle. Endocrinology 148(11):5385-5395. doi: 10.1210/en.2007-0541 PMID: 17690168
Related Products: Corticotropin Releasing Hormone Rabbit Polyclonal (Cat. #AB-02)
Experimental dissociation of neural circuits underlying conditioned avoidance and hypophagic responses to lithium chloride.
Rinaman L, Dzmura V (2007) Experimental dissociation of neural circuits underlying conditioned avoidance and hypophagic responses to lithium chloride. Am J Physiol Regul Integr Comp Physiol 293(4):R1495-1503. doi: 10.1152/ajpregu.00393.2007
Summary: Lithium chloride (LiCl) is frequently used to study neural attributes of “sickness behavior.” Previous work by these authors showed that noradrenergic neurons (NA) in the nucleus of the solitary tract (NST) are involved in the inhibition of food uptake by cholecystokinin. Here, 20 ng total of anti-DBH-SAP (Cat. #IT-03) was injected into the NST of rats. Lesioned animals demonstrated significantly reduced inhibition of food intake in response to LiCl, but conditioned flavor avoidance was left intact.
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Behavioral and immunohistological effects of cholinergic damage in immunolesioned rats: Alteration of c-Fos and polysialylated neural cell adhesion molecule expression.
Chambon C, Paban V, Manrique C, Alescio-Lautier B (2007) Behavioral and immunohistological effects of cholinergic damage in immunolesioned rats: Alteration of c-Fos and polysialylated neural cell adhesion molecule expression. Neuroscience 147:893-905. doi: 10.1016/j.neuroscience.2007.05.022
Summary: In this work the authors looked to expand the knowledge of molecular events and brain structure changes following cholinergic immunolesion. Rats were treated with bilateral injections of 192-IgG-SAP (Cat. #IT-01); 37.5 ng per side into the medial septum, and 75 ng per side into the nucleus basalis magnocellularis. 1 month after treatment behavioral deficits were drastic and cholinergic neurons had completely disappeared. Elevated levels of polysialylated neural cell adhesion molecule were temporarily able to compensate for the loss of cholinergic neurons. NOTE: material from Chemicon, Paris.
Related Products: 192-IgG-SAP (Cat. #IT-01)
A limited role for microglia in antibody mediated plaque clearance in APP mice.
Garcia-Alloza M, Ferrara BJ, Dodwell SA, Hickey GA, Hyman BT, Bacskai BJ (2007) A limited role for microglia in antibody mediated plaque clearance in APP mice. Neurobiol Dis 28(3):286-292. doi: 10.1016/j.nbd.2007.07.019
Summary: Microglia are thought to play a key role in the clearance of amyloid-b (Ab) in Alzheimer’s disease. To examine this role the authors applied 30 µl of 0.5 mg/ml Mac-1-SAP (Cat. #IT-06) to the brain surface of mice for 20 minutes. The number of microglia and plaques was determined by counting of immunohistochemical samples. Results indicate that microglia play a minor role in clearing Ab plaques, although the interaction of microglia-mediated inflammation and anti-Ab antibodies appears to be vital in this process.
Related Products: Mac-1-SAP mouse/human (Cat. #IT-06)
Cortical cholinergic deficiency enhances amphetamine-induced dopamine release in the accumbens but not in the striatum.
Mattsson A, Olson L, Svensson TH, Schilstrom B (2007) Cortical cholinergic deficiency enhances amphetamine-induced dopamine release in the accumbens but not in the striatum. Exp Neurol 208(1):73-79. doi: 10.1016/j.expneurol.2007.07.012
Summary: Previous data has implicated cholinergic dysfunction in the pathogenesis of schizophrenia. Here the authors investigated whether increased amphetamine-induced release of dopamine was a response to cortical cholinergic denervation. Rats received bilateral 0.067 µg injections of 192-IgG-SAP (Cat. #IT-01) into the nucleus basalis magnocellularis, and dopamine release was monitored in the nucleus accumbens and striatum. Surprisingly, the increased dopamine release was not linked to loss of cholinergic neurons, but to blocking of muscarinic receptors.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Respiratory plasticity in response to changes in oxygen supply and demand
Bavis RW, Powell FL, Bradford A, Hsia CCW, Peltonen JE, Soliz J, Zeis B, Fergusson ED, Fu Z, Gassmann M, Kim CB, Maurer J, McGuire M, Miller BM, O’Halloran KD, Paul RJ, Reid SG, Rusko HK, Tikkanen HO, Wilkinson KA (2007) Respiratory plasticity in response to changes in oxygen supply and demand. Integ and Comp Biol 47(4):532-551. doi: 10.1093/icb/icm070
Summary: This paper covers data presented at the First Annual Congress of Respiratory Biology. One of the subjects discussed is the use of SP-SAP (Cat. #IT-07) to elucidate the role of central chemoreceptors in the nucleus tractus solitarius during ventilatory acclimatization to hypoxia.
Related Products: SP-SAP (Cat. #IT-07)
Ketanserin-induced baroreflex enhancement in spontaneously hypertensive rats depends on central 5-HT(2A) receptors.
Shen FM, Wang J, Ni CR, Yu JG, Wang WZ, Su DF (2007) Ketanserin-induced baroreflex enhancement in spontaneously hypertensive rats depends on central 5-HT(2A) receptors. Clin Exp Pharmacol Physiol 34:702-707. doi: 10.1111/j.1440-1681.2007.04626.x
Summary: Ketanserin is an anytihypertensive drug that effectively lowers blood pressure, decreases blood pressure variability, and enhances blood pressure response in spontaneously hypertensive rats. Using the fact that ketanserin is a selective 5-HT2A antagonist the authors investigated which of these effects utilized the 5-HT2A receptor. Following a 5 nmol ventricular injection of anti-SERT-SAP (Cat. #IT-23) the blood pressure parameters modified by ketanserin were monitored. The data suggest that the baroreflex sensitivity-enhancing effects of ketanserin use the 5-HT2A pathway, but antihypertensive effects follow a different route.
Related Products: Anti-SERT-SAP (Cat. #IT-23)
Superficial NK1 expressing spinal dorsal horn neurones modulate inhibitory neurotransmission mediated by spinal GABA(A) receptors.
Rahman W, Sikander S, Suzuki R, Hunt SP, Dickenson AH (2007) Superficial NK1 expressing spinal dorsal horn neurones modulate inhibitory neurotransmission mediated by spinal GABA(A) receptors. Neurosci Lett 419:278-283. doi: 10.1016/j.neulet.2007.04.039
Summary: It has been shown that elimination of lamina 1 NK1 receptor-expressing neurons affects pain behaviors. The authors investigated whether eliminating these neurons would alter GABAergic spinal inhibitory systems. Rats received 10-µl injections of 10-µM SP-SAP (Cat. #IT-07) into the L4-5 regions. Data generated by electrical and mechanical stimuli suggest that although GABAergic transmission is dependent on NK1 receptor-expressing neurons, loss of these cells results in a decrease in spinal cord excitability.
Related Products: SP-SAP (Cat. #IT-07)
