tt2005

43 entries

Possible role of CRF peptides in burn-induced hypermetabolism.

Chance WT, Dayal R, Friend LA, Sheriff S (2006) Possible role of CRF peptides in burn-induced hypermetabolism. Life Sci 78(7):694-703. doi: 10.1016/j.lfs.2005.05.083

Summary: Burn trauma has been associated with hypermetabolism and anorexia. Corticotropin releasing factor (CRF) elevates metabolic rate and elicits anorexia, while neuropeptide Y (NPY) reduces metabolic rate while stimulating feeding. After burn treatment, rats were injected with 2.5 µg CRF-SAP (Cat. #IT-13) into the third ventricle. Several parameters, including resting energy expenditure, NPY concentrations in the paraventricular nucleus, and CRFr-2 density were evaluated post-treatment. The results indicate that the CRFr-2 is important in maintaining hypermetabolism resulting from burn trauma.

Related Products: CRF-SAP (Cat. #IT-13)

Septal innervation regulates the function of alpha7 nicotinic receptors in CA1 hippocampal interneurons.

Thinschmidt JS, Frazier CJ, King MA, Meyer EM, Papke RL (2005) Septal innervation regulates the function of alpha7 nicotinic receptors in CA1 hippocampal interneurons. Exp Neurol 195(2):342-352. doi: 10.1016/j.expneurol.2005.05.006

Summary: The authors examined whether hippocampal innervation by medial septum/diagonal band of Broca projections is necessary for normal a7 receptor function. 1 µg of 192-Saporin (Cat. #IT-01) was injected into the medial septum of rats. Various methods, including whole-cell patch clamping and immunohistochemistry, were used to evaluate the effects of these lesions. Lesioning with 192-Saporin did not affect a7 receptor currents, indicating that cholinergic neurons are not linked to a7 function.

Related Products: 192-IgG-SAP (Cat. #IT-01)

Spinal-supraspinal serotonergic circuits regulating neuropathic pain and its treatment with gabapentin.

Suzuki R, Rahman W, Rygh LJ, Webber M, Hunt SP, Dickenson AH (2005) Spinal-supraspinal serotonergic circuits regulating neuropathic pain and its treatment with gabapentin. Pain 117(3):292-303. doi: 10.1016/j.pain.2005.06.015

Summary: The anticonvulsant, gabapentin, is thought to modulate calcium channel function. In animals, it also affects abnormal pain function. 10 µl of 1 µM SP-SAP (Cat. #IT-07) was injected into the subarachnoid space of rats. It was found that the effects of gabapentin were blocked when NK-1r expressing neurons in the dorsal horn were eliminated. The results suggest that not only is the NK-1r pathway a determinant of neuronal and behavioral manifestations of neuropathy, it is also involved in the action of gabapentin.

Related Products: SP-SAP (Cat. #IT-07)

Ablation of vagal preganglionic neurons innervating the extra-thoracic trachea affects ventilatory responses to hypercapnia and hypoxia.

Wu M, Kc P, Mack SO, Haxhiu MA (2006) Ablation of vagal preganglionic neurons innervating the extra-thoracic trachea affects ventilatory responses to hypercapnia and hypoxia. Respir Physiol Neurobiol 152(1):36-50. doi: 10.1016/j.resp.2005.07.002

Summary: Hypercapnia, an excess of CO2 in the blood, is thought to stimulate the release of acetylcholine by airway-related vagal preganglionic neurons (AVPNs). AVPNs in the nucleus ambiguus (NA) were lesioned with ten 1-µl injections of CTB-SAP (Cat. #IT-14) into the trachealis muscle of rats. Treated animals maintained rhythmic breathing patterns, but episodes of increased respiratory rate in response to hypercapnia were significantly reduced.

Related Products: CTB-SAP (Cat. #IT-14)

Autonomic brainstem nuclei are linked to the hippocampus.

Castle M, Comoli E, Loewy AD (2005) Autonomic brainstem nuclei are linked to the hippocampus. Neuroscience 134(2):657-669. doi: 10.1016/j.neuroscience.2005.04.031

Summary: Stimulation of the vagal nerve has been reported to enhance memory, as well as be an effective treatment for epilepsy. The authors examined the underlying synaptic pathway. The right ventral CA1 hippocampal field of rats was lesioned with 42 ng of either anti-DBH-SAP (Cat. #IT-03), or 192-Saporin (Cat. #IT-01). The results indicate that both noradrenergic and cholinergic neurons are relay sites for this pathway.

Related Products: 192-IgG-SAP (Cat. #IT-01), Anti-DBH-SAP (Cat. #IT-03)

Origin and immunolesioning of cholinergic basal forebrain innervation of cat primary auditory cortex.

Kamke MR, Brown M, Irvine DR (2005) Origin and immunolesioning of cholinergic basal forebrain innervation of cat primary auditory cortex. Hear Res 206(1-2):89-106. doi: 10.1016/j.heares.2004.12.014

Summary: In this study the authors assessed the use of a cholinergic immunotoxin while examining cholinergic basal forebrain input to the primary auditory cortex in cat. Six 0.5 µg injections of ME20.4-SAP (Cat. #IT-15) were made into the putamen/globus pallidus, and cholinergic cell survival was examined by immunohistochemistry. The injected area showed a large reduction in number of AChE-positive fibers in the primary auditory cortex. This provides the evidence of the efficacy of ME20.4-SAP for investigating plasticity in cat auditory cortex.

Related Products: ME20.4-SAP (Cat. #IT-15)

Susceptibility to seizure-induced injury and acquired microencephaly following intraventricular injection of saporin-conjugated 192 IgG in developing rat brain.

Koh S, Santos TC, Cole AJ (2005) Susceptibility to seizure-induced injury and acquired microencephaly following intraventricular injection of saporin-conjugated 192 IgG in developing rat brain. Exp Neurol 194(2):457-466. doi: 10.1016/j.expneurol.2005.03.002

Summary: It is thought that one mechanism for resistance to seizure-induced injury in immature animals is an abundance of neurotrophic growth factors. Rat pups were treated with 2 µg of 192-Saporin (Cat. #IT-01) injected into the left lateral ventricle to examine how cholinergic basal forebrain projections might affect this type of injury. The results indicate that these neurons may be critical for normal brain growth, and that they play a protective role in preventing excitotoxic neuronal injury.

Related Products: 192-IgG-SAP (Cat. #IT-01)

Neonatal lesion of forebrain cholinergic neurons: Further characterization of behavioral effects and permanency.

Pappas BA, Payne KB, Fortin T, Sherren N (2005) Neonatal lesion of forebrain cholinergic neurons: Further characterization of behavioral effects and permanency. Neuroscience 133(2):485-492. doi: 10.1016/j.neuroscience.2005.02.040

Summary: Neonatal rats treated with bilateral intracerebroventricular injections of 300 ng of 192-Saporin (Cat. #IT-01) showed basal forebrain cholinergic neuron loss that was still evident at 24 months of age. The authors tested the reference memory and attentional processing of these rats in a Morris water maze. The results suggest that impaired performance of the treated animals in complex maze tasks reflects reduced problem solving ability rather than a deficit in attentional processing.

Related Products: 192-IgG-SAP (Cat. #IT-01)

Elimination of neurokinin-1 receptor neurons in caudal nucleus reverses the effects of systemic bicuculline on c-Fos expression in rat trigeminal sensory nucleus: I. High intensity electrical stimulation of the trigeminal ganglion.

Abe T, Ohshita N, Sugiyo S, Moritani M, Kobayashi M, Takemura M (2005) Elimination of neurokinin-1 receptor neurons in caudal nucleus reverses the effects of systemic bicuculline on c-Fos expression in rat trigeminal sensory nucleus: I. High intensity electrical stimulation of the trigeminal ganglion. Neuroscience 133(3):739-747. doi: 10.1016/j.neuroscience.2005.03.021

Summary: The authors investigated the role of NK-1r + neurons in lamina 1 of the trigeminal caudal nucleus (Vc) for ora-facial nociception. After a 5 µl injection of 5 µM SP-SAP (Cat. #IT-07) into the cisterna magna, c-fos expression in the Vc was evaluated. SP-SAP treatment, along with use of bicuculline, a GABAA receptor antagonist, showed that NK-1r+ neurons in laminae I and III of the Vc are involved in nociceptive processing in the trigeminal sensory nucleus.

Related Products: SP-SAP (Cat. #IT-07)

Aging and cholinergic deafferentation alter GluR1 expression in rat frontal cortex.

Kim I, Wilson RE, Wellman CL (2005) Aging and cholinergic deafferentation alter GluR1 expression in rat frontal cortex. Neurobiol Aging 26(7):1073-1081. doi: 10.1016/j.neurobiolaging.2004.09.005

Summary: Neuronal plasticity is involved in several processes during adulthood, including learning and memory, and recovery from injury. Recent evidence suggests that aging reduces this plasticity. The authors used 0.15 µg injections of 192-Saporin (Cat. #IT-01) into the nucleus basalis magnocellularis of rats to investigate how the loss of cortical plasticity would affect the expression of GluR1. Younger animals displayed a marked increase in the number of GluR1-expressing neurons, a compensatory response not seen in older animals.

Related Products: 192-IgG-SAP (Cat. #IT-01)

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