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Spinal neurons involved in the generation of at-level pain following spinal injury in the rat.
Yezierski RP, Yu CG, Mantyh PW, Vierck CJ, Lappi DA (2004) Spinal neurons involved in the generation of at-level pain following spinal injury in the rat. Neurosci Lett 361(1-3):232-236. doi: 10.1016/j.neulet.2003.12.035
Summary: The elimination of substance P receptor-expressing neurons in lamina I of the spinal cord using SP-SAP (Cat. #IT-07) has been shown to reduce behavior associated with chronic pain. The authors investigated the effects of 150 or 300 ng SP-SAP treatment during or after intraspinal administration of quisqualic acid in rats. Both treatments resulted in a reduction of pain-associated behavior. These results demonstrate that pain following spinal cord injury involves a population of spinal neurons expressing the substance P receptor.
Related Products: SP-SAP (Cat. #IT-07)
Recurrent paraplegia after remyelination of the spinal cord.
Jasmin L, Ohara PT (2004) Recurrent paraplegia after remyelination of the spinal cord. J Neurosci Res 77(2):277-284. doi: 10.1002/jnr.20143
Summary: Previously, the authors demonstrated that a 3 µg-injection of CTB-SAP (Cat. #IT-14) into the lumbosacral intrathecal space caused a loss of motor function due to spinal demyelination. The motor function was recovered and stable for up to 9 months, after which the rats exhibited a slow deterioration of motor function, loss of spinal white matter, and the appearance of calcium deposits. The results indicate that the CTB-SAP-induced demyelination model is useful for investigating long term effects of axon and motoneuron loss.
Related Products: CTB-SAP (Cat. #IT-14)
Loss of cortical acetylcholine enhances amphetamine-induced locomotor activity.
Mattsson A, Pernold K, Ogren SO, Olson L (2004) Loss of cortical acetylcholine enhances amphetamine-induced locomotor activity. Neuroscience 127(3):579-591. doi: 10.1016/j.neuroscience.2004.05.038
Summary: The authors have recently shown that cholinergic denervation of the basal forebrain in rats leads to an increased motor response to d-amphetamine, a hallmark of schizophrenia. In the present study 192-Saporin (Cat. #IT-01) was injected into the nucleus basalis magnocellularis or the medial septum/diagonal band of Broca, and OX7-SAP (Cat. #IT-02) was injected intracerebroventricularly. The dopaminergic hyper-reactivity was induced by lesions to the cortex cerebri, but not by damage to the cerebellum or hippocampus.
Related Products: 192-IgG-SAP (Cat. #IT-01), OX7-SAP (Cat. #IT-02)
Intrathecal application of saporin conjugates leads to development of pituitary adenomas in rats
Margeta M, Ohara PT, Bollen AW, Jasmin L (2004) Intrathecal application of saporin conjugates leads to development of pituitary adenomas in rats. J Neuropathol Exp Neurology 63(5):518.
Objective: To study the recovery from spinal cord demyelination or the effects of decreased central noradrenergic tone on pain behavior.
Summary: The spectrum of findings varied from small, sometimes multifocal nodules to large neoplasms that entirely replaced the normal gland and showed a significant degree of mitotic activity and nuclear pleomorphism. Development of this novel animal model will enable investigation of non-hormonal factors important in the pathogenesis of pituitary adenomas
Usage: Rats were injected intrathecally with CTB-SAP (IT-14) or to the anti-DBH-SAP (IT-03)
Related Products: CTB-SAP (Cat. #IT-14), Anti-DBH-SAP (Cat. #IT-03)
Altered neurotrophin receptor function in the developing prefrontal cortex leads to adult-onset dopaminergic hyperresponsivity and impaired prepulse inhibition of acoustic startle.
Rajakumar N, Leung LS, Ma J, Rajakumar B, Rushlow W (2004) Altered neurotrophin receptor function in the developing prefrontal cortex leads to adult-onset dopaminergic hyperresponsivity and impaired prepulse inhibition of acoustic startle. Biol Psychiatry 55(8):797-803. doi: 10.1016/j.biopsych.2003.12.015
Summary: Neurodevelopmental abnormalities are suspected to play a role in the pathogenesis of schizophrenia. The authors injected 0.75 µl of 192-Saporin (Cat. #IT-01) bilaterally into the prefrontal cortex of postnatal day 1 rats. The rats were then evaluated in tests designed to measure behavioral abnormalities relevant to schizophrenia. The behavior of the treated animals indicated that damage to p75-receptor-expressing neurons in the prefrontal cortex may be involved in the manifestation of schizophrenia.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Modulation of photic resetting in rats by lesions of projections to the suprachiasmatic nuclei expressing p75 neurotrophin receptor.
Erhardt C, Galani R, Jeltsch H, Cassel JC, Klosen P, Menet JS, Pevet P, Challet E (2004) Modulation of photic resetting in rats by lesions of projections to the suprachiasmatic nuclei expressing p75 neurotrophin receptor. Eur J Neurosci 19(7):1773-1788. doi: 10.1111/j.1460-9568.2004.03281.x
Summary: The circadian clock in mammals is located within suprachiasmatic nuclei of the hypothalamus (SCN). The authors investigated how cholinergic afferents from the basal forebrain may be involved in control of the circadian clock. 3 µg of 192-Saporin (Cat. #IT-01) was injected intracerebroventricularly, or 1 µg was injected in SCN of rats, and various aspects of the circadian system were investigated. The data suggest that the forebrain cholinergic system is involved in the phase resetting properties of light.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Featured Article: 192 IgG-saporin-induced lesions identify an inhibitory role in cocaine reward for cholinergic neuronal systems in the diagonal band and ventral pallidum
Smith J (2004) Featured Article: 192 IgG-saporin-induced lesions identify an inhibitory role in cocaine reward for cholinergic neuronal systems in the diagonal band and ventral pallidum. Targeting Trends 5(2)
Related Products: 192-IgG-SAP (Cat. #IT-01)
Read the featured article in Targeting Trends.
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Medullary serotonergic neurons and adjacent neurons that express neurokinin-1 receptors are both involved in chemoreception in vivo.
Nattie EE, Li A, Richerson GB, Lappi DA (2004) Medullary serotonergic neurons and adjacent neurons that express neurokinin-1 receptors are both involved in chemoreception in vivo. J Physiol 556(1):235-253. doi: 10.1113/jphysiol.2003.059766 PMID: 14724193
Summary: The retrotrapezoid nucleus contains neurokinin-1 receptor (NK-1r)-expressing neurons that are involved in chemoreception. NK-1r-expressing neurons are also present in areas that contain medullary serotonergic neurons. These serotonergic neurons have been shown to be chemosensitive in vitro. With two 100-nl injections of 1 µM SP-SAP (Cat. #IT-07), anti-SERT-SAP (Cat. #IT-23), or both, the authors examined whether both cell populations are involved in chemoreception in vivo in rats. The results support that separate populations of serotonergic and NK-1r-expressing neurons are each involved in chemoreception in vivo.
Related Products: SP-SAP (Cat. #IT-07), Anti-SERT-SAP (Cat. #IT-23), Antibody to Serotonin Transporter (SERT, Cat. #AB-N09)
Habituation to stress and dexamethasone suppression in rats with selective basal forebrain cholinergic lesions.
Helm KA, Ziegler DR, Gallagher M (2004) Habituation to stress and dexamethasone suppression in rats with selective basal forebrain cholinergic lesions. Hippocampus 14(5):628-635. doi: 10.1002/hipo.10203
Summary: Basal forebrain cholinergic neurons may be involved in hippocampal and medial prefrontal cortex inhibition of glucocorticoid stress responses. The authors investigated the effects of 0.05 to 0.075 µg injections of 192-Saporin (Cat. #IT-01) into the medial septum/vertical limb of the diagonal band of rats by measuring corticosterone levels during a restraint stress test. Lesioned rats displayed less stress suppression on the administration of dexamethasone than controls, indicating that cholinergic neurons are involved in these stress responses.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Macrophage-derived tumor necrosis factor alpha, an early developmental signal for motoneuron death.
Sedel F, Béchade C, Vyas S, Triller A (2004) Macrophage-derived tumor necrosis factor alpha, an early developmental signal for motoneuron death. J Neurosci 24(9):2236-2246. doi: 10.1523/JNEUROSCI.4464-03.2004
Related Products: IB4-SAP (Cat. #IT-10)
