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Effects of lesions of the histaminergic tuberomammillary nucleus on spontaneous sleep in rats.
Gerashchenko D, Chou TC, Blanco-Centurion CA, Saper CB, Shiromani PJ (2004) Effects of lesions of the histaminergic tuberomammillary nucleus on spontaneous sleep in rats. Sleep 27(7):1275-1281. doi: 10.1093/sleep/27.7.1275
Summary: Although evidence suggests that histaminergic neurons in the tuberomammillary nucleus (TMN) promote wakefulness, this has not been investigated using specific lesioning agents. In this study, the authors utilize the fact that TMN neurons express the orexin-B receptor by eliminating these neurons with an injection of 50 ng of orexin-SAP (Cat. #IT-20) into the posterior hypothalamus. The data indicate that histaminergic neurons are not required for the homeostatic regulation of sleep.
Related Products: Orexin-B-SAP (Cat. #IT-20)
Organized development from human embryonic stem cells after injection into immunodeficient mice
Gertow K, Wolbank S, Rozell B, Sugars R, Andang M, Parish CL, Imreh MP, Wendel M, Ahrlund-Richter L (2004) Organized development from human embryonic stem cells after injection into immunodeficient mice. Stem Cells Dev 13:421-435. doi: 10.1089/scd.2004.13.421 PMID: 15345136
Summary: After thawing and brief drying, sections were fixed with 4% paraformaldehyde in PBS pH 7.4 for 40 min. Sections were blocked [PBS, 1% bovine serum albumin (BSA), 0.3% Triton X-100], washed, and incubated with primary antibodies for Tuj1 (-tubulin type III), glial fibrillary acid protein (GFAP), tyrosine hydroxylase (TH), and vesicular GABA transporter (vGAT; 1:400) overnight at 4°C. After rinsing in PBS, slides were incubated with Cy2- or Cy3-conjugated secondary antibodies.
Related Products: vGAT Rabbit Polyclonal (Cat. #AB-N44)
Hindbrain catecholamine neurons mediate consummatory responses to glucoprivation.
Hudson B, Ritter S (2004) Hindbrain catecholamine neurons mediate consummatory responses to glucoprivation. Physiol Behav 82(2-3):241-250. doi: 10.1016/j.physbeh.2004.03.032
Summary: Norepinephrine (NE) and epinephrine (E) neurons appear to potently stimulate feeding behavior when administered to the hypothalamus. Previous work has indicated that these neurons play important roles in feeding responses due to glucoprivation. Bilateral 42 ng-injections of anti-DBH-SAP (Cat. #IT-03) were administered to rats to investigate the roles of NE and E neurons in the consummatory phase of the glucoprivic response. The results indicate that catecholaminergic neurons are involved in both appetitive and consummatory responses to glucoprivation.
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Sound sequence discrimination learning is dependent on cholinergic inputs to the rat auditory cortex.
Kudoh M, Seki K, Shibuki K (2004) Sound sequence discrimination learning is dependent on cholinergic inputs to the rat auditory cortex. Neurosci Res 50(1):113-123. doi: 10.1016/j.neures.2004.06.007
Summary: The auditory cortex (AC) is thought to play a role in the discrimination of sound sequences. The authors investigated the role of cholinergic inputs to the AC in processing these sequences by injecting 5 µg of 192-Saporin (Cat. #IT-01) into either the lateral ventricle or bilateral AC of rats. Treated animals displayed suppressed sound discrimination learning, but discrimination between two sound components was unaffected. The results suggest that cholinergic neurons in the AC are highly involved in sound sequence learning.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Cognitive and neurological deficits induced by early and prolonged basal forebrain cholinergic hypofunction in rats.
Ricceri L, Minghetti L, Moles A, Popoli P, Confaloni A, De Simone R, Piscopo P, Scattoni ML, di Luca M, Calamandrei G (2004) Cognitive and neurological deficits induced by early and prolonged basal forebrain cholinergic hypofunction in rats. Exp Neurol 189(1):162-172. doi: 10.1016/j.expneurol.2004.05.025
Summary: A distinctive feature of Alzheimer’s disease is the loss of cholinergic neurons in the basal forebrain (BF). The authors investigated long-term effects of BF cholinergic lesions on several parameters. Administration of 0.21 µg of 192-Saporin (Cat. #IT-01) to the third ventricle of 7 day-old rats was followed by an evaluation of protein levels and cortical EEG patterns at 6 months of age. The findings indicate that permanent neonatal BF cholinergic damage may provide a model for abnormal adult cholinergic function.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Age-dependent effect of cholinergic lesion on dendritic morphology in rat frontal cortex.
Works SJ, Wilson RE, Wellman CL (2004) Age-dependent effect of cholinergic lesion on dendritic morphology in rat frontal cortex. Neurobiol Aging 25(7):963-974. doi: 10.1016/j.neurobiolaging.2003.08.003
Summary: Aged rats display more dramatic and longer lasting effects due to brain injury than young animals. The authors examined the role cholinergic neurons may play in brain plasticity after injury in rats of varying ages. 0.15 µg of 192-Saporin (Cat. #IT-01) was injected into the nucleus basalis magnocellularis of young, middle-aged, and aged rats. Some types of injury were only seen in middle-aged and aged rats, and changes in dendritic morphology were least marked in the young animals.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Facilitation of cholinergic transmission by combined treatment of ondansetron with flumazenil after cortical cholinergic deafferentation.
Gil-Bea FJ, Dominguez J, Garcia-Alloza M, Marcos B, Lasheras B, Ramirez MJ (2004) Facilitation of cholinergic transmission by combined treatment of ondansetron with flumazenil after cortical cholinergic deafferentation. Neuropharmacology 47(2):225-232. doi: 10.1016/j.neuropharm.2004.03.014
Summary: Previous studies from this group demonstrated that 5-HT(3) receptor antagonists potentiated by GABA(A) antagonists increased acetylcholine (ACh) release in the rat cerebral cortex. This series of experiments investigated the effects of these antagonists on rats with 0.067 µg-bilateral infusions of 192-Saporin (Cat. #IT-01) into the nucleus basalis magnocellularis. Even after lesioning with 192-Saporin, rats treated with the 5-HT(3) and GABA(A) receptor antagonists displayed increased ACh release, indicating that these antagonists may have use as treatments for cognitive disorders.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Cortical cholinergic function and deficits in visual attentional performance in rats following 192 IgG-Saporin-induced lesions of the medial prefrontal cortex.
Dalley JW, Theobald DE, Bouger P, Chudasama Y, Cardinal RN, Robbins TW (2004) Cortical cholinergic function and deficits in visual attentional performance in rats following 192 IgG-Saporin-induced lesions of the medial prefrontal cortex. Cereb Cortex 14(8):922-932. doi: 10.1093/cercor/bhh052
Summary: Prior work has demonstrated that lesions of the cortical cholinergic system of the basal forebrain impair performance in attentional tasks. The authors examined the effects of selective depletion of acetylcholine from the prefrontal cortex (PFC) on these same attentional tasks. 50 or 100 ng of 192-Saporin (Cat. #IT-01) was infused into the PFC of rats. Treated animals displayed deficits in specific aspects of the attentional tasks, indicating a modulatory role in PFC function by basal forebrain cholinergic neurons.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Featured Article: The discovery of saporin
Stirpe F (2004) Featured Article: The discovery of saporin. Targeting Trends 5(3)
Related Products: Saporin (Cat. #PR-01)
Effects of isolectin B4-conjugated saporin, a targeting cytotoxin, on bladder overactivity induced by bladder irritation.
Nishiguchi J, Sasaki K, Seki S, Chancellor MB, Erickson KA, de Groat WC, Kumon H, Yoshimura N (2004) Effects of isolectin B4-conjugated saporin, a targeting cytotoxin, on bladder overactivity induced by bladder irritation. Eur J Neurosci 20(2):474-482. doi: 10.1111/j.1460-9568.2004.03508.x
Summary: It has been demonstrated that IB4-binding non-peptidergic C-fiber neuronal populations are present in afferent pathways to the bladder. The authors used intrathecal administration of 8 µl of 2.5 µM IB4-SAP (Cat. #IT-10) to investigate what roles these neurons play in bladder function. Treated animals displayed a reduction of IB4 afferent nerve terminal staining, as well as a suppression of bladder overactivity due to bladder irritation, without a change in normal bladder function.
Related Products: IB4-SAP (Cat. #IT-10)
