tt2006

Li A, Nattie E (2006) Catecholamine neurones in rats modulate sleep, breathing, central chemoreception and breathing variability. J Physiol 570(Pt 2):385-396. doi: 10.1113/jphysiol.2005.099325

Summary: Brainstem catecholamine (CA) neurons are thought to modulate the processing of sensory information and participate in the control of breathing. Using a 5 µg injection of anti-DBH-SAP (Cat. #IT-03), or a control injection of mouse-IgG-SAP (Cat. #IT-18) into the fourth ventricle, the authors investigated breathing frequency and wakefulness. The results suggest that CA neurons promote wakefulness, participate in central respiratory chemoreception, stimulate breathing frequency, and minimize breathing variability during REM sleep.

Related Products: Anti-DBH-SAP (Cat. #IT-03), Mouse IgG-SAP (Cat. #IT-18)

Emgard M, Paradisi M, Pirondi S, Fernandez M, Giardino L, Calza L (2007) Prenatal glucocorticoid exposure affects learning and vulnerability of cholinergic neurons. Neurobiol Aging 28(1):112-121. doi: 10.1016/j.neurobiolaging.2005.11.015

Summary: Women at risk of preterm delivery are commonly treated with synthetic glucocorticoids such as dexamethasone and betamethasone. Here the authors examined adult rats that were prenatally exposed to glucocorticoids. After 2.5 µg intracerebroventricular injections of 192-IgG-SAP (Cat. #IT-01) or 0.44 µg of saporin (Cat. #PR-01), the rats were tested in a water maze pool. The evidence suggests that not only do prenatal glucocorticoids affect adult cognitive function, they also make cholinergic neurons more susceptible to challenges later in life.

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

Saurer TB, Carrigan KA, Ijames SG, Lysle DT (2006) Suppression of natural killer cell activity by morphine is mediated by the nucleus accumbens shell. J Neuroimmunol 173(1-2):3-11. doi: 10.1016/j.jneuroim.2005.11.009

Summary: In this work the authors investigated the role of dopaminergic projections to the nucleus accumbens in modulation of immune parameters such as morphine-induced suppression of splenic natural killer (NK) cell activity. Studies have indicated that acute exposure to opioids decrease NK cell-mediated cytotoxicity. Rats received bilateral 0.5 µg-injections of anti-DAT-SAP (Cat. #IT-25) into the nucleus accumbens shell. Treated animals showed no immunosuppression upon administration of morphine, indicating that dopaminergic neurons in the nucleus accumbens play a major role in this pathway.

Related Products: Anti-DAT-SAP (Cat. #IT-25)

Gerashchenko D, Blanco-Centurion CA, Miller JD, Shiromani PJ (2006) Insomnia following hypocretin2-saporin lesions of the substantia nigra. Neuroscience 137(1):29-36. doi: 10.1016/j.neuroscience.2005.08.088

Objective: To investigate which regions of major arousal areas might be responsible for the changes in sleep-wake architecture

Summary: It is known that orexin (also known as hypocretin) is involved in waking. The results suggest that motor activity is under inhibitory control of the substantia nigra.

Usage: Bilateral injection of Orexin-SAP (92 and 184 ng/ml, 0.25 ml in the ventral tegmental area and 0.5 ml in the substantia nigra) of rats induced insomnia, as well as hyperactivity and stereotypic movements.

Related Products: Orexin-B-SAP (Cat. #IT-20)

Mattsson A, Lindqvist E, Ogren SO, Olson L (2005) Increased phencyclidine-induced hyperactivity following cortical cholinergic denervation. Neuroreport 16(16):1815-1819. doi: 10.1097/01.wnr.0000185018.29316.87

Summary: A potential contribution to schizophrenia is altered cholinergic function. The authors investigated how lesioning cholinergic corticopetal projections might affect glutaminergic activity. Rats were injected with 0.134 µg of 192-IgG-SAP (Cat. #IT-01) into the nucleus basalis magnocellularis. The authors found that cholinergic lesioning of the neocortex led to enhanced sensitivity to phencyclidine, which has been shown to induce clinical symptoms similar to those of schizophrenia. These data suggest that glutaminergic dysfunction may be relevant to schizophrenia pathophysiology.

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

Vago R, Marsden CJ, Lord JM, Ippoliti R, Flavell DJ, Flavell SU, Ceriotti A, Fabbrini MS (2005) Saporin and ricin A chain follow different intracellular routes to enter the cytosol of intoxicated cells. FEBS J 272(19):4983-4995. doi: 10.1111/j.1742-4658.2005.04908.x

Summary: Some bacterial toxins such as Pseudomonas aeruginosa exotoxin A carry a KDEL-like C-terminal peptide sequence, which targets the protein to the endoplasmic reticulum. Saporin (Cat. #PR-01) is a plant ribosome-inactivating protein, which does not contain a KDEL-like sequence. Here the authors examined the intracellular pathways utilized by saporin. Although ricin, another plant ribosome-inactivating protein, could be visualized in the Golgi complex, saporin was not. The data suggest that saporin may utilize endosomes during its journey through the cell.

Related Products: Saporin (Cat. #PR-01)

Sherren N, Pappas BA (2005) Selective acetylcholine and dopamine lesions in neonatal rats produce distinct patterns of cortical dendritic atrophy in adulthood. Neuroscience 136(2):445-456. doi: 10.1016/j.neuroscience.2005.08.053

Summary: In this work the authors examined lesions of acetylcholine afferents in 7-day-old rat pups, and the effect on dendritic development. 600 ng of 192-IgG-SAP (Cat. #IT-01) were administered to the ventricles of test animals. Various morphological changes in the retrosplenial cortex were observed, including smaller apical tufts and fewer basilar dendritic branches in layer V medial prefrontal cells. The data demonstrate that ascending acetylcholine afferents are very important in the development of cortical cytoarchitecture.

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

Fontan-Lozano A, Troncoso J, Munera A, Carrion AM, Delgado-Garcia JM (2005) Cholinergic septo-hippocampal innervation is required for trace eyeblink classical conditioning. Learn Mem 12(6):557-563. doi: 10.1101/lm.28105

Summary: Classical conditioning of eyeblink responses can be used to evaluate cognitive deficits. The authors lesioned the medial septum/diagonal band of rats with 200 ng of 192-IgG-SAP (Cat. #IT-01), then examined classical and instrumental conditioning paradigms. Lesioned animals displayed a deficit in the acquisition, but not retrieval of eyeblink classical conditioning. The deficit was reversed by carbachol, a cholinergic muscarinic agonist, suggesting a role for the muscarinic system in the acquisition of new motor abilities.

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

Hawkes C, Jhamandas JH, Kar S (2005) Selective loss of basal forebrain cholinergic neurons by 192 IgG-saporin is associated with decreased phosphorylation of Ser glycogen synthase kinase-3beta. J Neurochem 95(1):263-272. doi: 10.1111/j.1471-4159.2005.03363.x

Summary: Glycogen synthase kinase-3ß (GSK-3ß) is an enzyme involved in a variety of biological events. In this study the authors examined the potential role of GSK-3ß in degeneration of basal forebrain cholinergic neurons. Rats were treated with 2.0 µg per ventricle injections of 192-IgG-SAP (Cat. #IT-01), then GSK-3ß and other cholinergic marker levels were assayed. The results indicate that increased GSK-3ß activity can provide some protection from 192-IgG-SAP-induced degeneration of forebrain cholinergic neurons.

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

Yamazaki Y, Jia Y, Hamaue N, Sumikawa K (2005) Nicotine-induced switch in the nicotinic cholinergic mechanisms of facilitation of long-term potentiation induction. Eur J Neurosci 22(4):845-860. doi: 10.1111/j.1460-9568.2005.04259.x

Summary: The authors investigated cellular mechanisms underlying improved cognitive function in Alzheimer’s disease patients upon the administration of nicotine. To model Alzheimer’s disease in rats, 2 µg of 192-IgG-SAP (Cat. #IT-01) was injected into the lateral cerebral ventricle. Examination of the lesioned animals suggests that nicotine promotes the induction of long-term potentiation by enhancing N-methyl-D-aspartate responses, and suppressing acetylcholine-mediated mechanisms in pyramidal cells.

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