References

Saenz C, Dominguez R, de Lacalle S (2006) Estrogen contributes to structural recovery after a lesion. Neurosci Lett 392(3):198-201. doi: 10.1016/j.neulet.2005.09.023

Summary: The authors evaluated the trophic effects of 17ß-estradiol (E2) on cholinergic neurons of the basal forebrain after lesioning with 192-IgG-SAP (Cat. #IT-01). Ovariectomized female rats received 200 nl of 0.075 mg/ml 192-IgG-SAP followed by a subcutaneous pellet of E2, which was released over 60 days. Dendritic size in ovariectomized rats receiving the E2 was the same as in control animals, while ovariectomized rats receiving a placebo displayed a significant reduction in dendritic arborization.

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

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)

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)

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)

Lai J, Zhang W, Badghisi H, Hruby VJ, Porreca F (2006) Featured Article: The biologically active cholecystokinin (26-33) peptide, [Tyr2-SO3]CCK-8, retains high affinity for CCK2 receptors after covalent conjugation to saporin. Targeting Trends 7(1)

Related Products: CCK-SAP (Cat. #IT-31)

Read the featured article in Targeting Trends.

See Also:

• Lai J et al. Featured Article: The biologically active cholecystokinin (26-33) peptide, [Tyr2-SO3]CCK-8, retains high affinity for CCK2 receptors after covalent conjugation to saporin. Targeting Trends 7(1), 2006.

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)

Chen J, Zhou Y, Mueller-Steiner S, Chen LF, Kwon H, Yi S, Mucke L, Gan L (2005) SIRT1 protects against microglia-dependent amyloid-beta toxicity through inhibiting NF-κB signaling. J Biol Chem 280(48):40364-40374. doi: 10.1074/jbc.M509329200

Usage: To eliminate microglia in mixed cortical cultures, cultures were treated with either Ac-LDL-SAP at 3 ug/ml for 18 h or 5mM leucine methyl ester for 12 h. These agents selectively kill microglia in mixed cultures.

Related Products: Acetylated LDL-SAP (Cat. #IT-08)

Gibbs RB, Fitz NF, Johnson DA (2005) Cholinergic lesions produce selective effects on cognitive performance in rats. Neuroscience 2005 Abstracts 881.1. Society for Neuroscience, Washington, DC.

Summary: Cholinergic projections from the basal forebrain play an important role in cognitive processes; however, the degree to which damage to specific projections contributes to impairment within specific cognitive domains is unclear. In the present study, cholinergic projections to the hippocampus and/or frontal cortex of young adult, ovariectomized Sprague-Dawley rats were selectively destroyed by injecting 192 IgG-saporin (SAP) into the medial septum (MS), the nucleus basalis magnocellularis (NBM), or both the MS and NBM (MSNBM). Controls received injections of sterile saline. Animals were then tested for learning and memory impairments using a series of tasks, including a delayed matching-to-position (DMP) T-maze task, an operant configural association (CA) negative patterning task, and a 12-arm radial maze (RAM) task, administered in that order. Results reveal different effects of the lesions on the different tasks. For example, SAP lesions of the MS, as well as combined lesions of MS and NBM significantly impaired acquisition the DMP task; however, once animals had reached criterion, cholinergic lesions did not alter decrements in performance produced by increasing the intertrial delay. In contrast, SAP lesions of the MS had no significant effect on acquisition of the CA task, although combined lesions of MS and NBM produced a trend toward impairment on the CA task among animals with the most severe cholinergic depletion. Likewise, combined lesions significantly impaired acquisition of the RAM task. In general, combined lesions produced greater impairments than lesions of either the MS or NBM alone. Significant correlations between acquisition of the DMP and RAM tasks and ChAT activity in the hippocampus, frontal cortex, and occipital cortex, were also detected. These data demonstrate that removal of cholinergic projections to the hippocampus and frontal cortex produce cognitive impairments that are lesion specific as well as task dependent.

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

Bailey AM, St Germain J, Tyler MM (2005) 192 IgG-saporin lesions to the nucleus basalis magnocellularis (NBM) do not disrupt the retention of learning set formation. Neuroscience 2005 Abstracts 881.2. Society for Neuroscience, Washington, DC.

Summary: Male Long Evans rats (Rattus norvegicus) were used to investigate the role of the nucleus basalis magnocellularis (nBM) in the retention of a previously acquired learning set rule. All rats had successfully acquired an olfactory discrimination learning set by demonstrating above chance performance on trial 2 across 42 olfactory discrimination problems. Following the initial acquisition of learning set, animals were given bilateral 192 IgG-saporin (0.375 µg/µl; 0.4 µl per hemisphere) lesions to the nBM. Assessment of open field activity indicated that there were no group differences in general activity levels or emotionality before or after surgery. Retention of learning set was tested 10 days following surgery with 20 novel, odor-unique olfactory discrimination learning set problems. Control and nBM lesioned animals performed significantly higher than expected by chance on trial 2 of the novel problems suggesting retention of a learning set hypothesis. However, rats with 192 IgG-saporin nBM lesions performed learning set at a significantly lower level than control animals as measured by trial 2 percentage correct. Results suggest that damage to the nBM disrupts general performance on a cognitively demanding task, but does not block retention of the learning set rule.

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

Ferry B, Herbeaux K, Petoukhova-Traissard N, Galani R, Cassel J, Majchrzak M (2005) Facilitation of conditioned odor aversion by entorhinal cortex lesion in the rat is reversed by cholinergic lesion in the basal forebrain. Neuroscience 2005 Abstracts 881.6. Society for Neuroscience, Washington, DC.

Summary: In the rat, conditioned odor aversion (COA) corresponds to the avoidance of an odorized-tasteless solution (conditioned stimulus, CS) previously associated with toxicosis (unconditioned stimulus, US). Evidence suggests that the entorhinal cortex (EC) is part of the neural substrate involved in the acquisition of COA. Indeed, we showed that EC lesion facilitated CS-US association and rendered it resistant to lengthening of the interstimulus interval (ISI). This facilitation phenomenon might correspond to a lengthening of the olfactory CS memory trace, rendering the association with the subsequent US possible. Because i) all our EC-lesioned rats showed septo-hippocampal cholinergic sprouting, and ii) scopolamine infusions into the dentate gyrus reversed performance in EC-lesioned but not in sham-operated rats in a spontaneous olfactory preference test, we suggested that COA facilitation resulted from enhanced cholinergic activity in the hippocampus. In order to test this hypothesis, we studied the effect of a cholinergic basal forebrain lesion combined to an EC-lesion during COA. Male Long-Evans rats subjected to bilateral EC lesions and intraventricular infusions of the selective toxin 192 IgG-saporin received odor-US pairings with a short or long ISI. Results showed that sham-lesioned rats displayed COA with the short, but not the long ISI, whereas EC-lesioned rats showed COA with both ISI. More interestingly, rats with double lesions did not differ from controls, suggesting that the cholinergic lesion suppressed the effect of EC-lesions. These results strongly suggest that the facilitative effects observed in EC-lesioned animals during COA are due, at least in part, to the septo-hippocampal cholinergic sprouting elicited by the EC lesion. Moreover, they suggest that the hippocampal cholinergic system is involved in the control of memory processes underlying the association between the olfactory CS and the US during acquisition of COA.

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