References

Turchi JN, Saunders RC, Mishkin M (2002) Effects of cholinergic deafferentation of rhinal cortex on visual recognition in monkeys. Neuroscience 2002 Abstracts 82.5. Society for Neuroscience, Orlando, FL.

Summary: Excitotoxic lesions of the rhinal (perirhinal/entorhinal) cortices yield substantial deficits in visual recognition (Baxter and Murray, 2001; Malkova et al., 2001). To evaluate the mnemonic role of cholinergic inputs to this region, we compared the visual recognition performance of untreated monkeys with that of monkeys given rhinal cortex infusions of the selective cholinergic immunotoxin ME20.4-SAP. This toxin binds to the p75 receptor, borne by corticopetal cholinergic neurons of the basal forebrain, and is retrogradely transported to the cell body where it permanently destroys ribosomal function. Both groups were first trained to criterion in the rule for delayed nonmatching-to-sample (DNMS) with trial-unique stimuli at a 10-s delay in a Wisconsin General Testing Apparatus. This was followed by treatment and recovery for the experimental group (n=3) and an equivalent rest period for the control group (n=4), after which both groups were retrained on the DNMS rule and then given a memory performance test with increasing delays (30, 60, and 120 s) and list lengths (3, 5, 10, and 20 stimuli). The experimental group relearned the DNMS rule without significant impairment but then demonstrated robust deficits when tested with increasing delays (a mean of 83% vs 95% for controls) and list lengths (67% vs 86% for controls). The findings complement results obtained in a study of muscarinic receptor blockade in the perirhinal cortex (Tang et al., 1997) and indicate that cholinergic integrity of the rhinal cortex is critical for visual recognition memory.

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

Suzuki R, Morcuende S, Webber M, Hunt SP, Dickenson AH (2002) Superficial NK1-expressing neurons control spinal excitability through activation of descending pathways. Nat Neurosci 5(12):1319-1326. doi: 10.1038/nn966

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

Tokuno H, Chiken S, Kametani K, Moriizumi T (2002) Efferent projections from the striatal patch compartment: anterograde degeneration after selective ablation of neurons expressing mu-opioid receptor in rats. Neurosci Lett 332(1):5-8. doi: 10.1016/s0304-3940(02)00837-6

Summary: Taking advantage of the fact that neurons in patch compartments of the striatum express µ-opioid receptors, the authors injected 8.5 ng of dermorphin-SAP (Cat. #IT-12) into the striatum of rats. This lesion produced a degeneration of patch neurons as well as anterograde degeneration of efferent fibers from patch compartments, allowing further elucidation of the functional organization of the striatum.

Related Products: Dermorphin-SAP / MOR-SAP (Cat. #IT-12)

Bechade C, Mallecourt C, Sedel F, Vyas S, Triller A (2002) Motoneuron-derived neurotrophin-3 is a survival factor for PAX2-expressing spinal interneurons. J Neurosci 22(20):8779-8784. doi: 10.1523/JNEUROSCI.22-20-08779.2002

Summary: In the rat, half of motoneurons die between embryonic day 15 and postnatal day 1. Programmed cell death of interneurons is not as well characterized. The authors cultured explants of brachial neural tubes from rat embryos in the presence of 200 ng/ml of 192-Saporin (Cat. #IT-01). Although 192-Saporin had no direct effect on interneurons in culture, elimination of p75-neurotrophin receptor-expressing neurons caused the interneurons to die.

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

Khasabov SG, Rogers SD, Ghilardi JR, Peters CM, Mantyh PW, Simone DA (2002) Spinal neurons that possess the substance P receptor are required for the development of central sensitization. J Neurosci 22(20):9086-9098. doi: 10.1523/JNEUROSCI.22-20-09086.2002

Summary: Using 5 x 10-5 M intrathecal injections of SP-SAP (Cat. #IT-07) the authors examined the role of SPR-expressing neurons in modulation of pain and hyperalgesia. Treated animals exhibited highly attenuated sensitization to stimuli after capsaicin treatment as compared to controls, but normal responses in the absence of capsaicin

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

Cassel JC (2002) Featured Article: Does 192-IgG-Saporin or 5,7-DHT kill cognitive functions in the rat?. Targeting Trends 3(4)

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

Read the featured article in Targeting Trends.

See Also:

• Lehmann O et al. 5,7-DHT-induced hippocampal 5-HT depletion attenuates behavioural deficits produced by 192 IgG-saporin lesions of septal cholinergic neurons in the rat. Eur J Neurosci 15(12):1991-2006, 2002.
• Lehmann O et al. Combined 192 IgG-saporin and 5,7-dihydroxytryptamine lesions in the male rat brain: A neurochemical and behavioral study. Pharmacol Biochem Behav 72(4):899-912, 2002.
• Galani R et al. Selective immunolesions of CH4 cholinergic neurons do not disrupt spatial memory in rats. Physiol Behav 76:75-90, 2002.

Zeitschel U, Schliebs R, Rossner S, Bigl V, Eschrich K, Bigl M (2002) Changes in activity and expression of phosphofructokinase in different rat brain regions after basal forebrain cholinergic lesion. J Neurochem 83(2):371-380. doi: 10.1046/j.1471-4159.2002.01127.x

Summary: The authors used intraventricular injections of 4 µg of 192-Saporin (Cat. #IT-01) in rats to investigate whether impaired cholinergic transmission may cause metabolic changes. Although the results demonstrate an initial increase in a cortical glucose metabolic marker, this increase was transient. The authors conclude that cholinergic systems do not control cortical glucose metabolic mechanisms affected by Alzheimer’s disease.

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

Ballmaier M, Casamenti F, Scali C, Mazzoncini R, Zoli M, Pepeu G, Spano PF (2002) Rivastigmine antagonizes deficits in prepulse inhibition induced by selective immunolesioning of cholinergic neurons in nucleus basalis magnocellularis. Neuroscience 114(1):91-98. doi: 10.1016/s0306-4522(02)00234-8

Summary: The authors injected 300 nl of 400 ng/ml 192-Saporin (Cat. #IT-01) bilaterally into the nucleus basalis magnocellularis of rats, then treated the lesioned animals with rivastigmine, a cholinesterase inhibitor. Animals treated with rivistagmine exhibited raised levels of cortical acetylcholine, in contrast to undetectable acetylcholine levels in lesioned animals not treated with rivastigmine.

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

Cassel J, Gaurivaud M, Lazarus C, Bertrand F, Galani R, Jeltsch H (2002) Grafts of fetal septal cells after cholinergic immunotoxic denervation of the hippocampus: a functional dissociation between dorsal and ventral implantation sites. Neuroscience 113(4):871-882. doi: 10.1016/s0306-4522(02)00226-9

Summary: The authors lesioned rats with intraseptal infusions of 0.8 µg 192-Saporin (Cat. #IT-01), then implanted fetal cells in either the dorsal or ventral hippocampus. Only grafts into the dorsal hippocampus counteracted the effect of cholinergic lesions on spatial working memory performance.

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

Pizzo DP, Thal LJ, Winkler J (2002) Mnemonic deficits in animals depend upon the degree of cholinergic deficit and task complexity. Exp Neurol 177:292-305. doi: 10.1006/exnr.2002.7993

Summary: In this study, the authors compared icv and intraparenchymal injections of 192-Saporin (Cat. #IT-01, 3.3 µg and 450 ng, respectively). While a similar reduction in choline acetyltransferase activity was observed with each strategy, and performance in certain allocentric tasks was similar, an egocentric task showed a marked difference between the two groups.

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