targeted-toxins

Yu Y-Q, Barry DM, Hao Y, Liu X-T, Chen Z-F (2017) Molecular and neural basis of contagious itch behavior in mice. Science 355:1072. doi: 10.1126/science.aak9748

Summary: The authors selectively ablated the SCN gastrin-releasing peptide receptor (GRPR) neurons using Bombesin-SAP (Cat. #IT-40), a peptide-conjugated toxin that kills GRPR neurons in the spinal cord. After bilateral injection of Bombesin-SAP into the SCN, immunohistochemistry showed that Bombesin-SAP injection resulted in ablation of SCN GRPR+ neurons.

Related Products: Bombesin-SAP (Cat. #IT-40)

Maurice T, Goguadze N (2017) Sigma-1 (σ1) receptor in memory and neurodegenerative diseases. Handb Exp Pharmacol 244:81-108. doi: 10.1007/164_2017_15

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

Jeong D, Lee J, Chang W, Chang J (2017) Identifying the appropriate time for deep brain stimulation to achieve spatial memory improvement on the Morris water maze. BMC Neuroscience 18:29.. doi: 10.1186/s12868-017-0345-4

Summary: This study was performed to determine the stage of memory affected by medial septum deep brain stimulation (MS-DBS). Memory impairment due to cholinergic denervation can be improved by DBS. The improvement is significantly correlated with the up-regulation of BDNF expression and neurogenesis. Based on the results of this study, the use of MS-DBS during the early stage of disease may restore spatial memory impairment.

Usage: Rats were injected bilaterally with 8 μl of 192-IgG-SAP (0.63 μg/μl) at the cerebroventricle.

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

Burma NE, Bonin RP, Leduc-Pessah H, Baimel C, Cairncross ZF, Mousseau M, Shankara JV, Stemkowski PL, Baimoukhametova D, Bains JS, Antle MC, Zamponi GW, Cahill CM, Borgland SL, De Koninck Y, Trang T (2017) Blocking microglial pannexin-1 channels alleviates morphine withdrawal in rodents. Nat Med 23:355-360.. doi: 10.1038/nm.4281

Summary: The authors investigated the mechanisms underlying opiate withdrawal in rat. Depletion of spinal lumbar microglia by intrathecal injections of Mac-1–SAP (Cat. #IT-33; 20 mcg) decreased withdrawal behaviors and attenuated the severity of withdrawal without affecting morphine antinociception. Unconjugated Saporin (Cat. #PR-01; 20 mcg) was used as control and had no effect on spinal CD11b immunoreactivity or naloxone-induced morphine withdrawal.

Related Products: Mac-1-SAP rat (Cat. #IT-33), Saporin (Cat. #PR-01)

Bondarenko N, Dilmukhametova L, Kurina A, Murtazina A, Sapronova A, Sysoeva A, Ugrumov M (2017) Plasticity of central and peripheral sources of noradrenaline in rats during ontogenesis. Biochemistry (Mosc) 82:373-379.. doi: 10.1134/S0006297917030166

Related Products: Anti-DBH-SAP (Cat. #IT-03)

Martínez-Gardeazabal J, González de San Román E, Moreno-Rodríguez M, Llorente-Ovejero A, Manuel I, Rodríguez-Puertas R (2017) Lipid mapping of the rat brain for models of disease. Biochim Biophys Acta Biomembr 1859:1548-1557.. doi: 10.1016/j.bbamem.2017.02.011

Objective: To map the spatial distribution of different lipid species in the rat central nervous system (CNS) using IMS to find a possible relationship between anatomical localization and physiology. The data obtained were subsequently applied to a model of neurological disease, the 192IgG-saporin lesion model of memory impairment.

Summary: The specific distribution of different lipids supports their involvement not only in structural and metabolic functions but also as intracellular effectors or specific receptor ligands and/or precursors. Moreover, the specific localization in the CNS described here will enable us to analyze lipid distribution to identify their physiological conditions in rat models of neurodegenerative pathologies, such as Alzheimer’s disease.

Usage: 192 IgG-SAP in aCSF (135 ng/1 μl/hemisphere; 0.25 μl/min) was administered.

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

Gelfo F, Cutuli D, Nobili A, De Bartolo P, D’Amelio M, Petrosini L, Caltagirone C (2017) Chronic lithium treatment in a rat model of basal forebrain cholinergic depletion: Effects on memory impairment and neurodegeneration. J Alzheimers Dis 56:1505-1518. doi: 10.3233/JAD-160892 PMID: 28222508

Objective: To evaluate the potential beneficial effects of a chronic lithium treatment in preventing the damage that a basal forebrain cholinergic neurodegeneration provokes.

Summary: The chronic lithium treatment significantly rescued memory performances but did not modulate ChAT availability and caspase-3 activity. The present findings support the lithium protective effects against the cognitive impairment that characterizes the brain cholinergic depletion.

Usage: Neurodegeneration was induced by injecting the immunotoxin 192 IgG-SAP in the medial septum (0.5 ug/side) and nucleus basalis magnocellularis (0.4 ug/side).

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

Lecrux C, Sandoe C, Neupane S, Kropf P, Toussay X, Tong X, Lacalle-Aurioles M, Shmuel A, Hamel E (2017) Impact of altered cholinergic tones on the neurovascular coupling response to whisker stimulation. J Neurosci 37:1518-1531. doi: 10.1523/JNEUROSCI.1784-16.2016

Summary: The authors assessed the effects of varying ACh tone on whisker-evoked NVC responses in rat barrel cortex. ACh depletion was achieved via unilateral icv injection (4 mcg/2 mcl) with 192 IgG-SAP (Cat. #IT-01) or saline. They conclude that ACh is not only a facilitator, but also a prerequisite for the full expression of sensory-evoked NVC responses.

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

Kelly SC, Nelson PT, Counts SE (2017) Featured Article: The locus coeruleus: a potential link between cerebrovascular and neuronal pathology in Alzheimer’s disease. Targeting Trends 18

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

Read the featured article in Targeting Trends.

See Also:

• Kelly SC et al. The locus coeruleus: a potential link between cerebrovascular and neuronal pathology in Alzheimer’s disease. Neuroscience 2016 Abstracts 786.11 / H7, 2016. Society for Neuroscience, San Diego, CA

Turnbull M, Coulson E (2017) Cholinergic basal forebrain lesion decreases neurotrophin signaling without affecting tau hyperphosphorylation in genetically susceptible mice. J Alzheimers Dis 55:1141-1154.. doi: 10.3233/JAD-160805

Summary: Alzheimer’s disease(AD) is a progressive, irreversible neurodegenerative disease that destroys memory and cognitive function. Aggregates of hyperphosphorylated tau protein are a prominent feature in the brain of patients with AD, and area major contributor to neuronal toxicity and disease progression. However, the factors that initiate the toxic cascade that results in tau hyperphosphorylation in AD are unknown. The authors investigated whether degeneration of basal forebrain cholinergic neurons (BFCNs) and/or resultant decrease in neurotrophin signaling cause aberrant tau hyperphosphorylation. Two-month-old male and female pR5 mice were infused with murine p75-SAP (Cat. #IT-16) at a concentration of 0.4 mg/ml or 0.4 mg/ml of control Rabbit IgG-SAP (Cat. #IT-35) using a 30G needle attached to a 5 ml Hamilton syringe and pump. The needle was lowered into the medial septum according to coordinates in a mouse brain atlas, and the toxin was infused at a rate of 0.4 ul/min (1.5 u total volume). The results reveal that the loss of BFCNs in pre-symptomatic pR5 tau transgenic mice results in a decrease in hippocampal brain-derived neurotrophic factor levels and reduced TrkB receptor activation. However, there was no exacerbation of the levels of phosphorylated tau or its aggregation in the hippocampus of susceptible mice. Furthermore the animals’ performance in a hippocampal-dependent learning and memory task was unaltered, and no changes in hippocampal synaptic markers were observed. This suggests that tau pathology is likely to be regulated independently of BFCN degeneration and the corresponding decrease in hippocampal neurotrophin levels, although these features may still contribute to disease etiology.

Related Products: mu p75-SAP (Cat. #IT-16), Rabbit IgG-SAP (Cat. #IT-35)