References

Vierck C, Yezierski R, Wiley R (2016) Pain sensitivity following loss of cholinergic basal forebrain (CBF) neurons in the rat. Neuroscience 319:23-34. doi: 10.1016/j.neuroscience.2016.01.038

Objective: There is a large amount of research on the involvement of cholinergic mechanisms on spinal transmission of pain signals, indicating that cholinergic agonists can attenuate this kind of pain. In contrast, some studies have shown affective reactions to pain are suppressed by cholinergic antagonists. The authors investigated the disagreement between reflexive and affective reactions.

Summary: Lesioned rats displayed decreased escape from thermal stimulation, as well as loss of the normal hyperalgesic effect of sound stress. Results indicate that the basal forebrain cholinergic system plays a role in central processing of pain.

Usage: Administration of 192-IgG-SAP with a 4-μg injection into the left lateral ventricle of rats. Animals were tested in temperature escape and sound stress models.

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

Schwartz M, Nguyen A, Warrier D, Palmerston J, Thomas A, Morairty S, Neylan T, Kilduff T (2016) Locus coeruleus and tuberomammillary nuclei ablations attenuate hypocretin/orexin antagonist-mediated rem sleep. eNeuro 3:ENEURO.0018-0016.2016. doi: 10.1523/ENEURO.0018-16.2016

Summary: To examine the mechanism by which the Orexin 1r/Orexin 2r antagonist almorexant decreases wakefulness and increases NREM and REM sleep the authors utilized Anti-DBH-SAP (Cat. #IT-03) and Orexin-B-SAP (Cat. #IT-20). Rats received 3-μg injections of Anti-DBH-SAP into the LC, or bilateral 57-80 ng injections of Orexin-SAP into the TMN. Both conjugates attenuated the increased REM sleep seen upon administration of almorexant without altering almorexant-induced changes in NREM sleep.

Related Products: Anti-DBH-SAP (Cat. #IT-03), Orexin-B-SAP (Cat. #IT-20)

Mao C, Agca C, Mocko-Strand J, Wang J, Ullrich-Lüter E, Pan P, Wang S, Arnone M, Frishman L, Klein W (2016) Substituting mouse transcription factor Pou4f2 with a sea urchin orthologue restores retinal ganglion cell development. Proc Biol Sci 283:20152978. doi: 10.1098/rspb.2015.2978 PMID: 26962139

Summary: Pou4f2 is Pou domain transcription factor that is essential for the development of retinal ganglion cells (RGCs) in the vertebrate retina. The sea urchin genome contains SpPou4f1/2, a distant orthologue of Pou4f2, but they have no obvious eyes and their photoreceptors are located around their tube feet disc. Scientists replaced genomic Pou4f2 with an SpPou4f1/2 cDNA to see if SpPou4f1/2 could support RGC development in mice. Mice expressing SpPou4f1/2 developed retinas that looked like wild-type mice. Immunolabeling of retinas with a 1:1000 dilution of Anti-Melanopsin (Cat. #AB-N39) showed the presence of many well-bundled axons emanating from SpPou4f1/2-expressing RGCs. Electroretinogram recordings from these mice indicate that their RGCs are functionally active. These results suggest that there is a high degree of functional conservation between the two genes despite more than 540 million years of divergence from the common ancestor of mice and sea urchins.

Related Products: Melanopsin Rabbit Polyclonal, affinity-purified (Cat. #AB-N39)

Yao Y, Echeverry S, Shi X, Yang M, Yang Q, Wang G, Chambon J, Wu Y, Fu K, De Koninck Y, Zhang J (2016) Dynamics of spinal microglia repopulation following an acute depletion. Sci Rep 6:22839. doi: 10.1038/srep22839

Summary: This study confirms that similar to microglia in the brain, spinal microglia can repopulate rapidly following elimination, which is driven essentially by a self-renewal process. To deplete microglia in spinal cords, Mac-1-SAP (Cat. #IT-06) was injected i.t. (7 μl, 1.6  μg/μl) at the level of L4-L5 in mouse. The results support the concept that microglia repopulation, whether in the brain or in the spinal cord, is the consequence of onsite resident microglia proliferation. Newly generated microglia are fully functional and are able to respond to peripheral nerve injury and contribute to the development of neuropathic pain.

Related Products: Mac-1-SAP mouse/human (Cat. #IT-06)

Fei Y, Wang X, Chen S, Zhou Q, Zhang C, Li Y, Sun L, Zhang L (2016) Role of the RVM in descending pain regulation originating from the cerebrospinal fluid-contacting nucleus. Neurochem Res 41:1651-1661. doi: 10.1007/s11064-016-1880-6

Summary: The researchers investigated whether the CSF-contacting nucleus contributed to descending pain modulation in normal and neuropathic rats, and detected the 5-HT expression changes in both RVM and spinal dorsal cord. They also detected the possible anatomical and function correlation between the CSF-contacting nucleus and the RVM. Targeted ablation of the CSF-contacting nucleus was performed using CTB-SAP (Cat. #IT-14; 500 ng/3 μl), which was administered i.c.v. to the normal rats and rats 7 days before the CCI procedure. Based on the findings of the present study, they believe that the CSF-contacting nucleus may act as a component of descending pain regulation system. RVM, which acts as an important brain nucleus, is involved in the relay of nociceptive information between the CSF-contacting nucleus and spinal cord. Moreover, RVM 5-HT system plays a critical role in descending pain inhibition originating from the CSF-contacting nucleus.

Related Products: CTB-SAP (Cat. #IT-14)

Wang L, Conner J, Nagahara A, Tuszynski M (2016) Rehabilitation drives enhancement of neuronal structure in functionally relevant neuronal subsets. Proc Natl Acad Sci U S A 113:2750-2755. doi: 10.1073/pnas.1514682113

Summary: Rehabilitation is often prescribed after brain injury, but the basis for how training can influence brain plasticity and recovery is unclear. In this study, the authors show that intense rehabilitation training after focal brain injury drives significant structural changes in brain cells located adjacent to the injury. Importantly, a key brain modulatory system, the basal forebrain cholinergic system, is required for enabling rehabilitation to impact brain structure. Rats underwent cholinergic ablations by injecting 192-IgG-Saporin (Cat. #IT-01) into the nucleus basalis (0.2-0.25 mcl of 0.375 mg/ml solution in artificial CSF). Damage to the cholinergic system, which can occur naturally during aging, completely blocks brain plasticity mediated by rehabilitation and significantly attenuates functional recovery. These results provide new insights into how rehabilitation may promote recovery and suggest that brain cholinergic systems may be a possible therapeutic target for influencing recovery.

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

Gritsch S, Bali K, Kuner R, Vardeh D (2016) Functional characterization of a mouse model for central post-stroke pain. Mol Pain 12:1744806916629049. doi: 10.1177/1744806916629049

Summary: While clinical evidence has pointed toward central pain pathway dysfunction in central post-stroke pain (CPSP), the underlying mechanisms have not been defined. In this work the authors created a mouse model of CPSP through lesions of the thalamic ventral posterolateral nucleus. In order to examine the role of neurokinin-1 receptor-expressing (NK1R) neurons in lamina I/III of the spinal cord in the development and maintenance of CPSP the authors administered 1 μmol intrathecal injections of SSP-SAP (Cat. #IT-11). Saporin (Cat. #PR-01) was used as a control. While the NK1R+ neurons in the spinal cord were not involved in establishing CPSP, the data indicate that sensory changes in the mice are comparable to those observed in human patients with CPSP.

Related Products: SSP-SAP (Cat. #IT-11), Saporin (Cat. #PR-01)

Yuan X, Yang M, Chen X, Zhang X, Sukhadia S, Musolino N, Bao H, Chen T, Xu C, Wang Q, Santoro S, Ricklin D, Hu J, Lin R, Yang W, Li Z, Qin W, Zhao A (2017) Characterization of the first fully macropinocytosing human antibodies human anti-TEM1 scFv in models of solid tumor imaging and immunotoxin-based therapy. Cancer Immunol Immunother 66:367-378.. doi: 10.1007/s00262-016-1937-z

Summary: Tumor endothelial marker 1 (TEM1) has been identified as a novel surface marker upregulated on the blood vessels and stroma in many solid tumors. The authors previous isolated a single-chain variable fragment (scFv) 78 against TEM1 from a yeast display scFv library and evaluated potential applications of scFv78 as a tool for tumor molecular imaging, immunotoxin-based therapy and nanotherapy. MS1 and MS1-hTEM1 cells were treated with site-specifically biotinylated scFv78 conjugated with the Streptavidin-ZAP (Cat. #IT-27) at a molar ratio of 4:1 (scFv78:ZAP) starting from 40 nM serially diluted down to 0.04 nM. The scFv78-saporin immunoconjugate exerted dose-dependent cytotoxicity with high specificity to TEM1-positive cell in vitro. The data indicate that scFv78, the first fully human anti-TEM1 recombinant antibody, recognizes both human and mouse TEM1 and has features advantageous for the development of imaging probes or antibody-toxin conjugates for a large spectrum of human TEM1-positive solid tumors.

Related Products: Streptavidin-ZAP (Cat. #IT-27)

Vazquez-DeRose J, Schwartz M, Nguyen A, Warrier D, Gulati S, Mathew T, Neylan T, Kilduff T (2016) Hypocretin/orexin antagonism enhances sleep-related adenosine and GABA neurotransmission in rat basal forebrain. Brain Struct Funct 221:923-940. doi: 10.1007/s00429-014-0946-y

Summary: The basal forebrain (BF) is one of the regions receiving excitatory input from orexin neurons. The authors investigated the hypothesis that orexin antagonists induce sleep at least in part by interfering with the facilitation of BF neurons. Rats received bilateral 500-ng injections of 192-IgG-SAP (Cat. #IT-01) into the BF. Lesioned animals displayed no abnormal responses to a benzodiazepine agonist or vehicle. An orexin antagonist, however, was less effective than the control at inducing sleep in lesioned rats.

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

Mittelman-Smith M, Krajewski-Hall S, McMullen N, Rance N (2016) Ablation of KNDy neurons results in hypogonadotropic hypogonadism and amplifies the steroid-induced LH surge in female rats. Endocrinology 157:2015-2027. doi: 10.1210/en.2015-1740

Summary: KNDy neurons are a subpopulation of neurons in the infundibular nucleus that coexpress estrogen receptor α, kisspeptin, and neurokinin B (NKB) mRNA. Previous work indicated that altered signaling from KNDy neurons may play a role in the low levels of circulating sex steroids found in hypogonadotropic hypogonadism. Rats received bilateral 10-ng injections of NK3-SAP (Cat. #IT-63) dorsal to the arcuate nucleus. Blank-SAP (Cat. #IT-21) was used as control. In animals with intact ovaries the NK3-SAP lesion resulted in hypogonadotropic hypogonadism. In contrast, the LH surge in lesioned ovariectomized rats was 3-fold higher, demonstrating that KNDy neurons are integral for the control of serum LH levels, estrous cyclicity, and may also have some control over the magnitude of the LH surge.

Related Products: NKB-SAP (Cat. #IT-63), Blank-SAP (Cat. #IT-21)