References

Mendoza J, Pevet P, Felder-Schmittbuhl MP, Bailly Y, Challet E (2010) The cerebellum harbors a circadian oscillator involved in food anticipation. J Neurosci 30:1894-1904. doi: 10.1523/JNEUROSCI.5855-09.2010

Summary: The authors report on a circadian oscillator in the cerebellum that is sensitive to feeding cues. Mice received intracerebroventricular injections of 0.12, 0.25, or 0.50 µg of OX7-SAP (Cat. #IT-02). Lesioned animals displayed attenuated food-anticipatory activity, and less locomotor activity after fasting, indicating that Purkinje cells in the cerebellum are involved in the circadian connection to feeding.

Related Products: OX7-SAP (Cat. #IT-02)

Akasaka E, Watanabe S, Himaki T, Ohtsuka M, Yoshida M, Miyoshi K, Sato M (2010) Enrichment of xenograft-competent genetically modified pig cells using a targeted toxin, isolectin BS-I-B4 conjugate. Xenotransplantation 17:81-89. doi: 10.1111/j.1399-3089.2010.00568.x

Summary: Genetically modified pigs lacking the gala1-3gal epitope may be suitable for production of organs that could be transplanted to humans. The ability to select for a homozygous population of donor somatic cells would accelerate the process of generating these animals, which would otherwise take approximately 2 years. The authors incubated a heterozygous population of 107 porcine embryonic fibroblasts with 1.6 µg of IB4-SAP (Cat. #IT-10). Even after 6 months the treated cells were negative for the agal epitope.

Related Products: IB4-SAP (Cat. #IT-10)

Li AJ, Wang Q, Dinh TT, Ritter S (2010) Featured Article: Deletion of NPY/AGRP and POMC neurons in the arcuate nucleus by leptin-saporin produces hyperphagia, obesity and changes in diurnal feeding patterns in rats. Targeting Trends 11(1)

Related Products: Leptin-SAP (Cat. #IT-47), Blank-SAP (Cat. #IT-21)

Read the featured article in Targeting Trends.

See Also:

• Li A-J et al. Leptin-saporin injection into the arcuate nucleus lesions NPY/AGRP and POMC neurons and produces hyperphagia, obesity and changes in diurnal feeding patterns in rats. Neuroscience 2009 Abstracts 374.5/EE116, 2009. Society for Neuroscience, Chicago, IL

Thomsen MS, Hay-Schmidt A, Hansen HH, Mikkelsen JD (2010) Distinct neural pathways mediate alpha7 nicotinic acetylcholine receptor-dependent activation of the forebrain. Cereb Cortex 20(9):2092-2102. doi: 10.1093/cercor/bhp283

Summary: a7 nicotinic acetylcholine receptor (nAChR) agonists are potential treatments for some aspect of schizophrenia. The authors examine whether cholinergic neurons in the horizontal limb of the diagonal band of Broca (HDB) are a target for this treatment. Rats received 300 ng injections of 192-IgG-SAP (Cat. #IT-01) into the HDB. The results demonstrate that cholinergic neurons in the HDB are essential for a7 nAChR agonist activation of the medial prefrontal cortex.

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

Gibbs RB (2010) Estrogen therapy and cognition: a review of the cholinergic hypothesis. Endocr Rev 31(2):224-253. doi: 10.1210/er.2009-0036

Summary: This review discusses estrogen therapy for use in postmenopausal women. In this context the issues revolve around benefits vs. harm of such therapy on the brain and cognitive impairment associated with aging and Alzheimer’s disease. Use of 192-IgG-SAP (Cat. #IT-01) to investigate this paradigm is described.

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

Robertson RT, Baratta J, Yu J, LaFerla FM (2009) Amyloid-beta expression in retrosplenial cortex of triple transgenic mice: relationship to cholinergic axonal afferents from medial septum. Neuroscience 164:1334-1346. doi: 10.1016/j.neuroscience.2009.09.024

Summary: In this work the authors developed a model to examine the relationship between afferent projections and the formation of amyloid-beta (Aβ) deposits. Mice received 1.86 µg unilateral injections of 192-IgG-SAP (Cat. #IT-01) into the lateral ventricle. Lesioned animals had persistent Aβ immunoreactivity in layer III of the granular division of retrosplenial cortex (RSg). This data indicates that septal cholinergic axonal projections transport Aβ or amyloid precursor protein to layer III of the RSg.

Related Products: 192-IgG-SAP (Cat. #IT-01), mu p75-SAP (Cat. #IT-16)

Marshall AM, Nommsen-Rivers LA, Hernandez LL, Dewey KG, Chantry CJ, Gregerson KA, Horseman ND (2010) Serotonin transport and metabolism in the mammary gland modulates secretory activation and involution. J Clin Endocrinol Metab 95(2):837-846. doi: 10.1210/jc.2009-1575 PMID: 19965920

Summary: Serotonin is known to be a local regulator of lactation homeostasis. This work examined  the roles of the serotonin reuptake transporter (SERT) and monoamine oxidase in this system. Immunohistochemical and immunocytochemical staining was done on human primary mammary epithelial cells and mouse tissue with an anti-SERT antibody (Cat. #AB-N09). Additional data included epidemiological studies and selective serotonin reuptake inhibitor treatment of mice. The results suggest that women taking SSRI inhibitor medications were more likely to experience delayed secretory activation.

Related Products: Antibody to Serotonin Transporter (SERT, Cat. #AB-N09)

Wilson RE, Coons KD, Sengelaub DR (2009) Neuroprotective effects of testosterone on dendritic morphology following partial motoneuron depletion: efficacy in female rats. Neurosci Lett 465:123-127. doi: 10.1016/j.neulet.2009.09.007

Summary: Previous work has demonstrated a protective effect from testosterone in a motoneuron nerve injury model for male rats. This work investigated whether testosterone has the same effect in females. Female rats received 2 µg of CTB-SAP (Cat. #IT-14) into the left vastus medialis muscle. 4 weeks later surviving motoneurons were visualized with CTB conjugated to HRP. Testosterone treatment greatly attenuated the atrophy seen in control animals, suggesting that testosterone is also a neurotherapeutic agent in females.

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

Rennie KE, Ward C, Fréchette M, Pappas BA (2009) Effects of combined neonatal cholinergic lesion and chronic cerebral hypoperfusion on CA1 cytoarchitecture. Neuroscience 2009 Abstracts 736.23/M38. Society for Neuroscience, Chicago, IL.

Summary: Neonatal lesioning of the basal forebrain cholinergic (BFC) system alters cytoarchitecture of pyramidal cells in both the hippocampus and neocortex of the adult rat, indicating a role for the BFC in forebrain development. In addition to altering forebrain development, neonatal cholinergic lesion may also exacerbate the brain’s response to pathological factors that emerge as the brain ages. One factor that might interact with BFC lesion is reduced cerebral blood flow (hypoperfusion). Examining this interaction is especially interesting because both BFC degeneration and reduced cerebral blood flow are characteristics of Alzheimer’s disease. In the rat, chronic cerebrovascular insufficiency by itself reportedly causes the degeneration of hippocampal CA1 pyramidal cells, alters amyloid processing and produces spatial memory impairments. We hypothesized that neonatal cholinergic lesion using the cholinotoxin 192-IgG-saporin would render the hippocampus more vulnerable to the neuropathological effects of chronic forebrain hypoperfusion induced by permanent bilateral occlusion of the carotid arteries (2VO). We previously reported that combined BFC lesion and 2VO impaired working memory in the Morris water maze and increased anxiety-like behaviours on the elevated plus apparatus, whereas neither of these treatments alone caused any of these effects. Here we report the effects of neonatal BFC lesion, 2VO, or their combined application on hippocampal CA1 cytoarchitecture using quantitative Golgi analysis. Rats subjected to 2VO showed increased apical branch length and spines, and increased basal spines. Neonatal BFC lesion on its own had only restricted effects on apical branch length at certain branch orders and no effect on spines. However, at a number of branch orders the stimulating effect of 2VO on apical spines occurred only in animals subjected to neonatal BFC lesion, indicating that this lesion modulated the response to 2VO. To our knowledge, this is the first examination of the effects of 2VO on CA1 neuron cytoarchitecture. Surprisingly, it increased rather than decreased dendritic length and spines. Furthermore, while the BFC lesion had minimal effects on its own, it was permissive to some of the effects of 2VO on dendritic spines. Taken together with our previous data, this study suggests that pre-existing cholinergic dysfunction alters aspects of both the behavioural and neural consequences of chronic hypoperfusion. These results may have implications for Alzheimer’s disease where cholinergic dysfunction and hypoperfusion are co-expressed

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

Coons KD, Munoz F, Osborne MC, Sengelaub DR (2009) Dendritic atrophy following partial motoneuron depletion: Time course of recovery and protection with androgens and estrogens. Neuroscience 2009 Abstracts 743.2/R17. Society for Neuroscience, Chicago, IL.

Summary: We have previously demonstrated that partial depletion of motoneurons innervating the quadriceps muscles induces dendritic atrophy and loss of function in remaining motoneurons. Furthermore, treatment with testosterone is neuroprotective, and dendritic atrophy and loss of function following partial motoneuron depletion are attenuated in a dose-dependent fashion, and in both male and female rats. In the present study, we assessed dendritic atrophy after partial motoneuron depletion at a variety of time points to determine its time course and pattern with and without testosterone treatment. We also examined the potential neuroprotective effects of the androgenic and estrogenic metabolites of testosterone. Motoneurons innervating the vastus medialis muscle were selectively killed by intramuscular injection of cholera toxin-conjugated saporin. Simultaneously, saporin-injected males were given implants containing either testosterone (45mm), dihydrotestosterone (30mm), estradiol (10%, 10mm), or left untreated. At 2, 4, 6, or 10 weeks after partial motoneuron depletion, motoneurons innervating the ipsilateral vastus lateralis muscle were labeled with cholera toxin-conjugated HRP, and dendritic arbors were reconstructed in 3 dimensions. Animals treated with dihydrotestosterone or estradiol were assessed only at 4 weeks post depletion. Dendritic arbors were also assessed in a group of untreated normal males. Quadriceps motoneuron dendrites underwent a rapid atrophy and protracted recovery following partial motoneuron depletion. Dendritic atrophy in remaining quadriceps motoneurons was apparent at 2 weeks after motoneuron depletion, with a decrease of over 50% in dendritic length, and this atrophy remained through 6 weeks post-depletion; dendritic length recovered by 10 weeks post-depletion. Treatment with testosterone attenuated induced dendritic atrophy at all time points, and recovery to normal lengths was present at 6 weeks post-depletion. Treatment with dihydrotestosterone or estradiol was as effective as testosterone in attenuating dendritic atrophy in remaining quadriceps motoneurons. These results suggest that treatment with testosterone is neuroprotective, both attenuating induced dendritic atrophy and accelerating recovery. Furthermore, this effect can be achieved with both androgenic and estrogenic metabolites, further supporting a role for hormones as neurotherapeutic agents in the injured nervous system.

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