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Effect of medial prefrontal subregions electrical stimulation on the neuronal activity of the primary visual cortex and basal forebrain.
Nguyen HN, Huppé-Gourgues F, Vaucher E (2013) Effect of medial prefrontal subregions electrical stimulation on the neuronal activity of the primary visual cortex and basal forebrain. Neuroscience 2013 Abstracts 639.04. Society for Neuroscience, San Diego, CA.
Summary: The cholinergic system and the medial prefrontal cortex (mPFC) play an important role in visual attention through the modulation of neuronal responses in the primary visual cortex (V1). The mPFC doesn’t project directly to V1, but does project to the horizontal limb of the diagonal band of Broca (HDB), which contains cholinergic neurons and projections to V1. Here, we investigated a possible involvement of the mPFC subregions in the activation of basal forebrain cholinergic neurons to enhance cholinergic transmission in V1. The different subregions of the mPFC, the anterior cingulate (Cg1), the prelimbic (PrL) and the infralimbic (IL) cortices, have anatomical and functional differences. Therefore the objective of this study was to determine if electrical stimulation of the different regions of the PFC activated V1 neurons in mice and if this activation was mediated through the HDB cholinergic pathway. The neuronal activity was evaluated by early gene c-Fos immunoreactivity in V1 and HDB after unilateral electrical stimulation of mPFC subregions (trains of 100 Hz for 0.3s every 2s, 50 μA, 30 mins) provided through a tungsten electrode in urethane anesthetized mice (n=4 mice per subregion). After the mPFC stimulation, mice were kept in darkness for 1h and brains were harvested after 4% paraformaldehyde intracardiac perfusion. The c-Fos expression was quantified on 35 µm coronal brain sections in V1 and HDB: an equivalent threshold was applied to all microphotographs and a c-Fos automated particle analysis tools was used (ImageJ). Moreover, the effect of the selective lesion of cholinergic fibers by the immunotoxin mu p75-saporin (1 μg/μl injections) was evaluated. The results show that electrical stimulation of PrL (Mann-Whitney U, p=0.021) and IL (p=0.021) cortices significantly induced a higher expression of c-Fos neurons in V1 of the stimulated hemisphere, but not in the HDB. Electrical stimulation of Cg1 did not elicit V1 nor HDB c-Fos immunoreactivity (p=0.248). Furthermore, selective lesions of basal forebrain cholinergic neurons did not eliminate the IL-induced c-Fos expression in the ipsilateral V1. Therefore, the mPFC stimulation seems to activate V1 neurons without the contribution of the HDB cholinergic neurons. This suggests there is a functional link between the mPFC and V1 independent from HDB cholinergic projections.
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Featured Article: Medial ganglionic eminence-like cells derived from human embryonic stem cells correct learning and memory deficits in an NGFr-lesioned mouse model
Liu Y, Weick JP, Liu H, Krencik R, Zhang X, Ma L, Zhou GM, Ayala M, Zhang S (2013) Featured Article: Medial ganglionic eminence-like cells derived from human embryonic stem cells correct learning and memory deficits in an NGFr-lesioned mouse model. Targeting Trends 14(3)
Related Products: mu p75-SAP (Cat. #IT-16)
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Medial ganglionic eminence-like cells derived from human embryonic stem cells correct learning and memory deficits.
Liu Y, Weick JP, Liu H, Krencik R, Zhang X, Ma L, Zhou GM, Ayala M, Zhang SC (2013) Medial ganglionic eminence-like cells derived from human embryonic stem cells correct learning and memory deficits. Nat Biotechnol 31(5):440-447. doi: 10.1038/nbt.2565
Summary: Progenitor cells were transplanted into mice that had received 1.5 μg of mu p75-SAP (Cat. #IT-16) into the medial septum.
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Rapid beta-amyloid deposition and cognitive impairment after cholinergic denervation in app/ps1 mice.
Ramos-Rodriguez JJ, Pacheco-Herrero M, Thyssen D, Murillo-Carretero MI, Berrocoso E, Spires-Jones TL, Bacskai BJ, Garcia-Alloza M (2013) Rapid beta-amyloid deposition and cognitive impairment after cholinergic denervation in app/ps1 mice. J Neuropathol Exp Neurol 72(4):272-285. doi: 10.1097/NEN.0b013e318288a8dd
Summary: The authors investigated whether specific cholinergic neurodegeneration is responsible for the deposition of plaques. APPswe/PS1dE9 transgenic mice received bilateral icv injections of 1-1.2 μg of mu p75-SAP (Cat. #IT-16) into the basal forebrain. Although the transgenic mice show plaque deposition, they do not exhibit other signs of Alzheimer’s disease. Lesioned transgenic animals, however, displayed increased β-amyloid plaque deposition, increased Tau phosphorylation, and early memory impairment that worsened with age.
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Combinatorial treatment of tart cherry extract and essential fatty acids reduces cognitive impairments and inflammation in the mu-p75 saporin-induced mouse model of Alzheimer’s disease.
Matchynski JJ, Lowrance SA, Pappas C, Rossignol J, Puckett N, Sandstrom M, Dunbar GL (2013) Combinatorial treatment of tart cherry extract and essential fatty acids reduces cognitive impairments and inflammation in the mu-p75 saporin-induced mouse model of Alzheimer’s disease. J Med Food 16(4):288-295. doi: 10.1089/jmf.2012.0131 PMID: 23566055
Summary: The authors investigated the efficacy of a combinatorial therapy, Cerise Total-Body Rhythm (TBR) by treating mice with TBR prior to and following icv administration of 0.8 μg of mu p75-SAP (Cat. #IT-16).
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Cholinergic degeneration is associated with increased plaque deposition and cognitive impairment in APPswe/PS1dE9 mice.
Laursen B, Mork A, Plath N, Kristiansen U, Bastlund JF (2013) Cholinergic degeneration is associated with increased plaque deposition and cognitive impairment in APPswe/PS1dE9 mice. Behav Brain Res 240:146-152. doi: 10.1016/j.bbr.2012.11.012
Summary: Extracellular plaques containing amyloid β-peptides (Aβ) and cholinergic dysfunction are two of the main hallmarks of Alzheimer’s disease. Using a transgenic mouse line that displays an age-related increase in plaque deposition, the authors examined the relationship between cholinergic degeneration and Aβ overexpresssion. Mice received 0.9-μg bilateral icv injections of mu p75-SAP (Cat. #IT-16). Working memory was significantly impaired in lesioned mice with plaques, and the plaque burden was increased as compared to wild-type mice that also received a lesion.
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Partial loss in septo-hippocampal cholinergic neurons alters memory-dependent measures of brain connectivity without overt memory deficits.
Brayda-Bruno L, Mons N, Yee BK, Micheau J, Abrous DN, Nogues X, Marighetto A (2013) Partial loss in septo-hippocampal cholinergic neurons alters memory-dependent measures of brain connectivity without overt memory deficits. Neurobiol Dis 54:372-381. doi: 10.1016/j.nbd.2013.01.010
Summary: The authors examined whether partial degeneration of septo-hippocampal neurons alters brain activity patterns even without overt memory loss. Mice received 45 ng of mu p75-SAP (Cat. #IT-16) into the medial septal area. Lesioned animals had significantly altered functional activities in the brain, despite lack of an overt behavioral deficit. Some changes observed are also altered with the initial signs of Alzheimer’s disease.
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Lesions of the basal forebrain cholinergic system in mice disrupt idiothetic navigation.
Hamlin AS, Windels F, Boskovic Z, Sah P, Coulson EJ (2013) Lesions of the basal forebrain cholinergic system in mice disrupt idiothetic navigation. PLoS One 8(1):e53472. doi: 10.1371/journal.pone.0053472
Summary: Alzheimer’s disease patients perform poorly on spatial navigation tests requiring either distal cues (allothetic) or body-centered cues (idiothetic). The authors used 0.2 μg bilateral infusions of mu p75-SAP (Cat. #IT-16) into the lateral ventricles of mice to examine the hypothesis that the cholinergic medial septo-hippocampal circuit is important for idiothetic navigation. Rabbit IgG-SAP (Cat. #IT-35) was used as a control. Lesioned animals were similar to controls in contextual fear conditioning, spatial working memory, as well as several other parameters. But exploratory behavior requiring idiothetic signals was very disorganized, indicating that cholinergic cells are vital to idiothetic navigation.
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Diffusion-weighted magnetic resonance imaging detection of basal forebrain cholinergic degeneration in a mouse model.
Kerbler GM, Hamlin AS, Pannek K, Kurniawan ND, Keller MD, Rose SE, Coulson EJ (2013) Diffusion-weighted magnetic resonance imaging detection of basal forebrain cholinergic degeneration in a mouse model. Neuroimage 66C:133-141. doi: 10.1016/j.neuroimage.2012.10.075
Summary: The authors examined the effectiveness of diffusion MRI using diffusion tensor imaging (DTI) and probabilistic tractography in detecting cholinergic loss in a mouse model. Mice received bilateral 0.2-μg icv injections of mu p75-SAP (Cat. #IT-16). Rabbit IgG-SAP (Cat. #IT-35) was used as control. The animals were then examined using DTI. The data indicate that DTI is a valid technique for assessment of cholinergic loss in septo-hippocampal tracts as a result of Alzheimer’s disease.
Related Products: mu p75-SAP (Cat. #IT-16), Rabbit IgG-SAP (Cat. #IT-35)
Limited effect of serotonergic denervation on beta-amyloid and cognitive impairment in APPswe/PS1dE9 mice.
Ortiz-Barajas O, Ramos-Rodriguez J, Berrocoso E, Garcia Alloza M (2012) Limited effect of serotonergic denervation on beta-amyloid and cognitive impairment in APPswe/PS1dE9 mice. Neuroscience 2012 Abstracts 751.12. Society for Neuroscience, New Orleans, LA.
Summary: Alzheimer’s Disease (AD) is a neurodegenerative disease characterized by progressive cognitive and memory impairment. Amyloid-beta (Aβ) deposition, as senile plaques (SP), seems to play a key role in the development and progression of the illness. Moreover SP tend to accumulate in cortex and hippocampus, relevant areas in learning and memory. On the other hand neuronal loss is the pathological feature that best correlates with duration and severity of the illness and at present animal available animal models hardly reproduce the complexity of the disease. We have previously seen that selective cortical and hipocampal cholinergic denervation, using murine p-75 saporin, may worsen cognitive abilities in APPswe/PS1dE9 mice as well as increase SP deposition in denervated areas. In the present work we lesioned 7 months old APPswe/PS1dE9 mice with 1 µl of 5,7-dyhidroxytiptamine (0.16 µg/µl) injected in the raphe nucleus (RN). In order to guarantee selective removal of cortical and hipocampal serotonergic inervation, and protect noardernergic and dopaminergic neurons, animals were i.p. injected with desipramine and nomifensine before surgery. We observed a clear reduction of tryptophan hydroxilase staining in the RN. In the Morris water maze test we observed learning and memory impairment in APPswe/Ps1dE9 mice, without a synergistic effect of the serotonergic lesion. When we assessed SP deposition we did not observe a significant increase of SP in cortex or hipocampus 14 days after the lesion, as we observed after selective cholinergic denervation. Altogether our data suggest that cognitive impairment and induced SP depositioin observed after cholinergic denervation is not achieved when serotonergic system is affected, supporting a selective effect mediated by different neurotransmitter systems. Acknowledgements: MG-A: RYC-2008-02333, ISCIII-Subdirección General de Evaluación y Fomento de la Investigación (PS09/00969), Fundación Dr. Eugenio Rodriguez Pascual, Junta Andalucia Excelencia (CTS-7847).
Related Products: mu p75-SAP (Cat. #IT-16)