Social transmission of food preference in mice: Methodology and application to galanin-overexpressing transgenic mice.

Wrenn, Craige C.; Harris, Ashley P.; Saavedra, María C.; Crawley, Jacqueline N.

doi:10.1037/0735-7044.117.1.21

Cited by 102 publications

(92 citation statements)

References 84 publications

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“…Behavioral studies of the these mice show performance deficits on learning and memory tasks Wrenn et al, 2002), social and food preference tasks Wrenn et al, 2003), impaired long-term potentiation and evoked glutamate release in the hippocampus (Mazarati et al, 2000), reduced numbers of choline acetyltransferase-ir neurons in the basal forebrain , and a selective reduction in ventral hippocampal acetylcholine release (Laplante et al, 2004) compared with WT mice. In addition, GAL overexpression appears to play a role in affective behaviors such as anxiety Kinney et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Ectopic galanin expression and normal galanin receptor 2 and galanin receptor 3 mRNA levels in the forebrain of galanin transgenic mice

Counts

Pérez

et al. 2005

Neuroscience

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Abstract-The functional interactions of the neuropeptide galanin (GAL) occur through its binding to three G proteincoupled receptor subtypes: galanin receptor (GALR) 1, GALR2 and GALR3. Previously, we demonstrated that GALR1 mRNA expression was increased in the CA1 region of the hippocampus and discrete hypothalamic nuclei in galanin transgenic (GAL-tg) mice. This observation suggested a compensatory adjustment in cognate receptors in the face of chronic GAL exposure. To evaluate the molecular alterations to GALR2 and GALR3 in the forebrain of GAL overexpressing mice, we performed complementary quantitative, real-time PCR (qPCR), in situ hybridization, and immunohistochemistry in select forebrain regions of GAL-tg mice to characterize the neuronal distribution and magnitude of GAL mRNA and peptide expression and the consequences of genetically manipulating the neuropeptide GAL on the expression of GALR2 and GALR3 receptors. We found that GAL-tg mice displayed dramatic increases in GAL mRNA and peptide in the frontal cortex, posterior cortex, hippocampus, septal diagonal band complex, amygdala, piriform cortex, and olfactory bulb. Moreover, there was evidence for ectopic neuronal GAL expression in forebrain limbic regions that mediate cognitive and affective behaviors, including the piriform and entorhinal cortex and amygdala. Interestingly, regional qPCR analysis failed to reveal any changes in GALR2 or GALR3 expression in the GAL-tg mice, suggesting that, contrary to GALR1, these receptor genes are not under ligand-mediated regulatory control. The GAL-tg mouse model may provide a useful tool for the investigation of GAL ligand-receptor relationships and their role in normal cognitive and affective functions as well as in the onset of neurological disease.

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Section: Discussionmentioning

confidence: 99%

Ectopic galanin expression and normal galanin receptor 2 and galanin receptor 3 mRNA levels in the forebrain of galanin transgenic mice

Counts

Pérez

et al. 2005

Neuroscience

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“…Mice were tested for their ability to find buried food according to Wrenn et al (2003) with minor modifications. Briefly, mice were weaned at day 14 and tested beginning on day 16.…”

Section: Methodsmentioning

confidence: 99%

β1,3-N-Acetylglucosaminyltransferase 1 Glycosylation Is Required for Axon Pathfinding by Olfactory Sensory Neurons

Henion¹,

Raitcheva²,

Grosholz³

et al. 2005

J. Neurosci.

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During embryonic development, axons from sensory neurons in the olfactory epithelium (OE) extend into the olfactory bulb (OB) where they synapse with projection neurons and form glomerular structures. To determine whether glycans play a role in these processes, we analyzed mice deficient for the glycosyltransferase ␤1,3-N-acetylglucosaminyltransferase 1 (␤3GnT1), a key enzyme in lactosamine glycan synthesis. Terminal lactosamine expression, as shown by immunoreactivity with the monoclonal antibody 1B2, is dramatically reduced in the neonatal null OE. Postnatal ␤3GnT1 Ϫ/Ϫ mice exhibit severely disorganized OB innervation and defective glomerular formation. Beginning in embryonic development, specific subsets of odorant receptor-expressing neurons are progressively lost from the OE of null mice, which exhibit a postnatal smell perception deficit. Axon guidance errors and increased neuronal cell death result in an absence of P2, I7, and M72 glomeruli, indicating a reduction in the repertoire of odorant receptor-specific glomeruli. By ϳ2 weeks of age, lactosamine is unexpectedly reexpressed in sensory neurons of null mice through a secondary pathway, which is accompanied by the regrowth of axons into the OB glomerular layer and the return of smell perception. Thus, both neonatal OE degeneration and the postnatal regeneration are lactosamine dependent. Lactosamine expression in ␤3GnT1 Ϫ/Ϫ mice is also reduced in pheromone-receptive vomeronasal neurons and dorsal root ganglion cells, suggesting that ␤3GnT1 may perform a conserved function in multiple sensory systems. These results reveal an essential role for lactosamine in sensory axon pathfinding and in the formation of OB synaptic connections.

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“…Olfactory habituation/dishabituation to test social smells has been developed and used to test Galanin overexpressing transgenic mice. 36 The number three core symptom of autism is stereotyped repetitive behaviors and narrow restricted interests. Mice can be videotaped and scored for spontaneous stereotyped jumping, grooming, reduced exploration, repetitive behaviors, and restricted interests.…”

Section: Designing Mouse Behavioral Tasks Relevant To the Symptoms Ofmentioning

confidence: 99%

Epigenetics and Neural Developmental Disorders

Zhao

Pak²,

Smrt³

et al. 2007

Epigenetics

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Neural developmental disorders, such as autism, Rett Syndrome, Fragile X syndrome, and Angelman syndrome manifest during early postnatal neural development. Although the genes responsible for some of these disorders have been identified, how the mutations of these genes affect neural development is currently unclear. Emerging evidence suggest that these disorders share common underlying defects in neuronal morphology, synaptic connectivity and brain plasticity. In particular, alterations in dendritic branching and spine morphology play a central role in the pathophysiology of most mental retardation disorders, suggesting that common pathways regulating neuronal function may be affected. Epigenetic modulations, mediated by DNA methylation, RNA-associated silencing, and histone modification, can serve as an intermediate process that imprints dynamic environmental experiences on the "fixed" genome, resulting in stable alterations in phenotypes. Disturbance in epigenetic regulations can lead to inappropriate expression or silencing of genes, causing an array of multi-system disorders and neoplasias. Rett syndrome, the most common form of mental retardation in young girls, is due to l mutation of MECP2, encoding a methylated DNA binding protein that translates DNA methylation into gene repression. Angelman syndrome is due to faulty genomic imprinting or maternal mutations in UBE3A. Fragile X Syndrome, in most cases, results from the hypermethylation of FMR1 promoter, hence the loss of expression of functional FMRP protein. Autism, with its complex etiology, may have strong epigenetic link. Together, these observations strongly suggest that epigenetic mechanisms may play a critical role in brain development and etiology of related disorders. This report summarizes the scientific discussions and major conclusions from a recent conference that aimed to gain insight into the common molecular pathways affected among these disorders and discover potential therapeutic targets that have been missed by looking at one disorder at a time.

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Social transmission of food preference in mice: Methodology and application to galanin-overexpressing transgenic mice.

Cited by 102 publications

References 84 publications

Ectopic galanin expression and normal galanin receptor 2 and galanin receptor 3 mRNA levels in the forebrain of galanin transgenic mice

Ectopic galanin expression and normal galanin receptor 2 and galanin receptor 3 mRNA levels in the forebrain of galanin transgenic mice

β1,3-N-Acetylglucosaminyltransferase 1 Glycosylation Is Required for Axon Pathfinding by Olfactory Sensory Neurons

Epigenetics and Neural Developmental Disorders

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