Cancer & Metabolism, 1(1), 15.
Gershon TR, Crowther AJ, Liu H, Miller CR, Deshmukh M (2013).
PMID: 24280296 | DOI: 24280296
Sci Rep.
2017 Oct 27
Rocco BR, Oh H, Shukla R, Mechawar N, Sibille E.
PMID: 29079825 | DOI: 29079825
Cell-specific molecular investigations of the human brain are essential for understanding the neurobiology of diseases, but are hindered by postmortem conditions and technical challenges. To address these issues we developed a multi-label fluorescence in situ hybridization protocol and a novel optical filter device to identify cell types and control for tissue autofluorescence. We show that these methods can be used with laser-capture microdissection for human brain tissue cell-specific molecular analysis.
Nature Neuroscience
2017 Nov 13
Ryan PJ, Ross SI, Campos CA, Derkach VA, Palmiter RD.
PMID: - | DOI: -
Brain regions that regulate fluid satiation are not well characterized, yet are essential for understanding fluid homeostasis. We found that oxytocin-receptor-expressing neurons in the parabrachial nucleus of mice (OxtrPBN neurons) are key regulators of fluid satiation. Chemogenetic activation of OxtrPBN neurons robustly suppressed noncaloric fluid intake, but did not decrease food intake after fasting or salt intake following salt depletion; inactivation increased saline intake after dehydration and hypertonic saline injection. Under physiological conditions, OxtrPBN neurons were activated by fluid satiation and hypertonic saline injection. OxtrPBN neurons were directly innervated by oxytocin neurons in the paraventricular hypothalamus (OxtPVH neurons), which mildly attenuated fluid intake. Activation of neurons in the nucleus of the solitary tract substantially suppressed fluid intake and activated OxtrPBN neurons. Our results suggest that OxtrPBN neurons act as a key node in the fluid satiation neurocircuitry, which acts to decrease water and/or saline intake to prevent or attenuate hypervolemia and hypernatremia.
Molecular and Cellular Neuroscience
2017 Dec 15
Wijayatunge R, Liu F, Shpargel KB, Wayne NJ, Chan U, Boua JV, Magnuson T, West AE.
PMID: - | DOI: -
The histone H3 lysine 27 (H3K27) demethylase Kdm6b (Jmjd3) can promote cellular differentiation, however its physiological functions in neurons remain to be fully determined. We studied the expression and function of Kdm6b in differentiating granule neurons of the developing postnatal mouse cerebellum. At postnatal day 7, Kdm6b is expressed throughout the layers of the developing cerebellar cortex, but its expression is upregulated in newborn cerebellar granule neurons (CGNs). Atoh1-Cre mediated conditional knockout of Kdm6b in CGN precursors either alone or in combination with Kdm6a did not disturb the gross morphological development of the cerebellum. Furthermore, RNAi-mediated knockdown of Kdm6b in cultured CGN precursors did not alter the induced expression of early neuronal marker genes upon cell cycle exit. By contrast, knockdown of Kdm6b significantly impaired the induction of a mature neuronal gene expression program, which includes gene products required for functional synapse maturation. Loss of Kdm6b also impaired the ability of Brain-Derived Neurotrophic Factor (BDNF) to induce expression of Grin2c and Tiam1 in maturing CGNs. Taken together, these data reveal a previously unknown role for Kdm6b in the postmitotic stages of CGN maturation and suggest that Kdm6b may work, at least in part, by a transcriptional mechanism that promotes gene sensitivity to regulation by BDNF.
PLoS One.
2018 Feb 27
Wu Y, Luna MJ, Bonilla LS, Ryba NJP, Pickel JM.
PMID: 29485996 | DOI: 29485996
Design and engineering of complex knockin mice has revolutionized the in vivo manipulation of genetically defined cells. Recently development of the bacterial clustered regularly interspersed short palindromic repeats (CRISPR) associated protein 9 (Cas9) system for single site cleavage of mammalian genomes has opened the way for rapid generation of knockin mice by targeting homology directed repair to selected cleavage sites. We used this approach to generate new lines of mice that will be useful for a variety of aspects of neuroscience research. These lines have been bred to homozygosity and details of the expression and function of the transgenes are reported. Two lines target the Rosa26-locus and have been engineered to allow Cre-dependent expression of the avian tva receptor, and Cre-dependent expression of a cell surface targeted spaghetti-monster carrying many copies of the "ollas-tag". Another line expresses red fluorescent protein and tva in Tac1-positive neurons; the fourth line targets FlpO expression to Plekhg1 expressing neurons, providing a powerful approach to modify gene expression in thalamic excitatory neurons.
Neuropharmacology. 2015 Jul 25.
Granger AJ, Mulder N, Saunders A, Sabatini BL.
PMID: 26220313 | DOI: 26220313
Neurobiol Dis. 2015 Apr 2.
Razafsky D, Hodzic D.
PMID: 25843669 | DOI: 25843669
J Neurosci. 2015 Feb 25;35(8):3312-8.
Wu Z, Kim ER, Sun H, Xu Y, Mangieri LR, Li DP, Pan HL, Xu Y, Arenkiel BR, Tong Q.
PMID: 25716832 | DOI: 25716832
J Neurooncol. 2014 May 28.
Abiria SA, Williams TV, Munden AL, Grover VK, Wallace A, Lundberg CJ, Valadez JG, Cooper MK.
PMID: 24867209 | DOI: 24867209
Nat Commun.
2016 Jan 25
Alexander GM, Farris S, Pirone JR, Zheng C, Colgin LL, Dudek SM.
PMID: 26806606 | DOI: 26806606
The hippocampus supports a cognitive map of space and is critical for encoding declarative memory (who, what, when and where). Recent studies have implicated hippocampal subfield CA2 in social and contextual memory but how it does so remains unknown. Here we find that in adult male rats, presentation of a social stimulus (novel or familiar rat) or a novel object induces global remapping of place fields in CA2 with no effect on neuronal firing rate or immediate early gene expression. This remapping did not occur in CA1, suggesting this effect is specific for CA2. Thus, modification of existing spatial representations might be a potential mechanism by which CA2 encodes social and novel contextual information.
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