@article{sciolino_plummer_chen_alexander_robertson_dudek_mcelligott_jensen_2016, title={Recombinase-Dependent Mouse Lines for Chemogenetic Activation of Genetically Defined Cell Types}, volume={15}, ISSN={["2211-1247"]}, DOI={10.1016/j.celrep.2016.05.034}, abstractNote={Chemogenetic technologies, including the mutated human Gq-coupled M3 muscarinic receptor (hM3Dq), have greatly facilitated our ability to directly link changes in cellular activity to altered physiology and behavior. Here, we extend the hM3Dq toolkit with recombinase-responsive mouse lines that permit hM3Dq expression in virtually any cell type. These alleles encode a fusion protein designed to increase effective expression levels by concentrating hM3Dq to the cell body and dendrites. To illustrate their broad utility, we targeted three different genetically defined cell populations: noradrenergic neurons of the compact, bilateral locus coeruleus and two dispersed populations, Camk2a+ neurons and GFAP+ glia. In all three populations, we observed reproducible expression and confirmed that activation of hM3Dq is sufficient to dose-dependently evoke phenotypic changes, without extreme phenotypes associated with hM3Dq overexpression. These alleles offer the ability to non-invasively control activity of diverse cell types to uncover their function and dysfunction at any developmental stage.}, number={11}, journal={CELL REPORTS}, author={Sciolino, Natale R. and Plummer, Nicholas W. and Chen, Yu-Wei and Alexander, Georgia M. and Robertson, Sabrina D. and Dudek, Serena M. and McElligott, Zoe A. and Jensen, Patricia}, year={2016}, month={Jun}, pages={2563–2573} }
 @article{robertson_plummer_jensen_2016, title={Uncovering diversity in the development of central noradrenergic neurons and their efferents}, volume={1641}, ISSN={["1872-6240"]}, DOI={10.1016/j.brainres.2015.11.023}, abstractNote={Uncovering the mechanisms that underlie central noradrenergic neuron heterogeneity is essential to understanding selective subtype vulnerability to disease and environmental insult. Using recombinase-based intersectional genetic fate mapping we have previously demonstrated that molecularly distinct progenitor populations give rise to mature noradrenergic neurons differing in their anatomical location, axon morphology and efferent projection pattern. Here we review the findings from our previous study and extend our analysis of the noradrenergic subpopulation defined by transient developmental expression of Hoxb1. Using a combination of intersectional genetic fate mapping and analysis of a targeted loss of function mutation in Hoxb1, we have now uncovered additional heterogeneity based on the requirement of some noradrenergic neurons for Hoxb1 expression. By comparing the distribution of noradrenergic neurons derived from the Hoxb1 expression domain in wild-type and mutant mice, we demonstrate that Hoxb1 expression is required by a subset of neurons in the pons. Additional fate mapping, using a Hoxb1 enhancer element that drives Cre recombinase expression exclusively in rhombomere 4 of the hindbrain, reveals the existence of a subpopulation of noradrenergic neurons in the pons with more restricted axonal targets than the full Hoxb1-derived subpopulation. The unique projection profile of this newly defined subpopulation suggests that it may be functionally distinct. These analyses shed new light on the molecular determinants of noradrenergic identity in the pons and the overall complexity of the central noradrenergic system. This article is part of a Special Issue entitled SI: Noradrenergic System.}, journal={BRAIN RESEARCH}, author={Robertson, Sabrina D. and Plummer, Nicholas W. and Jensen, Patricia}, year={2016}, month={Jun}, pages={234–244} }