@article{lubischer_2022, title={Decision-Making and the Shadowy Brain — Part 1}, volume={1}, url={https://doi.org/10.52750/975523}, DOI={10.52750/975523}, abstractNote={When we're faced with decisions about anything -including how to respond to a health-related threat like a pandemic -knowing how our brains work can make us better decision-makers.Dr. Lubischer shares what your brain can learn without your approval, and how you can use this knowledge to become a better critical thinker and to take more control over your own decisions (what to do, what to believe, how to think critically).Jane Lubischer, Ph.D., is passionate about using the science of learning as a framework for better learning, better teaching and better design of courses and curricula.She grew up in California and earned degrees from}, publisher={North Carolina State University}, author={Lubischer, Jane}, year={2022}, month={Jan} }
 @article{lubischer_2022, title={Decision-Making and the Shadowy Brain — Part 2}, volume={1}, url={https://doi.org/10.52750/274958}, DOI={10.52750/274958}, abstractNote={When we're faced with decisions about anything -including how to respond to a health-related threat like a pandemic -knowing how our brains work can make us better decision-makers.Dr. Lubischer shares what your brain can learn without your approval, and how you can use this knowledge to become a better critical thinker and to take more control over your own decisions (what to do, what to believe, how to think critically).Jane Lubischer, Ph.D., is passionate about using the science of learning as a framework for better learning, better teaching and better design of courses and curricula.She grew up in California and earned degrees from}, publisher={North Carolina State University}, author={Lubischer, Jane}, year={2022}, month={Jan} }
 @article{lubischer_2022, title={The Secret of Learning}, url={https://doi.org/10.52750/976724}, DOI={10.52750/976724}, abstractNote={Dr. Jane Lubischer challenges students to be intentional and to use a big picture way of thinking about their own academic interests as they build their education.Jane Lubischer went to college to become an}, author={Lubischer, Jane}, year={2022}, month={Jul} }
 @inproceedings{the formation of student learning communities in a life science first year course.  parks ld and lubischer jl_2016, booktitle={Experimental Biology}, year={2016} }
 @inproceedings{critical and creative thinking in the life sciences (lsc 101): equipping and challenging students to be intentional learners. lubischer jl, flores jf, kuo h-c, parks ld_2015, booktitle={Teaching and Learning Symposium, NC State}, year={2015} }
 @inproceedings{nc state life sciences first year program (lsfy): administrative implementation of a holistic approach to first year student success._2015, booktitle={Gordon Research Conference on Undergraduate Biology Education Research}, year={2015} }
 @inproceedings{the science of learning and the w-curve: two impactful lessons for freshmen in the life sciences first year program. flores jf, kuo h-c, parks ld, lubischer jl_2015, booktitle={Teaching and Learning Symposium, NC State}, year={2015} }
 @article{lee_lubischer_2014, title={Close Encounters of the Amphibious Kind}, volume={051}, DOI={10.2505/4/sc14_051_06_50}, number={06}, journal={Science and Children}, publisher={National Science Teachers Association (NSTA)}, author={Lee, Tammy and Lubischer, Jane}, year={2014} }
 @article{mccullen_mcquilling_grossfeld_lubischer_clarke_loboa_2010, title={Application of Low-Frequency Alternating Current Electric Fields Via Interdigitated Electrodes: Effects on Cellular Viability, Cytoplasmic Calcium, and Osteogenic Differentiation of Human Adipose-Derived Stem Cells}, volume={16}, ISSN={["1937-3392"]}, url={https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/20367249/?tool=EBI}, DOI={10.1089/ten.tec.2009.0751}, abstractNote={Electric stimulation is known to initiate signaling pathways and provides a technique to enhance osteogenic differentiation of stem and/or progenitor cells. There are a variety of in vitro stimulation devices to apply electric fields to such cells. Herein, we describe and highlight the use of interdigitated electrodes to characterize signaling pathways and the effect of electric fields on the proliferation and osteogenic differentiation of human adipose-derived stem cells (hASCs). The advantage of the interdigitated electrode configuration is that cells can be easily imaged during short-term (acute) stimulation, and this identical configuration can be utilized for long-term (chronic) studies. Acute exposure of hASCs to alternating current (AC) sinusoidal electric fields of 1 Hz induced a dose-dependent increase in cytoplasmic calcium in response to electric field magnitude, as observed by fluorescence microscopy. hASCs that were chronically exposed to AC electric field treatment of 1 V/cm (4 h/day for 14 days, cultured in the osteogenic differentiation medium containing dexamethasone, ascorbic acid, and β-glycerol phosphate) displayed a significant increase in mineral deposition relative to unstimulated controls. This is the first study to evaluate the effects of sinusoidal AC electric fields on hASCs and to demonstrate that acute and chronic electric field exposure can significantly increase intracellular calcium signaling and the deposition of accreted calcium under osteogenic stimulation, respectively.}, number={6}, journal={TISSUE ENGINEERING PART C-METHODS}, author={McCullen, Seth D. and McQuilling, John P. and Grossfeld, Robert M. and Lubischer, Jane L. and Clarke, Laura I. and Loboa, Elizabeth G.}, year={2010}, month={Dec}, pages={1377–1386} }
 @article{cahoy_emery_kaushal_foo_zamanian_christopherson_xing_lubischer_krieg_krupenko_et al._2008, title={A transcriptome database for astrocytes, neurons, and oligodendrocytes: A new resource for understanding brain development and function}, volume={28}, ISSN={["1529-2401"]}, url={https://europepmc.org/articles/PMC6671143}, DOI={10.1523/JNEUROSCI.4178-07.2008}, abstractNote={Understanding the cell–cell interactions that control CNS development and function has long been limited by the lack of methods to cleanly separate neural cell types. Here we describe methods for the prospective isolation and purification of astrocytes, neurons, and oligodendrocytes from developing and mature mouse forebrain. We used FACS (fluorescent-activated cell sorting) to isolate astrocytes from transgenic mice that express enhanced green fluorescent protein (EGFP) under the control of an S100β promoter. Using Affymetrix GeneChip Arrays, we then created a transcriptome database of the expression levels of >20,000 genes by gene profiling these three main CNS neural cell types at various postnatal ages between postnatal day 1 (P1) and P30. This database provides a detailed global characterization and comparison of the genes expressed by acutely isolated astrocytes, neurons, and oligodendrocytes. We found that Aldh1L1 is a highly specific antigenic marker for astrocytes with a substantially broader pattern of astrocyte expression than the traditional astrocyte marker GFAP. Astrocytes were enriched in specific metabolic and lipid synthetic pathways, as well as the draper/Megf10 and Mertk/integrin αvβ5phagocytic pathways suggesting that astrocytes are professional phagocytes. Our findings call into question the concept of a “glial” cell class as the gene profiles of astrocytes and oligodendrocytes are as dissimilar to each other as they are to neurons. This transcriptome database of acutely isolated purified astrocytes, neurons, and oligodendrocytes provides a resource to the neuroscience community by providing improved cell-type-specific markers and for better understanding of neural development, function, and disease.}, number={1}, journal={JOURNAL OF NEUROSCIENCE}, author={Cahoy, John D. and Emery, Ben and Kaushal, Amit and Foo, Lynette C. and Zamanian, Jennifer L. and Christopherson, Karen S. and Xing, Yi and Lubischer, Jane L. and Krieg, Paul A. and Krupenko, Sergey A. and et al.}, year={2008}, month={Jan}, pages={264–278} }
 @article{malomouzh_nikolsky_lieberman_sherman_lubischer_grossfeld_urazaev_2005, title={Effect of N-acetylaspartylglutamate (NAAG) on non-quantal and spontaneous quantal release of acetylcholine at the neuromuscular synapse of rat}, volume={94}, ISSN={["1471-4159"]}, url={https://doi.org/10.1111/j.1471-4159.2005.03194.x}, DOI={10.1111/j.1471-4159.2005.03194.x}, abstractNote={Abstract N‐Acetylaspartylglutamate (NAAG), known to be present in rat motor neurons, may participate in neuronal modulation of non‐quantal secretion of acetylcholine (ACh) from motor nerve terminals. Non‐quantal release of ACh was estimated by the amplitude of the endplate membrane hyperpolarization (H‐effect) caused by inhibition of nicotinic receptors by (+)‐tubocurarine and acetylcholinesterase by armin (diethoxy‐p‐nitrophenyl phosphate). Application of exogenous NAAG decreased the H‐effect in a dose‐dependent manner. The reduction of the H‐effect by NAAG was completely removed when N‐acetyl‐β‐aspartylglutamate (βNAAG) or 2‐(phosphonomethyl)‐pentanedioic acid (2‐PMPA) was used to inhibit glutamate carboxypeptidase II (GCP II), a presynaptic Schwann cell membrane‐associated ectoenzyme that hydrolyzes NAAG to glutamate and N‐acetylaspartate. Bath application of glutamate decreased the H‐effect similarly to the action of NAAG but N‐acetylaspartate was without effect. Inhibition of NMDA receptors by dl‐2‐amino‐5‐phosphopentanoic acid, (+)‐5‐methyl‐10,11‐dihydro‐5H‐dibenzocyclohepten‐5,10‐imine (MK801), and 7‐chlorokynurenic acid or inhibition of muscle nitric oxide synthase (NO synthase) by NG‐nitro‐l‐arginine methyl ester and 3‐bromo‐7‐nitroindazole completely prevented the decrease of the H‐effect by NAAG. These results suggest that glutamate, produced by enzymatic hydrolysis of bath‐applied NAAG, can modulate non‐quantal secretion of ACh from the presynaptic terminal of the neuromuscular synapse via activation of postsynaptic NMDA receptors and synthesis of nitric oxide (NO) in muscle fibers. NAAG also increased the frequency of miniature endplate potentials (mEPPs) generated by spontaneous quantal secretion of ACh, whereas the mean amplitude and time constants for rise time and for decay of mEPPs did not change.}, number={1}, journal={JOURNAL OF NEUROCHEMISTRY}, author={Malomouzh, AI and Nikolsky, EE and Lieberman, EM and Sherman, JA and Lubischer, JL and Grossfeld, RM and Urazaev, AK}, year={2005}, month={Jul}, pages={257–267} }
 @article{lubischer_unguez_pierotti_roy_edgerton_2005, title={Reinnervation of the rat levator ani muscle after neonatal denervation}, volume={63}, ISSN={["0022-3034"]}, url={https://doi.org/10.1002/neu.20129}, DOI={10.1002/neu.20129}, abstractNote={After axonal injury on postnatal day 14 (P14), but not P21, motoneurons in the spinal nucleus of the bulbocavernosus (SNB) do not display their normal response to circulating testosterone levels. This could result from a permanent disruption of communication between motoneurons and their testosterone-sensitive target muscles. We assessed the extent of reinnervation of one of these target muscles, the levator ani (LA) muscle, 5 months after the pudendal nerve was cut either on P14 or P21. The number of motoneurons innervating the LA in control and nerve cut animals was determined using retrograde labeling procedures. Functional recovery of the LA muscle was determined via the testing of its in situ contractile properties. Compared to control muscles, reinnervated LA muscles were smaller, had fewer muscle fibers, generated a lower maximum tetanic tension, and were more fatigable. In spite of the fact that fewer motoneurons reinnervated the LA muscle after nerve cut on P14 than on P21, there were no differences in the weight or contractile properties of the LA muscle between these two groups. These data suggest that motoneurons that survived injury on P14 innervated more muscle fibers than normal and exhibited a similar ability to functionally reinnervate the target muscle as those motoneurons that survived injury on P21.}, number={3}, journal={JOURNAL OF NEUROBIOLOGY}, author={Lubischer, JL and Unguez, GA and Pierotti, DJ and Roy, RR and Edgerton, VR}, year={2005}, month={Jun}, pages={188–198} }
 @article{fluorescent proteins expressed in mouse transgenic lines mark subsets of glia, neurons, macrophages, and dendritic cells for vital examination._2004, url={https://europepmc.org/articles/PMC6730273}, DOI={10.1523/JNEUROSCI.3934-04.2004}, abstractNote={To enable vital observation of glia at the neuromuscular junction, transgenic mice were generated that express proteins of the green fluorescent protein family under control of transcriptional regulatory sequences of the human S100B gene. Terminal Schwann cells were imaged repetitively in living animals of one of the transgenic lines to show that, except for extension and retraction of short processes, the glial coverings of the adult neuromuscular synapse are stable. In other lines, subsets of Schwann cells were labeled. The distribution of label suggests that Schwann cells at individual synapses are clonally related, a finding with implications for how these cells might be sorted during postnatal development. Other labeling patterns, some present in unique lines, included astrocytes, microglia, and subsets of cerebellar Bergmann glia, spinal motor neurons, macrophages, and dendritic cells. We show that lines with labeled macrophages can be used to follow the accumulation of these cells at sites of injury.}, journal={The Journal of neuroscience : the official journal of the Society for Neuroscience}, year={2004}, month={Dec} }
 @article{neonatal partial denervation results in nodal but not terminal sprouting and a decrease in efficacy of remaining neuromuscular junctions in rat soleus muscle._1999, url={https://europepmc.org/articles/PMC6782755}, DOI={10.1523/JNEUROSCI.19-20-08931.1999}, abstractNote={Mature motoneurons respond to partial denervation of their target muscle by sprouting to reinnervate denervated fibers, thus maintaining muscle strength in the face of motoneuronal loss caused by injury or disease. Neonatal motoneurons, however, do not expand to innervate more muscle fibers. The present work seeks to understand this developmental change in motoneuron response to partial denervation. It has been suggested that neonatal motor units cannot increase in size because they are already at their maximum size (approximately five times larger than in adulthood). We ruled out this explanation by showing that after partial denervation on postnatal day 14 (P14), when motor units have decreased to their adult size, motoneurons still did not sprout to reinnervate as many fibers as in adulthood. Instead, we found evidence supporting an alternative explanation involving terminal Schwann cells. After partial denervation of neonatal (but not adult) muscles, terminal Schwann cells at denervated endplates undergo apoptosis. We found that terminal (but not nodal) sprouting was absent in partially denervated neonatal muscles. This finding suggests that terminal Schwann cells, previously reported to guide terminal sprouts to denervated endplates in adult muscles, are necessary for the formation and growth of terminal sprouts. Moreover, partial denervation on P14 severely weakened the remaining, uninjured synapses, suggesting that neonatal motoneurons may withdraw terminals after the denervation of nearby fibers. These findings have implications for the interpretation of previous studies on synapse elimination and offer insight into the failure of young motor units to expand after partial denervation.}, journal={The Journal of neuroscience : the official journal of the Society for Neuroscience}, year={1999}, month={Oct} }
 @article{regulation of terminal schwann cell number at the adult neuromuscular junction._1999, url={https://europepmc.org/articles/PMC6784930}, DOI={10.1523/JNEUROSCI.19-24-j0004.1999}, abstractNote={Terminal Schwann cells (TSCs), neuroglia that cover motoneuron terminals, play a role in regulating the structure and function of the neuromuscular junction. In rats, the number of TSCs at each junction increases rapidly in early postnatal life and more slowly in young adults. It is possible that TSC number increases to match increasing endplate area. Alternatively, the increase in TSC number may reflect a developmental process independent of endplate size or terminal function. To experimentally test the relationship between endplate size and TSC number, we manipulated endplate area in an androgen-sensitive muscle of the rat, the levator ani (LA), by castration and by androgen replacement. We found that TSC number not only increased as endplates enlarged but also decreased when endplates shrank. Ninety days after castration, TSC number decreased by approximately 20% (one cell per junction) as endplate size decreased by 30%. These effects were reversed by testosterone. Testosterone levels did not affect TSC number in the extensor digitorum longus (EDL) muscle, where endplate area was unaffected by castration or testosterone treatment. TSC number was, however, significantly correlated with endplate area in both LA and EDL muscles. Furthermore, the relationship between endplate size and TSC number, as defined by the slope of the regression line, was the same in LA and EDL muscles, indicating that this relationship is not a unique feature of the LA muscle. These data suggest that TSC number is a dynamic property of the neuromuscular synapse that is actively regulated throughout life.}, journal={The Journal of neuroscience : the official journal of the Society for Neuroscience}, year={1999}, month={Dec} }
 @article{respecified larval proleg and body wall muscles circulate hemolymph in developing wings of manduca sexta pupae._1999, journal={The Journal of experimental biology}, year={1999}, month={Apr} }
 @article{target muscles and sensory afferents do not influence steroid-regulated, segment-specific death of identified motoneurons in manduca sexta._1996, url={https://doi.org/10.1002/(SICI)1097-4695(199612)31:4<449::AID-NEU5>3.0.CO;2-9}, DOI={10.1002/(sici)1097-4695(199612)31:4<449::aid-neu5>3.3.co;2-8}, abstractNote={Journal of NeurobiologyVolume 31, Issue 4 p. 449-460 Target muscles and sensory afferents do not influence steroid-regulated, segment-specific death of identified motoneurons in Manduca sexta Jane L. Lubischer, (e-mail: jlubi@uts.cc.utexas.edu) Institute of Neuroscience, University of Oregon, Eugene, Oregon 97403-1254Search for more papers by this authorJanis C. Weeks, Corresponding Author (e-mail: adg@jlnrc.medsch.ucla.edu) Institute of Neuroscience, University of Oregon, Eugene, Oregon 97403-1254Institute of Neuroscience, University of Oregon, Eugene, Oregon 97403-1254Search for more papers by this author Jane L. Lubischer, (e-mail: jlubi@uts.cc.utexas.edu) Institute of Neuroscience, University of Oregon, Eugene, Oregon 97403-1254Search for more papers by this authorJanis C. Weeks, Corresponding Author (e-mail: adg@jlnrc.medsch.ucla.edu) Institute of Neuroscience, University of Oregon, Eugene, Oregon 97403-1254Institute of Neuroscience, University of Oregon, Eugene, Oregon 97403-1254Search for more papers by this author First published: December 1996 https://doi.org/10.1002/(SICI)1097-4695(199612)31:4<449::AID-NEU5>3.0.CO;2-9Citations: 11AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinked InRedditWechat Abstract Programmed cell death plays a critical role in sculpting the nervous system during embryonic development. In holometabolous insects, cell death also plays an important role in the reorganization of the nervous system during metamorphosis. In Manduca sexta, cell death and the factors that regulate it can be studied at the level of individually identified neurons. The accessory planta retractor (APR) motoneurons undergo segment-specific death during the larval-pupal transformation. APRs in abdominal segments 1, 5, and 6 die at pupation; those in abdominal segments 2, 3, and 4 survive until adulthood. Juvenile hormone and ecdysteroids regulate the metamorphic restructuring of the nervous system, but the factors that determine which APRs will live and which will die are not known. The present study assessed the possible importance of cell-cell interactions in determining APR survival at pupation by removing APR's target muscle or mechanosensory input early in the final larval instar, prior to the hormonal cues that trigger the larval-pupal transformation. The motoneurons showed their normal, segment-specific pattern of death in nearly all cases. These results suggest that target muscles and sensory input play little or no role in determining the segment-specific pattern of APR survival at pupation. © 1996 John Wiley & Sons, Inc. Citing Literature Volume31, Issue4December 1996Pages 449-460 RelatedInformation}, journal={Journal of neurobiology}, year={1996}, month={Dec} }
 @article{axotomy of developing rat spinal motoneurons: cell survival, soma size, muscle recovery, and the influence of testosterone._1995, url={https://doi.org/10.1002/neu.480260207}, DOI={10.1002/neu.480260207}, abstractNote={AbstractDuring the period of synapse elimination, motoneurons are impaired in their ability to generate or regenerate axonal branches: following partial denervation of their target muscle, young motoneurons do not sprout to nearby denervated fibers and after axonal injury, they fail to reinnervate the muscle. In the rat levator ani (LA) muscle, which is innervated by motoneurons in the spinal nucleus of the bulbocavernosus (SNB), synapse elemination ends relatively late in development and can be regulated by testosterone. We took advantage of this system to determine if the end of synapse elimination and the development of regenerative capabilities by motoneurons share a common mechanism, or, alternatively, if these two events can be dissociated in time. Axotomy on or before postnatal day 14 (P14) caused the death of SNB motoneurons. By P21, toward the end of synapse elimination in the LA muscle, SNB motoneurons had developed the ability to survive axonal injury. Altering testosterone levels by castration on P7 followed by 4 weeks of either testosterone propionate or control injections did not change the ability of SNB motoneurons to survive axonal injury during development, although these same treatments alter the time course of synapse elimination in the LA muscle. Thus, we dissociated the inability of SNB motoneurons to recover from axonal injury from their developmental elimination of synaptic terminals. We also measured the effect of early axotomy on motoneuronal soma size and on target muscle weight. Axotomy on P14 caused a long‐lasting decrease in the soma size of surviving SNB motoneurons, whereas motoneurons axotomized on P28 recovered their normal soma size. Axotomy on or before P7 caused severe atrophy of the target muscles, matching the extensive loss of motoneurons. However, target muscle recovery after axotomy on P14 was as good as recovery after axotomy at later ages, despite greater motoneuronal death after axotomy on P14. This result may reflect an increase in motor unit size, a decrease in polyneuronal innervation by SNB motoneurons that survive axotomy on P14, or a combination of the two. © 1995 John Wiley & Sons, Inc.}, journal={Journal of neurobiology}, year={1995}, month={Feb} }
 @article{axotomy transiently down-regulates androgen receptors in motoneurons of the spinal nucleus of the bulbocavernosus._1995, url={https://doi.org/10.1016/0006-8993(95)00766-j}, DOI={10.1016/0006-8993(95)00766-j}, abstractNote={Testosterone is an important trophic factor for motoneurons in the spinal nucleus of the bulbocavernosus (SNB), and SNB motoneurons are more responsive to testosterone than are other motoneurons. Axonal injury during early postnatal life prevents the normal development of steroid-sensitivity by adult SNB motoneurons. Axonal injury also causes changes in the expression by motoneurons of a wide range of proteins, including the up-regulation of trophic factor receptors. We have used a polyclonal antibody (PG-21; G.S. Prins) to study the expression of androgen receptors in SNB motoneurons after axonal injury. PG-21 labeled motoneuronal nuclei in the lower lumbar spinal cord of rats in a pattern that matched autoradiograpic reports of androgen accumulation in this region of the nervous system. A population of numerous, small cells located dorsal to the central canal also showed evidence of androgen receptor expression. Cutting the axons of SNB motoneurons in adulthood or in development caused a decrease in androgen receptor immunoreactivity in SNB motoneurons. This is the first report that a trophic factor receptor in motoneurons is down-regulated after axonal injury, and is interesting in light of reports that testosterone treatment can facilitate motoneuronal regeneration after nerve cut. Androgen receptor levels subsequently returned to normal, regardless of the age at axotomy, providing no evidence for a lasting effect of developmental axotomy on androgen receptor levels in SNB motoneurons. Thus, axotomy-induced down-regulation of androgen receptors does not underlie the inability of SNB motoneurons to respond to androgen treatment several months after pudendal nerve cut in development.}, journal={Brain research}, year={1995}, month={Oct} }
 @article{evidence for target regulation of the development of androgen sensitivity in rat spinal motoneurons._1995, url={https://doi.org/10.1159/000111279}, DOI={10.1159/000111279}, abstractNote={Specific neuronal circuits within the vertebrate nervous system express high levels of steroid receptors and are sensitive to the effects of steroid hormones. The mechanisms by which these neuronal circuits develop their unique steroid sensitivity are unknown. One intriguing hypothesis is that retrograde influences during early postnatal life play a role in determining which central nervous system (CNS) neurons become sensitive to steroids. We now present evidence that during a critical period in early postnatal development, axonal injury disrupts the normal development of steroid sensitivity. The spinal nucleus of the bulbocavernosus (SNB) is a neuromuscular system that is highly androgen-sensitive at the level of both the motoneurons and their target muscles. Testosterone levels regulate the size of SNB motoneurons and their muscles in adult rats. Cutting the axons of SNB motoneurons on postnatal day 14 (P14) caused permanent decreases in SNB motoneuronal soma size, as well as in SNB target muscle weight. Interestingly, SNB motoneurons that survived axotomy on P14 failed to develop their normal ability to respond to testosterone in adulthood. That is, they did not respond to changes in testosterone levels with changes in soma size. The same effect was not seen after axotomy 1 week later in development, suggesting a critical period for this effect. Thus, separation from the target muscles during an early critical period in development blocked the differentiation of androgen sensitivity by SNB motoneurons, consistent with a role for the target in the normal development of steroid sensitivity by CNS neurons.}, journal={Developmental neuroscience}, year={1995}, month={Jan} }
 @article{transient and permanent effects of androgen during synapse elimination in the levator ani muscle of the rat._1992, url={https://doi.org/10.1002/neu.480230102}, DOI={10.1002/neu.480230102}, abstractNote={AbstractYoung male rats were castrated at 7 days of age, and treated with testosterone propionate daily from 7 to 34 days of age. At 13 months of age, motor axons and terminals innervating the levator ani (LA) muscle were stained with tetranitroblue tetrazolium (TNBT). The number of separate axons innervating individual muscle fibers was counted, and muscle fiber diameter was measured. Previous studies have shown that this androgen treatment increases muscle fiber diameter and delays synapse elimination, measured as (1) a greater percentage of muscle fibers innervated by multiple axons and (2) larger motor units. The present results indicate that the androgenic effect on synapse elimination is permanent, in that high levels of multiple innervation persisted for 12 months after the end of androgen treatment. In contrast, the effect on muscle fiber diameter was not maintained for this period. This dissociation of androgenic effects on the pattern of innervation from androgenic effects on muscle fiber diameter offers further evidence that the androgenic maintenance of multiple innervation is not dependent on muscle fiber size. In addition, circulating testosterone levels were measured at 50 and 60 days of age in animals similarly treated with androgen or oil from 7 to 34 days of age. By 60 days of age, testosterone levels in hormone‐treated animals had dropped below detectability, comparable to levels in oil‐treated controls. This provides additional evidence that androgen treatment during juvenile development can have permanent effects on the adult pattern of innervation in the LA muscle.}, journal={Journal of neurobiology}, year={1992}, month={Feb} }
 @article{autoradiographic localization of progestin-concentrating cells in the brain of the zebra finch._1990, url={https://doi.org/10.1002/cne.902910310}, DOI={10.1002/cne.902910310}, abstractNote={AbstractThe production of song in passerine birds is under the control of steroid hormones, and brain regions involved in song production have been shown to contain androgen and/or estrogen receptors. Studies to date, however, have not considered the possible role of progestins in this behavior. As one approach to this question, the autoradiographic method was used to investigate the distribution of progestin‐concentrating cells in the brain of the adult male zebra finch (Poephila guttata) after injection of the radiolabeled synthetic progestin [17α‐methyl‐3H]‐promegestone. In the telencephalon, identifiable groups of progestin‐accumulating cells were found in the hyperstriatum dorsale, at the medial edge of the lobus parolfactorius, and in the medial septum. In the diencephalon, labeled groups of cells were found in the preoptic area, through much of the medial hypothalamus‐‐including nucleus periventricularis magnocellularis, nucleus medialis hypothalami posterialis, and area infundibularis‐‐and in the medial spiriform nucleus and dorsomedial thalamus. In the myelencephalon, labeled cells are described at the dorsal edge of the medulla and scattered lateral to nXII. These findings offer no support for the hypothesis that progestin acts on any of the known song regions, but do suggest areas of progestin action in the avian central nervous system outside of the known song system. Not surprisingly, these include many areas of the medial hypothalamus and other midline structures.}, journal={The Journal of comparative neurology}, year={1990}, month={Jan} }
 @article{the effects of d1 and d2 receptor antagonists on pain sensitivity and morphine analgesia in the rat._1987, journal={Proceedings of the Western Pharmacology Society}, year={1987}, month={Jan} }