Time Zones, Screencasts, and Becoming Real: Lessons Learned as a Distance Librarian

The library literature abounds with articles, presentations, and books on using various sorts of distance learning tools and techniques for library services. (I direct you to the excellent 5th Bibliography of Library Services for Distance Learning Resources from the Distance Learning Section of ACRL or practically any library conference proceedings for numerous examples.) Many of those resources will discuss how a particular type of tool, say, webchat, can be used for library services, with examples of successful, and sometimes unsuccessful, use in various types of libraries. I have, however, very rarely seen any discussion of when to use such tools, or any theoretical discussion of why some tools work better than others in different situations. This article lays out the conclusions and suppositions I have come to in 7 years of being a distance librarian (plus several extra years working intensively with commuter students and with the benefit of a Master’s degree in Adult Education and Distance Learning), in the hopes of spurring a new discussion and new research into both how and when to use different types of tools and techniques

Selective neurodegeneration in Huntington's disease

No Abstract.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/50358/1/410380602_ftp.pd

Some histochemical observations on the telencephalon of the bullfrog, Rana catesbeiana shaw

The histochemically determined distribution of acetylcholinesterase, monoamine oxidase and succinate dehydrogenase in the telencephalon of the bullfrog supports the classically recognized divisions of the pallium and subpallium. Analysis also corroborates the following gernerally recognized anuran-amniotic homologies: anuran medial pallium to amniotic medial cortex anuran septal nuclei to amniotic septal nuclei, anuran striatum to amniotic corpus striatum. On topographical and histochemical criteria the ventrocaudal and basomedial portions of the anuran telencephalon are considered possible homologues to the mammalian amygdala. It is suggested that two divisions can be recognized: a pars lateralis which may be homologous to the mammalian cortico-medial group. And a pars medialis which may be homologous to the mammalian baso-lateral group. Further analysis suggests, particularly when viewed in the light of recent experimental anatomical studies, that the anuran lateral pallium consists of a pars dorsalis and a pars ventralis. The pars dorsalis may be the reptilian homologue of the dorsal cortex and the pars ventralis may be the field homologue of both the reptilian piriform cortex and the dorsal ventricular ridge.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/49994/1/901570403_ftp.pd

Preproenkephalin messenger RNA—containing neurons in striatum of patients with symptomatic and presymptomatic huntington's disease: An in situ hybridization study

Previous studies have revealed a loss of enkephalin immunoreactivity in the terminals of striatal neurons projecting to the external globus pallidus in patients with early grades of Huntington's disease (HD). To assess the status of the perikarya of striatal enkephalinergic neurons, we performed in situ hybridization histochemistry with a radiolabeled RNA probe complementary to preproenkephalin messenger RNA. We studied postmortem brain tissue of 6 patients with symptomatic HD, 7 control subjects, and 2 presymptomatic carriers of the HD allele. There was a significant reduction in the areal density of striatal neurons expressing preproenkephalin messenger RNA in the patients with symptomatic HD, but the level of labeling in the remaining cells was not altered compared with the control subjects. In the specimens from presymptomatic individuals, there was no reduction of areal density of preproenkephalin messenger RNA-containing neurons in the striatum, despite the fact that loss of enkephalin immunoreactivity in the external globus pallidus had been previously demonstrated in the same brains. The results correlate with the previous demonstration of depleted enkephalin immunoreactive terminals in the external globus pallidus in patients with symptomatic HD. They also suggest that the early loss of enkephalin immunoreactivity observed in the external globus pallidus of presymptomatic carriers of the HD allele is not related to a generalized death of striatal enkephalinergic neurons early in the course of the disease.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/50345/1/410300406_ftp.pd

An experimental study of the ventral striatum of the golden hamster. I. Neuronal connections of the nucleus accumbens

As part of an experimental study of the ventral striatum, the horseradish peroxidase (HRP) method was used to examine the afferent and efferent neuronal connections of the nucleus accumbens. Following iontophoretic applications or hydraulic injections of HRP in nucleus accumbens, cells labeled by retrograde transport of HRP were observed in the ipsilateral telencephalon in the posterior agranular insular, perirhinal, entorhinal, and primary olfactory cortices, in the subiculum and hippocampal field CA1, and in the anterior and posterior divisions of the basolateral amygdaloid nucleus. In the diencephalon, labeled neurons were present ipsilaterally in the central medial, paracentral and parafascicular intralaminar nuclei, and in the midline nuclei parataenialis, paraventricularis, and reuniens. Retrograde labeling was observed in the ipsilateral brainstem in cells of the ventral tegmental area and dorsal raphe. Many of these projections to nucleus accumbens were found to be topographically organized. Anterograde transport of HRP from nucleus accumbens demonstrated ipsilateral terminal fields in the ventral pallidum and substantia nigra, pars reticulata. The afferent projections to nucleus accumbens from the posterior insular and perirhinal neocortices, intralaminar thalamus, and the dopamine-containing ventral tegmental area are analogous to the connections of the caudatoputamen, as are the efferents from nucleus accumbens to the substantia nigra and ventral globus pallidus. These connections substantiate the classification of nucleus accumbens as a striatal structure and provide support for the recently proposed concept of the ventral striatum. Furthermore, the demonstration that a number of limbic system structures, including the amygdala, hippocampal formation, entorhinal cortex, and olfactory cortex are important sources of afferents to the nucleus accumbens, suggests that the ventral striatum may serve to integrate limbic information into the striatal system.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/50009/1/901910203_ftp.pd

Caldag-Gefi Down-Regulation in the Striatum as a Neuroprotective Change in Huntington's Disease.

Huntingtin protein (Htt) is ubiquitously expressed, yet Huntington’s disease (HD), a fatal neurologic disorder produced by expansion of an Htt polyglutamine tract, is characterized by neurodegeneration that occurs primarily in the striatum and cerebral cortex. Such discrepancies between sites of expression and pathology occur in multiple neurodegenerative disorders associated with expanded polyglutamine tracts. One possible reason is that disease-modifying factors are tissue-specific. Here we show that the striatum-enriched protein, CalDAG-GEFI, is severely down-regulated in the striatum of mouse HD models and is down-regulated in HD individuals. In the R6/2 transgenic mouse model of HD, striatal neurons with the largest aggregates of mutant Htt have the lowest levels of CalDAG-GEFI. In a brain-slice explant model of HD, knock-down of CalDAG-GEFI expression rescues striatal neurons from pathology induced by transfection of polyglutamine-expanded Htt exon 1. These findings suggest that the striking down-regulation of CalDAG-GEFI in HD could be a protective mechanism that mitigates Htt-induced degeneration.Eunice Kennedy Shriver National Institute of Child Health and Human Development (U.S.) (R01-HD28341)National Institute of Mental Health (U.S.) (F32-MH065815)Wellcome Trust (London, England)Cure Huntington’s Disease Initiative, Inc.MGH/MIT Morris Udall Center of Excellence in Parkinson Disease Research (P50-NS038372

Impaired extinction of learned fear in rats selectively bred for high anxiety – evidence of altered neuronal processing in prefrontal-amygdala pathways

The impaired extinction of acquired fear is a core symptom of anxiety disorders, such as post-traumatic stress disorder, phobias or panic disorder, and is known to be particularly resistant to existing pharmacotherapy. We provide here evidence that a similar relationship between trait anxiety and resistance to extinction of fear memory can be mimicked in a psychopathologic animal model. Wistar rat lines selectively bred for high (HAB) or low (LAB) anxiety-related behaviour were tested in a classical cued fear conditioning task utilizing freezing responses as a measure of fear. Fear acquisition was similar in both lines. In the extinction trial, however, HAB rats showed a marked deficit in the attenuation of freezing responses to repeated auditory conditioned stimulus presentations as compared with LAB rats, which exhibited rapid extinction. To gain information concerning the putatively altered neuronal processing associated with the differential behavioural response between HAB and LAB rats, c-Fos expression was investigated in the main prefrontal-amygdala pathways important for cued fear extinction. HAB compared to LAB rats showed an attenuated c-Fos response to repeated conditioned stimulus presentations in infralimbic and cingulate cortices, as well as in the lateral amygdala, but facilitated the c-Fos response in the medial part of the central amygdala. In conclusion, the present results support the notion that impaired extinction in high anxiety rats is accompanied by an aberrant activation profile in extinction-relevant prefrontal-amygdala circuits. Thus, HAB rats may represent a clinically relevant model to study the mechanisms and potential targets to accelerate delayed extinction processes in subjects with enhanced trait anxiety