FlyBase provides a centralized resource for the genetic and genomic data of Drosophila melanogaster. As FlyBase enters our fourth decade of service to the research community, we reflect on our unique aspects and look forward to our continued collaboration with the larger research and model organism communities. In this paper, we emphasize the dedicated reports and tools we’ve constructed to meet the specialized needs of fly researchers but also to facilitate use by other research communities. We also highlight ways that we support the fly community, including an external resources page, help resources, and multiple avenues by which researchers can interact with FlyBase.
Multiple types of cell death exist including necrosis, apoptosis, and autophagic cell death. The Drosophila ovary provides a valuable model to study the diversity of cell death modalities, and we review recent progress to elucidate these pathways. At least five distinct types of cell death occur in the ovary, and we focus on two that have been studied extensively. Cell death of mid-stage egg chambers uses a novel caspase-dependent pathway that involves autophagy, and triggers phagocytosis by surrounding somatic epithelial cells. For every egg, fifteen germline nurse cells undergo developmental programmed cell death, which occurs independently of most known cell death genes. These forms of cell death are strikingly similar to cell death observed in the germline of other organisms.
Abbreviations used: ABC, avidin-biotin reagent; ADN, aortic depressor nerve; BDNF, brain-derived neurotrophic factor; DAB, diaminobenzidine; DB, dilution buffer; FDD, frequency-dependent depression; HCN1, hyperpolarization-activated cyclic nucleotide-gated ion channel protein 1; HRP, horseradish peroxidase; IR, immunoreactive or immunoreactivity; NG, nodose ganglion; NPG, nodose-petrosal ganglion complex; NTS, nucleus tractus solitarius; P, postnatal day; PBS, phosphate-buffered saline; SDS, sodium dodecyl sulfate; TRPV1, transient receptor potential vanilloid type 1. AbstractFunctional characteristics of the arterial baroreceptor reflex change throughout ontogenesis, including perinatal adjustments of the reflex gain and adult resetting during hypertension. However, the cellular mechanisms that underlie these functional changes are not completely understood. Here, we provide evidence that brain-derived neurotrophic factor (BDNF), a neurotrophin with a well-established role in activitydependent neuronal plasticity, is abundantly expressed in vivo by a large subset of developing and adult rat baroreceptor afferents. Immunoreactivity to BDNF is present in the cell bodies of baroafferent neurons in the nodose ganglion, their central projections in the solitary tract, and terminal-like structures in the lower brainstem nucleus tractus solitarius. Using ELISA in situ combined with electrical field stimulation, we show that native BDNF is released from cultured newborn nodose ganglion neurons in response to patterns that mimic the in vivo activity of baroreceptor afferents. In particular, highfrequency bursting patterns of baroreceptor firing, which are known to evoke plastic changes at baroreceptor synapses, are significantly more effective at releasing BDNF than tonic patterns of the same average frequency. Together, our study indicates that BDNF expressed by first-order baroreceptor neurons is a likely mediator of both developmental and postdevelopmental modifications at first-order synapses in arterial baroreceptor pathways. Keywords: calcium channels, electrical field stimulation, frequency-dependent depression, nodose ganglion, nucleus tractus solitarius. (Scheuer et al. 1996;Liu et al. 1998Liu et al. , 2000Chen et al. 1999;Doyle and Andresen 2001), a form of synaptic plasticity that may influence baroreflex function (Liu et al. 2000). However, the exact molecular mechanisms underlying changes in either the perinatal or adult system are not well understood.In recent years, brain-derived neurotrophic factor (BDNF), a member of the neurotrophin family of growth factors, has emerged as a key mediator of mechanisms regulating activity-dependent synaptic maturation and plasticity (Huang and Reichardt 2001;Poo 2001), including sensory plasticity (Malcangio and Lessmann 2003). During embryonic development, BDNF is required for the survival of a large subset of NPG neurons, including cardio-respiratory control neurons (Erickson et al. 1996), and specifically arterial baroreceptors (Brady et al. 1999). Namely, BDNF is e...
Nociceptive pathways with first-order neurons located in the trigeminal ganglion (TG) provide sensory innervation to the head, and are responsible for a number of common chronic pain conditions, including migraines, temporomandibular disorders and trigeminal neuralgias. Many of those conditions are associated with inflammation. Yet, the mechanisms of chronic inflammatory pain remain poorly understood. Our previous studies show that the neurotrophin brain-derived neurotrophic factor (BDNF) is expressed by adult rat TG neurons, and released from cultured newborn rat TG neurons by electrical stimulation and calcitonin gene-related peptide (CGRP), a well-established mediator of trigeminal inflammatory pain. These data suggest that BDNF plays a role in activity-dependent plasticity at first-order trigeminal synapses, including functional changes that take place in trigeminal nociceptive pathways during chronic inflammation. The present study was designed to determine the effects of peripheral inflammation, using tooth pulp inflammation as a model, on regulation of BDNF expression in TG neurons of juvenile rats and mice. Cavities were prepared in right-side maxillary first and second molars of 4-week-old animals, and left open to oral microflora. BDNF expression in right TG was compared with contralateral TG of the same animal, and with right TG of sham-operated controls, 7 and 28 days after cavity preparation. Our ELISA data indicate that exposing the tooth pulp for 28 days, with confirmed inflammation, leads to a significant upregulation of BDNF in the TG ipsilateral to the affected teeth. Double-immunohistochemistry with antibodies against BDNF combined with one of nociceptor markers, CGRP or TRPV1, revealed that BDNF is significantly upregulated in TRPV1-immunoreactive (IR) neurons in both rats and mice, and CGRP-IR neurons in mice, but not rats. Overall, the inflammation-induced upregulation of BDNF is stronger in mice compared to rats. Thus, mouse TG provides a suitable model to study molecular mechanisms of inflammation-dependent regulation of BDNF expression in vivo.
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