The glial cells in abdominal ganglia of the horse leech Haemopis sanguisuga were studied by electron microscopy and analysed quantitatively to evaluate the suitability of this easily obtainable carnivorous species for physiological studies. Each abdominal ganglion contains eight giant glial cells, 12,000-14,000 small glial cells, and approximately 300 neurons. The giant glial cells constituted 44.6% and the small glial cells 6.4% of the ganglion's volume. The giant glial cells contain glycogen and bundles of filaments that are chiefly located in their periphery, close to the neurons into which they send processes. The small glial cells are frequently surrounded by the giant glial cells but also occur around neuronal perikarya and axon tracts, as well as against the basal lamina and connective tissue layers. The small glial cells contain lysosomes and sometimes form a trophospongium with the neurons. A system of extracellular channels, which is continuous with the basal lamina, indents the giant glial cells and extends around parts of the neurons. The extracellular channels contain a matrix that appears very similar to the basal lamina and to the cytoplasm in the processes of the small glial cells. Some of the extracellular channels contain collagen fibrils. Hemidesmosomes join the matrix-filled extracellular channels to both the neurons and the giant glial cells. Ionic lanthanum has a free access to the neurons and glial cells via the extracellular spaces and matrix-filled channels. Areas of synaptic intermingling rarely contain glial cell processes.
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Sci Rep
December 2024
Center for Medical Genetics, School of Life Sciences, Central South University, Changsha, 410078, Hunan, P. R. China.
Dopamine (DA) plays important roles in various behaviors, including learning and motivation. Recently, THOC5 was identified as an important regulator in the development of dopaminergic neurons. However, how THOC5 is regulated has not been explored.
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December 2024
Institute of Medical Sciences, University of Toronto, 1 King's College Circle, Toronto, ON, M5S 1A8, Canada.
Astrocyte to neuron reprogramming has been performed using viral delivery of neurogenic transcription factors in GFAP expressing cells. Recent reports of off-target expression in cortical neurons following adeno-associated virus (AAV) transduction to deliver the neurogenic factors have confounded our understanding of the efficacy of direct cellular reprogramming. To shed light on potential mechanisms that may underlie the neuronal off-target expression of GFAP promoter driven expression of neurogenic factors in neurons, two regionally distinct cortices were compared-the motor cortex (MC) and medial prefrontal cortex (mPFC)-and investigated: (1) the regional tropism and astrocyte transduction with an AAV5-GFAP vector, (2) the expression of Gfap in MC and mPFC neurons; and (3) material transfer between astrocytes and neurons.
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December 2024
Department of Neuroscience, Baylor College of Medicine, Houston, TX, 77030, USA.
The bipolar disorder (BD) risk gene ANK3 encodes the scaffolding protein AnkyrinG (AnkG). In neurons, AnkG regulates polarity and ion channel clustering at axon initial segments and nodes of Ranvier. Disruption of neuronal AnkG causes BD-like phenotypes in mice.
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December 2024
KU Leuven Department of Microbiology, Immunology and Transplantation, Virology, Antiviral Drug & Vaccine Research Group, Rega Institute for Medical Research, Leuven, Belgium.
The 2015-2016 Zika virus (ZIKV) outbreak in the Americas revealed the ability of ZIKV from the Asian lineage to cause birth defects, generically called congenital Zika syndrome (CZS). Notwithstanding the long circulation history of Asian ZIKV, no ZIKV-associated CZS cases were reported prior to the outbreaks in French Polynesia (2013) and Brazil (2015). Whether the sudden emergence of CZS resulted from an evolutionary event of Asian ZIKV has remained unclear.
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December 2024
Faculty of Biology, Medicine and Health, University of Manchester, Manchester, UK.
Growth differentiation factor 15, GDF15, and glucagon-like peptide-1 (GLP-1) analogues act through brainstem neurons that co-localise their receptors, GDNF-family receptor α-like (GFRAL) and GLP1R, to reduce food intake and body weight. However, their use as clinical treatments is partially hampered since both can also induce sickness-like behaviours, including aversion, that are mediated through a well-characterised pathway via the exterolateral parabrachial nucleus. Here, in mice, we describe a separate pathway downstream of GFRAL/GLP1R neurons that involves a distinct population of brain-derived neurotrophic factor (BDNF) cells in the medial nucleus of the tractus solitarius.
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