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Jonas Broman

Researcher at Lund University

Publications -  37
Citations -  1712

Jonas Broman is an academic researcher from Lund University. The author has contributed to research in topics: Spinal cord & Glutamate receptor. The author has an hindex of 24, co-authored 37 publications receiving 1644 citations. Previous affiliations of Jonas Broman include Health Science University & Karolinska Institutet.

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Cholesterol Depletion Impairs Vascular Reactivity to Endothelin-1 by Reducing Store-Operated Ca2+ Entry Dependent on TRPC1

TL;DR: It is suggested that cholesterol influences vascular reactivity to ET-1 by affecting the caveolar localization of TRPC1 through manipulating membrane cholesterol and disrupting caveolae in intact rat arteries.
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Regulated exocytosis of GABA-containing synaptic-like microvesicles in pancreatic beta-cells.

TL;DR: There are two parallel pathways of exocytosis in pancreatic β-cells and that release of GABA may accordingly be temporally and spatially separated from insulin secretion, providing a basis for paracrine GABAergic signaling within the islet.
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Enrichment of glutamate-like immunoreactivity in primary afferent terminals throughout the spinal cord dorsal horn.

TL;DR: Findings suggest that glutamate, alone or in combination with other neuroactive compounds, is involved in the transfer of all sensory modalities from primary afferent fibres to dorsal horn neurons.
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Distribution of vesicular glutamate transporters 1 and 2 in the rat spinal cord, with a note on the spinocervical tract.

TL;DR: The principal distribution patterns of VGLUT1 and V GLUT2 are essentially similar throughout the rostrocaudal extension of the spinal cord, suggesting dual origins of VglUT1‐immunoreactive varicosities in this region.
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Translocation of GluR1-Containing AMPA Receptors to a Spinal Nociceptive Synapse during Acute Noxious Stimulation

TL;DR: In this article, the authors show that a model of acute inflammatory hyperalgesia is associated with an elevated density of GluR1-containing AMPA receptors, as well as an increased synaptic ratio, at synapses established by C-fibers that lack the neuropeptide substance P.