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Virginia S. Seybold, Ph.D.
Professor, Department of Neuroscience
vseybold@umn.edu |
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 Cellular
mechanisms underlying hyperalgesia.
Although acute pain is an important adaptive mechanism that alerts
an organism to tissue injury and initiates behavior to avoid further
injury, chronic pain seems to serve no useful purpose. My research
program addresses mechanisms underlying hyperalgesia, the increased
sensation of pain that is felt following tissue injury. Mechanisms
for hyperalgesia are explored at both ends of sensory neurons: at
the peripheral process, where the signal of a noxious stimulus is
first transduced, and in the spinal cord, where the first synapse
in the pathway for sensation of pain is located. Sensitization
of sensory neurons occurs in conjunction with hyperalgesia.
Sensitization is the cellular process responsible for the increased
response of sensory neurons to noxious stimuli. The mechanism underlying
sensitization, however, is not understood. Using activity-dependent
fluorescent dyes, we are exploring whether substances generated in
injured tissue by cells of the immune system act directly on sensory
neurons to enhance the response of these neurons to noxious stimuli.
In addition, molecular biology is used to study plasticity in the
expression of peptides, neurotransmitters and receptors in sensory
neurons in conjunction with inflammation.
Recently, it has been shown that neurons in the spinal cord exhibit
increased excitability in parallel with hyperalgesia following peripheral
injury. The second area of my research addresses whether peptides
released from sensory neurons contribute to the increased excitability
of spinal neurons. Modulation of the flexor reflex by receptor antagonists
is used to assess the role of specific transmitters in the hyperexcitability
of spinal neurons that accompanies peripheral inflammation and hyperalgesia.
Biochemical studies of spinal neurons in vitro are used to explore
the intracellular pathways by which receptor activation leads to a
change in neuronal excitability. |
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Selected Publications
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 | Seybold VS, Coicou LG, Groth RD, Mermelstein PG.
Substance P initiates NFAT-dependent gene expression in spinal neurons.
J Neurochem. 2006 Apr;97(2):397-407. Epub 2006 Mar 15. |
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Khasabova IA, Harding-Rose C, Simone DA, Seybold VS
Differential effects of CB1 and opioid agonists on two populations
of adult rat dorsal root ganglion neurons.
J
Neurosci. 2004 Feb 18;24(7):1744-53 |
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Seybold VS, Jia YP, Abrahams LG
Cyclo-oxygenase-2 contributes to central sensitization in rats with
peripheral inflammation. Pain.
2003 Sep;105(1-2):47-55 |
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Seybold VS, McCarson KE, Mermelstein PG, Groth RD,
Abrahams LG
Calcitonin gene-related peptide regulates expression of neurokinin1
receptors by rat spinal neurons.
J
Neurosci. 2003 Mar 1;23(5):1816-24 |
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Khasabova IA, Simone DA, Seybold VS
Cannabinoids attenuate depolarization-dependent Ca2+ influx in intermediate-size
primary afferent neurons of adult rats.
Neuroscience.
2002;115(2):613-25 |
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Linden DR, Reutter MA, McCarson KE, Seybold VS
Time-dependent changes in neurokinin(3) receptors and tachykinins
during adjuvant-induced peripheral inflammation in the rat.
Neuroscience
2000;98(4):801-11 |
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Linden DR, Chehl M, El-Fakahanay, Seybold VS
Neurokinin 3 receptors couple to the activation of neuronal nitric
oxide synthase in stably transfected Chinese hamster ovary cells.
J
Pharm Expt Ther 2000;293:559-569 |
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