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Spasticity therapy reacts to astrocyte GluA1 receptor upregulation following spinal cord injury
Author(s) -
GómezSoriano Julio,
Goiriena Eider,
Taylor Julian
Publication year - 2010
Publication title -
british journal of pharmacology
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.2010.00964.x
Subject(s) - spasticity , medicine , baclofen , spinal cord injury , spinal cord , astrocyte , hyperreflexia , ampa receptor , anesthesia , neuropathic pain , neuroscience , glutamate receptor , central nervous system , receptor , psychology , agonist , psychiatry
For almost three decades intrathecal baclofen therapy has been the standard treatment for spinal cord injury spasticity when oral medication is ineffective or produces serious side effects. Although intrathecal baclofen therapy has a good clinical benefit-risk ratio for spinal spasticity, tolerance and the life-threatening withdrawal syndrome present serious problems for its management. Now, in an experimental model of spinal cord injury spasticity, AMPA receptor blockade with NGX424(Tezampanel) has been shown to reduce stretch reflex activity alone and during tolerance to intrathecal baclofen therapy.These results stem from the observation that GluA1 receptors are overexpressed on reactive astrocytes following experimental ischaemic spinal cord injury. Although further validation is required, the appropriate choice of AMPA receptor antagonists for treatment of stretch hyperreflexia based on our recent understanding of reactive astrocyte neurobiology following spinal cord injury may lead to the development of a better adjunct clinical therapy for spasticity without the side effects of intrathecal baclofen therapy.