ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004
A neuronal isoform of protein kinase G couples mitogen-activated protein kinase nuclear import to axotomy-induced long-term hyperexcitability in Aplysia sensory neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 66 citations in OpenAlex.
- The α isoform of cGMP-dependent protein kinase 1 (PKG1α) is expressed and functionally important in intrinsic primary afferent neurons of the guinea pig enteric nervous system.Neurogastroenterology and motility · 2021Article
- Changes in Metabolism and Proteostasis Drive Aging Phenotype inFrontiers in aging neuroscience · 2020Article
- A review of the actions of Nitric Oxide in development and neuronal function in major invertebrate model systems.AIMS neuroscience · 2019Review
- Nociceptive Biology of Molluscs and Arthropods: Evolutionary Clues About Functions and Mechanisms Potentially Related to Pain.Frontiers in physiology · 2018Review
- Article
- Synaptic generation of an intracellular retrograde signal requires activation of the tyrosine kinase and mitogen-activated protein kinase signaling cascades in Aplysia.Neurobiology of learning and memory · 2015Article
- Axon-soma communication in neuronal injury.Nature reviews. Neuroscience · 2014Review
- PKG-mediated MAPK signaling is necessary for long-term operant memory in Aplysia.Learning & memory (Cold Spring Harbor, N.Y.) · 2011Article
- Serum response factor mediated gene activity in physiological and pathological processes of neuronal motility.Frontiers in molecular neuroscience · 2011Article
- The regulation of AMPK signaling in a natural state of profound metabolic rate depression.Molecular and cellular biochemistry · 2010Article
- Molluscan memory of injury: evolutionary insights into chronic pain and neurological disorders.Brain, behavior and evolution · 2009Review
- Effects of axotomy on cultured sensory neurons of Aplysia: long-term injury-induced changes in excitability and morphology are mediated by different signaling pathways.Journal of neurophysiology · 2008Article
- Targeted mutation of EphB1 receptor prevents development of neuropathic hyperalgesia and physical dependence on morphine in mice.Molecular pain · 2008Article
- Intracellular signaling in primary sensory neurons and persistent pain.Neurochemical research · 2008Review
- Concepts of neural nitric oxide-mediated transmission.The European journal of neuroscience · 2008Review
- Enhanced transmission at a spinal synapse triggered in vivo by an injury signal independent of altered synaptic activity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- Role of nitric oxide in classical conditioning of siphon withdrawal in Aplysia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- Treatment of cancer pain with noninvasive brain stimulation.Journal of pain and symptom management · 2007Article
- Synaptogenesis regulates axotomy-induced activation of c-Jun-activator protein-1 transcription.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- Sunday Driver links axonal transport to damage signaling.The Journal of cell biology · 2005Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The induction of a long-term hyperexcitability (LTH) in vertebrate nociceptive sensory neurons (SNs) after nerve injury is an important contributor to neuropathic pain in humans, but the signaling cascades that induce this LTH have not been identified. In particular, it is not known how injuring an axon far from the cell soma elicits changes in gene expression in the nucleus that underlie LTH. The nociceptive SNs of Aplysia (ap) develop an LTH with electrophysiological properties after axotomy similar to those of mammalian neurons and are an experimentally useful model to examine these issues. We cloned an Aplysia PKG (cGMP-dependent protein kinase; protein kinase G) that is homologous to vertebrate type-I PKGs and found that apPKG is activated at the site of injury in the axon after peripheral nerve crush. The active apPKG is subsequently retrogradely transported to the somata of the SNs, but apPKG activity does not appear in other neurons whose axons are injured. In the soma, apPKG phosphorylates apMAPK (Aplysia mitogen-activated protein kinase), resulting in its entry into the nucleus. Surprisingly, studies using recombinant proteins in vivo and in vitro indicate that apPKG directly phosphorylates the threonine moiety in the T-E-Y activation site of apMAPK when the -Y- site contains a phosphate. We used inhibitors of nitric oxide synthase, soluble guanyl cyclase, or PKG after nerve injury, and found that each prevented the appearance of the LTH. Moreover, blocking apPKG activation prevented the nuclear import of apMAPK. Consequently, the nitric oxide-PKG-MAPK pathway is a potential target for treatment of neuropathic pain.
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