Journal article
Enhancement of presynaptic glutamate release and persistent inflammatory pain by increasing neuronal cAMP in the anterior cingulate cortex
Molecular pain, Vol.4(1), pp.40-40
09/29/2008
DOI: 10.1186/1744-8069-4-40
PMCID: PMC2570662
PMID: 18823548
Abstract
Both presynaptic and postsynaptic alterations are associated with plastic changes of brain circuits, such as learning and memory, drug addiction and chronic pain. However, the dissection of the relative contributions of pre- and postsynaptic components to brain functions is difficult. We have previously shown peripheral inflammation caused both presynaptic and postsynaptic changes and calcium-stimulated cyclic AMP (cAMP) pathway in the anterior cingulate cortex (ACC) is critical in the synaptic plasticity and behavioral sensitization to pain. It remains to be elucidated whether presynaptic or postsynaptic modulation by cAMP in the ACC could be sufficient for enhancing inflammatory pain. In order to address this question, we took advantage of a novel transgenic mouse model, heterologously expressing an
Aplysia
octopamine receptor (Ap oa
1
). This receptor is G protein-coupled and selectively activates the cAMP pathway. We found that activation of Ap oa
1
by octopamine enhanced glutamatergic synaptic transmission in the ACC by increasing presynaptic glutamate release
in vitro
. Bilateral microinjection of octopamine into the ACC significantly facilitated behavioral responses to inflammatory pain but not acute pain. The present study provides the first evidence linking enhanced presynaptic glutamate release in the ACC to behavioral sensitization caused by peripheral inflammation.
Details
- Title: Subtitle
- Enhancement of presynaptic glutamate release and persistent inflammatory pain by increasing neuronal cAMP in the anterior cingulate cortex
- Creators
- Long-Jun Wu - Department of Physiology, Faculty of Medicine, University of Toronto Centre for the Study of Pain, University of Toronto, 1 King's College Circle, Toronto, Ontario M5S 1A8, CanadaHendrik W Steenland - Department of Physiology, Faculty of Medicine, University of Toronto Centre for the Study of Pain, University of Toronto, 1 King's College Circle, Toronto, Ontario M5S 1A8, CanadaSusan S Kim - Department of Physiology, Faculty of Medicine, University of Toronto Centre for the Study of Pain, University of Toronto, 1 King's College Circle, Toronto, Ontario M5S 1A8, CanadaCarolina Isiegas - Department of Biology, University of Pennsylvania, Philadelphia, PA 19104, USATed Abel - Department of Biology, University of Pennsylvania, Philadelphia, PA 19104, USABong-Kiun Kaang - National Creative Research Initiative Center for Memory, Department of Biological Sciences, Seoul National University, San 56-1 Silim-dong Gwanak-gu, Seoul 151-747, KoreaMin Zhuo - Department of Physiology, Faculty of Medicine, University of Toronto Centre for the Study of Pain, University of Toronto, 1 King's College Circle, Toronto, Ontario M5S 1A8, Canada
- Resource Type
- Journal article
- Publication Details
- Molecular pain, Vol.4(1), pp.40-40
- DOI
- 10.1186/1744-8069-4-40
- PMID
- 18823548
- PMCID
- PMC2570662
- NLM abbreviation
- Mol Pain
- ISSN
- 1744-8069
- eISSN
- 1744-8069
- Publisher
- BioMed Central
- Language
- English
- Date published
- 09/29/2008
- Academic Unit
- Molecular Physiology and Biophysics; Psychiatry; Psychological and Brain Sciences; Iowa Neuroscience Institute; Neuroscience and Pharmacology; Biochemistry and Molecular Biology
- Record Identifier
- 9984065736002771
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