The extrasynaptic AMPA receptors functioning is altered under inflammatory pain

• Autorzy: Kopach O. , Park J. , Petralia R. , Sotnik A. , Belan P. , Tao Y. , Voitenko N.
• Języki publikacji: EN

Abstrakty

EN

We have recently shown that synaptic Ca2+-impearmable AMPA receptors (AMPARs) internalization in dorsal horn neurons underlies the maintenance of nociceptive hypersensitivity in infl ammatory pain. Here we have analyzed if traffi cking of extrasynaptic AMPARs is also changed during development and maintenance of persistent pain. We report that Complete Freund’s Adjuvant (CFA)-induced infl ammation causes an increase in functional expression of extrasynaptic AMPARs in rat substantia gelatinosa (SG) neurons during the maintenance rather than development of persistent pain. This increase, revealed as a signifi cant enhancement of AMPA-induced membrane currents and [Ca2+]i transients, was observed only in neurons characterized by an intrinsic tonic fi ring properties whereas no changes were observed in neurons exhibiting a strong adaptation. The increase was also accompanied by an enhancement of surface GluR1 expression and of the total amount of cobalt-positive neurons indicating an increase in a pool of GluR2-lacking AMPARs in extrasynaptic plasma membrane. These results suggest that functional changes in extrasynaptic AMPARs of tonic SG neurons that are associated with the maintenance of nociceptive hypersensitivity may also contribute to infl ammatory pain. We also suppose that there is a different contribution of tonic and transient neurons to the detection of peripheral painful stimuli and to maintenance of nociceptive hypersensitivity.

• Wydawca: -
• Czasopismo: Acta Neurobiologiae Experimentalis
• Rocznik: 2009
• Tom: 69
• Numer: 3
• Opis fizyczny: p.325-326

Twórcy

autor

Kopach O.

• Department of General Physiology of the Nervous System, Bogomoletz, Institute of Physiology, Kiev, Ukraine

autor

Park J.

• Department of Anesthesiology and Critical Care Medicine, John Hopkins University School of Medicine, Baltimore, Maryland, USA

autor

Petralia R.

• Laboratory of Neurochemistry, National Institute of Health, Bethesda, Maryland, USA

autor

Sotnik A.

• Department of General Physiology of the Nervous System, Bogomoletz, Institute of Physiology, Kiev, Ukraine

autor

Belan P.

• Department of General Physiology of the Nervous System, Bogomoletz, Institute of Physiology, Kiev, Ukraine

autor

Tao Y.

• Department of Anesthesiology and Critical Care Medicine, John Hopkins University School of Medicine, Baltimore, Maryland, USA

autor

Voitenko N.

• Department of General Physiology of the Nervous System, Bogomoletz, Institute of Physiology, Kiev, Ukraine