Neuropathic Pain Induces Interleukin-1β Sensitive Bimodal Glycinergic Activity in the Central Amygdala
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Fecha
2022-07-01
Profesor/a Guía
Facultad/escuela
Idioma
en
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MDPI
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Licencia CC
CC BY 4.0 DEED
Atribución 4.0 Internacional
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https://creativecommons.org/licenses/by/4.0/deed.es
Resumen
Neuropathic pain reduces GABA and glycine receptor (GlyR)-mediated activity in spinal and supraspinal regions associated with pain processing. Interleukin-1β (IL-1β) alters Central Amygdala (CeA) excitability by reducing glycinergic inhibition in a mechanism that involves the auxiliary β-subunit of GlyR (βGlyR), which is highly expressed in this region. However, GlyR activity and its modulation by IL-1β in supraspinal brain regions under neuropathic pain have not been studied. We performed chronic constriction injury (CCI) of the sciatic nerve in male Sprague Dawley rats, a procedure that induces hind paw plantar hyperalgesia and neuropathic pain. Ten days later, the rats were euthanized, and their brains were sliced. Glycinergic spontaneous inhibitory currents (sIPSCs) were recorded in the CeA slices. The sIPSCs from CeA neurons of CCI animals show a bimodal amplitude distribution, different from the normal distribution in Sham animals, with small and large amplitudes of similar decay constants. The perfusion of IL-1β (10 ng/mL) in these slices reduced the amplitudes within the first five minutes, with a pronounced effect on the largest amplitudes. Our data support a possible role for CeA GlyRs in pain processing and in the neuroimmune modulation of pain perception. © 2022 by the authors. Licensee MDPI, Basel, Switzerland.
Notas
Indexación: Scopus.
Palabras clave
CCI, Glycine receptors, Neuropathic pain, Spontaneous inhibitory currents
Citación
International Journal of Molecular Sciences, Volume 23, Issue 13, July-1 2022, Article number 7356
DOI
10.3390/ijms23137356