Neuropathic Pain Induces Interleukin-1 beta Sensitive Bimodal Glycinergic Activity in the Central Amygdala

Oliva, Carolina A; Stehberg, Jimmy; Barra, Rafael; Mariqueo, Trinidad

Abstract

Neuropathic pain reduces GABA and glycine receptor (GlyR)-mediated activity in spinal and supraspinal regions associated with pain processing. Interleukin-1 beta (IL-1 beta) alters Central Amygdala (CeA) excitability by reducing glycinergic inhibition in a mechanism that involves the auxiliary beta-subunit of GlyR (beta GlyR), which is highly expressed in this region. However, GlyR activity and its modulation by IL-1 beta 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-1 beta (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.

Más información

Título según WOS: ID WOS:000824090300001 Not found in local WOS DB
Título de la Revista: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volumen: 23
Número: 13
Editorial: MDPI
Fecha de publicación: 2022
DOI:

10.3390/ijms23137356

Notas: ISI