Input-dependent synaptic suppression by pregabalin in the central amygdala in male mice with inflammatory pain

Pregabalin (PGB) is a synthetic amino acid compound most widely prescribed for chronic peripheral and central neuropathic pain. PGB is a ligand for the α2δ1 subunit of voltage-dependent calcium channels, and its binding reduces neurotransmitter release and thus inhibits synaptic transmission. The ce...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Sumii Yamamoto, Yukari Takahashi, Fusao Kato
Formato:	article
Lenguaje:	EN
Publicado:	Elsevier 2021
Materias:	Pregabalin Central amygdala Latent inflammatory pain Formalin model Synaptic transmission Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571
Acceso en línea:	https://doaj.org/article/a42f59f715894d319de74b5616f5685c
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:a42f59f715894d319de74b5616f5685c
record_format	dspace
spelling	oai:doaj.org-article:a42f59f715894d319de74b5616f5685c2021-11-24T04:32:46ZInput-dependent synaptic suppression by pregabalin in the central amygdala in male mice with inflammatory pain2452-073X10.1016/j.ynpai.2021.100078https://doaj.org/article/a42f59f715894d319de74b5616f5685c2021-08-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S2452073X21000192https://doaj.org/toc/2452-073XPregabalin (PGB) is a synthetic amino acid compound most widely prescribed for chronic peripheral and central neuropathic pain. PGB is a ligand for the α2δ1 subunit of voltage-dependent calcium channels, and its binding reduces neurotransmitter release and thus inhibits synaptic transmission. The central nucleus of the amygdala (CeA) is a kernel site for the enhanced nociception-emotion link in chronic pain. The nociceptive information is conveyed to the CeA via the following two pathways: 1) the pathway arising from the basolateral amygdala (BLA), which carries nociceptive information mediated by the thalamocortical system, and 2) that arising from the external part of the pontine lateral parabrachial nucleus (LPB), that forms the final route of the spino-parabrachio-amygdaloid pathway that conveys nociceptive information directly from the superficial layer of the spinal dorsal horn. We compared the effects of PGB on the excitatory postsynaptic currents of neurons in the right CeA in response to electrical stimulation of BLA and LPB pathways using the whole-cell patch-clamp technique. Inflammatory pain was induced by intraplantar injection of formalin solution at the left hind paw.At eight hours post-formalin, PGB reduced EPSCs amplitude of the BLA-to-CeA synaptic transmission, accompanied by a significant increase in the PPR, suggesting a decreased release probability from the presynaptic terminals. In addition, these effects of PGB were only seen in inflammatory conditions. PGB did not affect the synaptic transmission at the LPB-to-CeA pathway, even in formalin-treated mice. These results suggest PGB improves not simply the aberrantly enhanced nociception but also various pain-associated cognitive and affective consequences in patients with chronic nociplastic pain.Sumii YamamotoYukari TakahashiFusao KatoElsevierarticlePregabalinCentral amygdalaLatent inflammatory painFormalin modelSynaptic transmissionNeurosciences. Biological psychiatry. NeuropsychiatryRC321-571ENNeurobiology of Pain, Vol 10, Iss , Pp 100078- (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Pregabalin Central amygdala Latent inflammatory pain Formalin model Synaptic transmission Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571
spellingShingle	Pregabalin Central amygdala Latent inflammatory pain Formalin model Synaptic transmission Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571 Sumii Yamamoto Yukari Takahashi Fusao Kato Input-dependent synaptic suppression by pregabalin in the central amygdala in male mice with inflammatory pain
description	Pregabalin (PGB) is a synthetic amino acid compound most widely prescribed for chronic peripheral and central neuropathic pain. PGB is a ligand for the α2δ1 subunit of voltage-dependent calcium channels, and its binding reduces neurotransmitter release and thus inhibits synaptic transmission. The central nucleus of the amygdala (CeA) is a kernel site for the enhanced nociception-emotion link in chronic pain. The nociceptive information is conveyed to the CeA via the following two pathways: 1) the pathway arising from the basolateral amygdala (BLA), which carries nociceptive information mediated by the thalamocortical system, and 2) that arising from the external part of the pontine lateral parabrachial nucleus (LPB), that forms the final route of the spino-parabrachio-amygdaloid pathway that conveys nociceptive information directly from the superficial layer of the spinal dorsal horn. We compared the effects of PGB on the excitatory postsynaptic currents of neurons in the right CeA in response to electrical stimulation of BLA and LPB pathways using the whole-cell patch-clamp technique. Inflammatory pain was induced by intraplantar injection of formalin solution at the left hind paw.At eight hours post-formalin, PGB reduced EPSCs amplitude of the BLA-to-CeA synaptic transmission, accompanied by a significant increase in the PPR, suggesting a decreased release probability from the presynaptic terminals. In addition, these effects of PGB were only seen in inflammatory conditions. PGB did not affect the synaptic transmission at the LPB-to-CeA pathway, even in formalin-treated mice. These results suggest PGB improves not simply the aberrantly enhanced nociception but also various pain-associated cognitive and affective consequences in patients with chronic nociplastic pain.
format	article
author	Sumii Yamamoto Yukari Takahashi Fusao Kato
author_facet	Sumii Yamamoto Yukari Takahashi Fusao Kato
author_sort	Sumii Yamamoto
title	Input-dependent synaptic suppression by pregabalin in the central amygdala in male mice with inflammatory pain
title_short	Input-dependent synaptic suppression by pregabalin in the central amygdala in male mice with inflammatory pain
title_full	Input-dependent synaptic suppression by pregabalin in the central amygdala in male mice with inflammatory pain
title_fullStr	Input-dependent synaptic suppression by pregabalin in the central amygdala in male mice with inflammatory pain
title_full_unstemmed	Input-dependent synaptic suppression by pregabalin in the central amygdala in male mice with inflammatory pain
title_sort	input-dependent synaptic suppression by pregabalin in the central amygdala in male mice with inflammatory pain
publisher	Elsevier
publishDate	2021
url	https://doaj.org/article/a42f59f715894d319de74b5616f5685c
work_keys_str_mv	AT sumiiyamamoto inputdependentsynapticsuppressionbypregabalininthecentralamygdalainmalemicewithinflammatorypain AT yukaritakahashi inputdependentsynapticsuppressionbypregabalininthecentralamygdalainmalemicewithinflammatorypain AT fusaokato inputdependentsynapticsuppressionbypregabalininthecentralamygdalainmalemicewithinflammatorypain
_version_	1718415994783793152

Input-dependent synaptic suppression by pregabalin in the central amygdala in male mice with inflammatory pain

Ejemplares similares