Role of metabotropic glutamate receptor 1 in the basolateral amygdala-driven prefrontal cortical deactivation in inflammatory pain in the rat

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• 作者：Livio Luongo^a ; ¹ ; Vito de Novellis^a ; ¹ ; Luisa Gatta^a ; Enza Palazzo^a ; Daniela Vita^a ; Francesca Guida^a ; Catia Giordano^a ; Dario Siniscalco^a ; Ida Marabese^a ; Maria De Chiaro^a ; Serena Boccella^a ; Francesca Rossi^b ; Sabatino Maione^a ; ^{sabatino.maione@unina2.it}
• 关键词：mGluRs ; Prefrontal cortex ; Basolateral amygdala ; Inflammatory pain ; Rat
• 刊名：Neuropharmacology
• 出版年：2013
• 出版时间：March, 2013
• 年：2013
• 卷：66
• 期：Complete
• 页码：317-329
• 全文大小：1613 K

文摘

Plastic changes in the amygdala and limbic cortex networks have been widely shown in chronic pain. We have here investigated the role of group I metabotropic glutamate receptors (mGluRs) in the basolateral amygdala (BLA) pre-infra-limbic (PL-IL) divisions of the medial prefrontal cortex (mPFC) neuron connections after carrageenan-induced inflammatory pain in the rat. Intra-plantar injection of carrageenan decreased either spontaneous or mechanically/electrically evoked activity of PL cortex pyramidal neurons which responded with excitation in a way prevented by CPCOOEt, a selective mGluR1 antagonist, though not by MPEP, a selective mGluR5 antagonist. Accordingly, intra-BLA microinjection of DHPG, a group I mGluR agonist, caused PL cortex neuron activity depression, antagonized by CPCCOEt. CPCOOEt, but not MPEP, reduced also carrageenan-induced mechanical allodynia. The PL cortex cell deactivation in inflammatory pain condition was associated with increased GABA (conversely glutamate was decreased) in the PL/IL cortex. The local application of bicuculline, a GABA_A receptor selective antagonist, reduced mechanical allodynia. An over-expression of mGluR1, but not mGluR5, have been observed in the PL-IL cortex after inflammatory pain suggesting an increased mGluR1-dependent cross-talk among BLA and IL-PL cortex neurons in inflammatory pain conditions.

This article is part of a Special Issue entitled ¡®Metabotropic Glutamate Receptors¡¯.