Characterization of pERK expression in amygdala and its role in nociceptive behavior

Abstract: Extracellular signal-regulated kinase (ERK), is a member of the mitogen-activated protein kinase (MAPK) family of serine/threonine protein kinases. Functioning as intracellular signaling molecules, they are responsible for multiple extracellular signals transduction into diverse intracellular responses through transcriptional and post-translational regulations. ERK is proposed to be a molecular substrate linked to several nociceptive-related processes such as central sensitization, corresponding to a drastical increase on synaptic effi-cacy of neurons involved in nociceptive-transmission, their threshold reduc-tion, pain signals enhancement, thus contributing to various chronic pain syndromes. Regulation of those pathways occurs primarily by MAPKs through central and peripheral mechanisms, whereby inhibition could provide significant anti-nociceptive effects. Although neurobiological mechanisms underlying pain pathways are extensively studied, many details remain un-clear. Herein, an immunohistochemical study was designed to investigate whether phosphorylated extracellular signal-regulated kinase (pERK) is found among neurons in nociceptive-related brain areas following mechanical noxious stimuli (pinch) applied to the tail and right hindpaw of three male Swiss-Webster B6 mice. Administration of ketamine was used for anesthetic pur-poses, while only one subject was viable for further experiments. Coronal sections were incubated on primary antibody rabbit anti-phospho-p44/42 ERK; 1:250, and immunostained using biotinylated donkey anti-rabbit sec-ondary antibody; 1:500. Confocal immunofluorescence microscopy revealed that phospho-ERK immunopositive cells were activated and expressed in integral amygdala regions of one brain sample, with higher intensity on the laterocapsular division of central amygdala. Accumulating evidences suggests pERK expression in amygdala to be responsible for pain modulation and emotional aspects. However, absence of control subjects leads to paucity of evidences, where no definitive conclusion can be drawn. Molecular mech-anisms of pain and modulation by the amygdala associated with pERK re-quire further elucidation.