• Renato Leonardo de Freitas, Priscila Medeiros, Juliana Almeida da Silva, Rithiele Cristina de Oliveira, Ricardo de Oliveira, Farhad Ullah, Asmat Ullah Khan, and Norberto Cysne Coimbra.
• Laboratory of Neuroanatomy and Neuropsychobiology, Department of Pharmacology, Ribeirão Preto Medical School of the University of São Paulo (FMRP-USP), Av. Bandeirantes, 3900, Ribeirão Preto, 14049-900 São Paulo, Brazil; Multiuser Centre of Neuroelectrophysiology, Department of Anatomy and Surgery, Ribeirão Preto Medical School of the University of São Paulo (FMRP-USP), Av. Bandeirantes, 3900, Ribeirão Preto, 14049-900 São Paulo, Brazil; Laboratory of Pain and Emotions, Department of Anatomy and Surgery, Ribeirão Preto Medical School of the University of São Paulo (FMRP-USP), Av. Bandeirantes, 3900, Ribeirão Preto, 14049-900 São Paulo, Brazil; Behavioural Neurosciences Institute (INeC), Avenida do Café, 2450, Ribeirão Preto, 14220-030 São Paulo, Brazil.
• Neuroscience. 2016 Nov 12; 336: 133-145.

AbstractIt has been proposed that the post-ictal state is associated with the expression of hypoalgesia. It is clear that the projections among the periaqueductal gray matter (PAG), dorsal raphe nucleus (DRN) and locus coeruleus (LC) play a role in pain management. These mesencephalic structures have direct reciprocal opioid and monoaminergic projections to the LC that can possibly modulate post-ictal hypoalgesia. The goal of this study was to examine if LC-opioid and serotonergic/noradrenergic mechanisms signal the post-ictal hypoalgesic responses to tonic-clonic seizures produced by intraperitoneal administration of pentylenetetrazole (PTZ at 64mg/kg), causing an ionophore γ-aminobutyric acid (GABA)-mediated Cl-influx antagonism. The rodents' nociceptive threshold was measured by the tail-flick test. Intra-LC cobalt chloride (1.0nM/0.2μL) microinjections produced intermittent local synaptic inhibition and were able to reduce post-ictal hypoalgesia. Central administration of naltrexone (a non-selective antagonist for opioid receptors), naloxonazine (a selective antagonist for μ1-opioid-receptors), methysergide (a non-selective antagonist for serotonergic receptors) or ketanserin (an antagonist for both α1-noradrenergic and 5-Hydroxytryptamine(HT)2A/2Creceptors) at 5.0μg/0.2μL, R-96544 (a 5-HT2Areceptor selective antagonist) at 10nM/0.2μL, or RS-102221 (a 5-HT2Creceptor selective antagonist) at 0.15μg/0.2μL into the LC also decreased post-ictal hypoalgesia. The data presented here suggest that the post-ictal antinociception mechanism involves the μ1-opiod, 5-HT2A- and 5-HT2C-serotonergic, and α1-noradrenergic receptors in the LC.Copyright © 2016 IBRO. Published by Elsevier Ltd. All rights reserved.

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