CEMO monthly seminar - Gustavo López-Córdoba

CEMO is delighted to announce the seminars of the department that will be given by PhD student and Postdoc.

The seminar is followed by a lunch (kindly provided by the department) in order to allow everybody to interact and promote collaboration between labs.

Agenda:

12:00 - "Pharmacological characterization of the spinal α2-adrenoceptors subtypes which modulates the nociception" - Gustavo López-Córdoba (Neuropharmacology group)

Abstract

The intrathecal administration of clonidine induces analgesia through the activation of spinal α2-adrenoceptors. These receptors are classified into three subtypes, α2A-, α2B- and α2C-adrenoceptors, without establishing the subtype or subtypes that could be mediating this antinociception. Through a behavioral and electrophysiological approach, the present study elucidated the pharmacological profile of the α2-adrenoceptor subtypes involved in clonidine-induced antinociception.

Male Wistar rats divided into two experimental groups were used. In the first experimental group, the antinociceptive effect of clonidine (0.1, 1, and 10 nmol/10 μl, intrathecal) and/or pretreatment with α2-antagonists was evaluated in a behavioral nociception model (1% formalin): (i) BRL 44408 (α2A- antagonist), (ii) imiloxan (α2B- antagonist) or (iii) JP-1302 (α2C- antagonist). In the second experimental group, unitary extracellular responses of wide dynamic range (WDR) neurons evoked by the stimulation of their peripheral receptive field (20 stimuli, 0.2 Hz, 1-msec duration, 0.1-3 mA) before and after spinal administration of clonidine (1-10 nmol/10 μL) and pretreatment with antagonist BRL 44408, or JP-1302.

The behavioral and neuronal nociception was inhibited by clonidine (0.1-10 nmol), this antinociception was only blocked by antagonist BRL 44408. In the case of behavioral nociception, intrathecal administration of JP-1302 inhibited nociception; this effect was blocked in animals pretreated with bicuculline (GABAA receptor antagonist).

This study suggests that clonidine exerts its antinociceptive effect through the activation of α2A-adrenoceptors. On the other hand, it is shown that blocking α2C-adrenoceptors exerts a behavioral antinociceptive effect, probably mediated by the participation of GABAergic mechanisms.

Gustavo López-Córdoba¹, Guadalupe Martínez-Lorenzana¹, Miguel Condés-Lara¹, Abimael González-Hernández¹.

¹Department of Developmental Neurobiology and Neurophysiology, Institute of Neurobiology, Universidad Nacional Autónoma of México, Campus UNAM Juriquilla, Querétaro, QRO, 76230, Mexico

12:45 - Q&A session

13:00 - Lunch