PhD: Lucie Blaszczyk-Gerand

Study of thalamic microglial and astrocytic cells in a neuropathic pain model of rat

Defended on: June 25th, 2015

Neuropathic pain due to nervous lesion concerns 400 million people worldwide and there is no cure to definitively alleviate such pain. So it is necessary to discover new therapeutic targets. Over the last years, numerous studies suggest that glial cells, astrocytes and microglia, could play a crucial role in the development and maintenance of neuropathic pain. Surprisingly, very little attention has been devoted to supra-spinal structures. As thalamus is a key structure in the nociceptive integration pathway, my PhD thesis project aimed at characterising thalamic astrocyte and microglia through quantitative real-time PCR (qRT-PCR) and immunohistochemistry methods in a rat neuropathic pain model (L5-L6 spinal nerve ligation).

Unexpectedly, at a time when neuropathic pain symptoms are present, as attested by behavioural tests, I show an early (14 days post-ligation = D14) and transient (non observed 28 days post-ligation = D28) thalamic decreased number of immunopositive cells for each of the 4 markers commonly used to study glia: Iba-1 and CD11b/c for microglia and GFAP and S100β for astrocytes. At the same time (D14) and late stage (D28), in neuropathic pain animals, I show an increased mRNA expression of the chemokine fractalkine, it’s microglial receptor and the microglial enzyme which gives rise to the soluble fractalkine by using qRT-PCR approach on microdissected thalamic nucleus. These results are correlated with pain symptoms intensity. These three factors are well-known to be involved in a spinal amplification pathway of nociceptive information, their over-expression attesting microglial reactivity. Then, I show at D28 a thalamic increase of GFAP immunostained surface in neuropathic pain animals without change in the number of GFAP immunopositive astrocytes. This implies an astrocytic hypertrophy and so establishes a thalamic astrocytic reactivity.

So, this work reveals an ambivalence in thalamic glial alterations in this neuropathic pain model: an early decrease in glial markers expression followed by a later astrocytic reactivity concomitant with microglial signs of reactivity. Numerous experiments are needed to understand the impact of such glial thalamic ambivalence, never described in the neuropathic pain field.


An Eighteen-Month Helicobacter Infection Does Not Induce Amyloid Plaques or Neuroinflammation in Brains of Wild Type C57BL/6J Mice.Baudron CR, Chambonnier L, Buissionnière A, Giese A, Macrez N, Cho Y, Fénelon V, Blaszczyk L, Dubus P, Lehours P, Mégraud F, Salles N, Varon C.
J Alzheimers Dis. 2015 Feb 19. [Epub ahead of print]

Cancer pain is not necessarily correlated with spinal overexpression of reactive glia markers. Ducourneau VR, Dolique T, Hachem-Delaunay S, Miraucourt LS, Amadio A, Blaszczyk L, Jacquot F, Ly J, Devoize L, Oliet SH, Dallel R, Mothet JP, Nagy F, Fénelon VS, Voisin DL. Pain. 2014 Feb;155(2):275-91. doi: 10.1016/j.pain.2013.10.008. Epub 2013 Oct 11.


  • Président : Marc Landry (Professeur, Bordeaux)
  • Rapporteur : Sophie Pezet (Maître de conférences, Paris)
  • Rapporteur : Lénaïc Monconduit (Maître de conférences, Clermont-Ferrand)
  • Examinateur : Luis Garcia-Larrea (Directeur de recherche, Lyon)
  • Directrice de thèse : Valérie Fénelon (Professeur, Bordeaux)

PhD supervisor

Valérie Fénelon
Professeur Université de Bordeaux

Team : « Relations Glie-Neurone », INSERM U862 Neurocentre Magendie et Université de Bordeaux, « Physiopathologie de la plasticité neuronale »

Last update: 9 April 2018