Olfactory function in an excitotoxic model for secondary neuronal degeneration: Role of dopaminergic interneurons. (19th November 2017)

• Record Type: Journal Article
• Authors: Marin, Concepció; Laxe, Sara; Langdon, Cristobal; Berenguer, Joan; Lehrer, Eduardo; Mariño-Sánchez, Franklin; Alobid, Isam; Bernabeu, Montserrat; Mullol, Joaquim
• Is Part Of: Neuroscience. Volume 364(2017)
• Page Start: 28
• Page End: 44
• Publication Date: 2017-11-19
• Subjects: ANOVA analysis of variance -- CCI controlled cortical impact -- DA dopamine -- FOV field of view -- FPI fluid percussion injury -- GABA gamma-aminobutyric acid -- GFAP Glial Fibrillary Acidic Protein -- MAP-2 microtubule-associated protein-2 -- MRI magnetic resonance imaging -- NeuN Neuronal Nuclear Antigen -- NMDA N-Methyl-D-Aspartate -- OB olfactory bulb -- OD optical density -- PBS phosphate-buffered saline -- PSA-NCAM polysialylated-neural cell adhesion molecule -- RAREVTR Relaxation Enhancement with Variable Repetition Time -- RMS rostral migratory stream -- SGZ subgranular zone -- SND secondary neuronal degeneration -- SVZ subventricular zone -- TBI traumatic brain injury -- TE echo times -- TH tyrosine hydroxylase -- TR repetition time; excitotoxicity -- traumatic brain injury -- olfaction -- secondary neuronal degeneration -- dopamine -- neurogenesis; Neurochemistry -- Periodicals; Neurophysiology -- Periodicals; Neurology -- Periodicals; Neurochimie -- Périodiques; Neurophysiologie -- Périodiques; Neurochemistry; Neurophysiology; Electronic journals; Periodicals; Electronic journals; 612.8
• DOI: 10.1016/j.neuroscience.2017.09.008
• Languages: English
• ISSNs: 0306-4522

Abstract

Highlights: Bilateral excitotoxic olfactory bulb (OB) lesions induce a decrease in the olfactory function. A partial spontaneous recovery of the olfactory function occurs after bilateral OB excitotoxic lesions. A lack of correlation exists between OB volumes and changes in olfactory function after OB excitotoxic lesions. A plasticity of the OB dopaminergic interneurons is relevant in the pathophysiology of recovery of loss of smell. Abstract: Secondary neuronal degeneration (SND) occurring in Traumatic brain injury (TBI) consists in downstream destructive events affecting cells that were not or only marginally affected by the initial wound, further increasing the effects of the primary injury. Glutamate excitotoxicity is hypothesized to play an important role in SND. TBI is a common cause of olfactory dysfunction that may be spontaneous and partially recovered. The role of the glutamate excitotoxicity in the TBI-induced olfactory dysfunction is still unknown. We investigated the effects of excitotoxicity induced by bilateral N-Methyl-D-Aspartate (NMDA) OB administration in the olfactory function, OB volumes, and subventricular zone (SVZ) and OB neurogenesis in rats. NMDA OB administration induced a decrease in the number of correct choices in the olfactory discrimination tests one week after lesions ( p < 0.01), and a spontaneous recovery of the olfactory deficit two weeks after lesions ( p < 0.05). A lack of correlation between OB volumes and olfactory function was observed. An increase in SVZ neurogenesis (Ki67+ cells, PSANCAM+ cells ( p < 0.01) associated with an increase in OB glomerular dopaminergic immunostaining ( p < 0.05) were related to olfactory function recovery. The present results show that changes in OB volumes cannot explain the recovery of the olfactory function and suggest a relevant role for dopaminergic OB interneurons in the pathophysiology of recovery of loss of smell in TBI.