Title:Multiple Intranigral Unilateral LPS Infusion Protocol Generates a Persistent Cognitive Impairment without Cumulative Dopaminergic Impairment
VOLUME: 12 ISSUE: 7
Author(s):Ana Marcia Delattre, Bruno Carabelli, Marco Aurélio Mori, Claudia Pudell, Danielle R.B.L. da Silva, Isabela Menezes, Paula R.G. Kempe, Pedro Vinícius Staziaki, Patrícia A. Dombrowski, Claudio da Cunha, Marcelo M.S. Lima and Anete C. Ferraz
Affiliation:Universidade Federal do Paraná, Setor de Ciências Biológicas, Departamento de Fisiologia, Av. Francisco H. dos Santos s/n, ZIP: 81.531 – 990, Caixa Postal: 19031, Curitiba, Paraná, Brazil.
Keywords:Parkinson’s disease, lipopolysaccharide, cognitive impairment, novel-object recognition test.
Abstract:Inflammation in Parkinson’s disease (PD) is a continuous process and might be implicated in the progression of
neuronal degeneration. Taking this into account, we proposed a new protocol with multiple and consecutive intranigral
lipopolysaccharide (LPS) administration in order to analyze its effects on cognitive behavior. Additionally, striatal
concentrations of the neurotransmitters dopamine (DA) and serotonin and their respective metabolites were assessed in
three different time-points with the purpose of identifying the consecutive and cumulative effects of LPS infusions. We
demonstrated that with a minimum administered dose there was stabilization of neuronal damage as revealed by absence
of synergic effect on DA concentration. Although the DA decrease (–43%) generates an animal model of early phase of
PD, without apparent motor impairment, the LPS group exhibited deficit in episodic-like memory behavior from the first
time-point until the last one, indicating persisted disturbances in memory-recognition responses. These findings provide
evidence that multiple intranigral LPS infusions are not sufficient to cause cumulative and progressive damage to
dopaminergic neurons, but confirm that the LPS model can be adopted as a useful tool providing insight about the
cognitive impairment observed in pre-motor phase of PD.
