International Journal of Molecular Sciences

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Dear Colleagues,

Various animal models have played a key role in neurological disorder research. These models aim to replicate various aspects of the disorders, including the genetic basis, histopathological lesions, and clinical symptoms. They provide us with improved comprehension of the etiopathogenesis of these disorders, with the end goal of mechanistically constructing therapeutics which can eventually lead to the modification and/or prevention of neurological disorders. Despite the vast amount of knowledge previously assimilated, researchers and the general public can still benefit from novel animal models that better recapitulate the human disease, in addition to updates concerning previously established animal models, as well as new insights regarding the molecular mechanisms underlying these disorders. This Special Issue intends to present new and interesting developments in the field. Articles offering innovative insights into the multifaceted pathophysiology of neurological disorders are welcome. This Special Issue may include, but is not limited to: original research articles focusing on differential gene expression analyses of genetic models, the development of new models, further characterization of established models, therapeutic studies utilizing animal models, and review articles which summarize and highlight recent advances in the field.

Prof. Dr. Changjong Moon
Guest Editor

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Keywords

neurological disorders
animal models
developmental models
genetic models
molecular mechanisms
genetic analysis
drug efficacy testing

Published Papers (1 paper)

Research

12 pages, 2744 KiB

Open AccessArticle

Effects of Intracerebral Aminophylline Dosing on Catalepsy and Gait in an Animal Model of Parkinson’s Disease

by Érica de Moraes Santos Corrêa, Gustavo Christofoletti and Albert Schiaveto de Souza

Int. J. Mol. Sci. 2024, 25(10), 5191; https://doi.org/10.3390/ijms25105191 - 10 May 2024

Viewed by 202

Abstract

Parkinson’s disease (PD) is a progressive disorder characterized by the apoptosis of dopaminergic neurons in the basal ganglia. This study explored the potential effects of aminophylline, a non-selective adenosine A₁ and A_2A receptor antagonist, on catalepsy and gait in a haloperidol-induced PD model. Sixty adult male Swiss mice were surgically implanted with guide cannulas that targeted the basal ganglia. After seven days, the mice received intraperitoneal injections of either haloperidol (experimental group, PD-induced model) or saline solution (control group, non-PD-induced model), followed by intracerebral infusions of aminophylline. The assessments included catalepsy testing on the bar and gait analysis using the Open Field Maze. A two-way repeated-measures analysis of variance (ANOVA), followed by Tukey’s post hoc tests, was employed to evaluate the impact of groups (experimental × control), aminophylline (60 nM × 120 nM × saline/placebo), and interactions. Significance was set at 5%. The results revealed that the systemic administration of haloperidol in the experimental group increased catalepsy and dysfunction of gait that paralleled the observations in PD. Co-treatment with aminophylline at 60 nM and 120 nM reversed catalepsy in the experimental group but did not restore the normal gait pattern of the animals. In the non-PD induced group, which did not present any signs of catalepsy or motor dysfunctions, the intracerebral dose of aminophylline did not exert any interference on reaction time for catalepsy but increased walking distance in the Open Field Maze. Considering the results, this study highlights important adenosine interactions in the basal ganglia of animals with and without signs comparable to those of PD. These findings offer valuable insights into the neurobiology of PD and emphasize the importance of exploring novel therapeutic strategies to improve patient’s catalepsy and gait. Full article

(This article belongs to the Special Issue Modeling Neurological Disorders in Experimental Animals: New Insights and Emerging Roles 4.0)

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Modeling Neurological Disorders in Experimental Animals: New Insights and Emerging Roles 4.0

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