Background: Three-dimensional (3D) motion analysis is established in investigating, human pathological motion. In the field of gait, its use results in the objective identification of primary, and secondary causes of deviations, many current interventions are the result of pre- and post-testing, and it was shown recently that it can result in decreased number of surgeries and overall cost of care. Consequently, recent attempts have implemented 3D motion analysis using rat models to study, parkinsonism.
View Article and Find Full Text PDFIntroduction: Prior research indicates methylphenidate (MPH) and alcohol (ethanol, EtOH) interact to significantly affect responses humans and mice. The present studies tested the hypothesis that MPH and EtOH interact to potentiate ethanol-related behaviors in mice.
Methods: We used several behavioral tasks including: drug discrimination in MPH-trained and EtOH-trained mice, conditioned place preference (CPP), rota-rod and the parallel rod apparatus.
We tested the hypothesis that the irreversible γ-amino butyric acid transaminase inhibitor, γ-vinyl γ-amino butyric acid [vigabatrin (VGB)], would reduce ethanol reinforcement and enhance the discriminative-stimulus effect of ethanol, effectively reducing ethanol intake. The present studies used adult C57BL/6J (B6) mice in well-established operant, two-bottle choice consumption, locomotor activity, and ethanol discrimination procedures to comprehensively examine the effects of VGB on ethanol-supported behaviors. VGB dose-dependently reduced operant responding for ethanol and ethanol consumption for long periods of time.
View Article and Find Full Text PDFMethylphenidate (MPH) therapy for attention-deficit/hyperactivity disorder is common in children and adults. Concerns regarding abuse of MPH prompted studies to better understand its pharmacology. We used an established drug discrimination task to determine whether MPH could be discriminated by C57BL/6J (B6) mice.
View Article and Find Full Text PDFGlial cell line-derived neurotrophic factor (GDNF) supports the viability of midbrain dopamine (DA) neurons that degenerate in Parkinson's disease. Middle-aged, 12 month old, Gdnf heterozygous (Gdnf(+/-)) mice have diminished spontaneous locomotor activity and enhanced synaptosomal DA uptake compared with wild type mice. In this study, dopamine transporter (DAT) function in middle-aged, 12 month old Gdnf(+/-) mice was more thoroughly investigated using in vivo electrochemistry.
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