Topic: 6-OHDA

Attention deficit/hyperactivity disorder (ADHD) is a common neurodevelopmental disorder in children and adults worldwide. It often coexists with anxiety, depression or alterations in sensitivity. Patients with ADHD report sensitization to pain and the prevalence of generalized pain is higher in ADHD patients (up to 80%) compared to control population (17%) (Stray LL et al., 2013). However, the mechanisms involved remain unknown. Neuroanatomical studies confirm that attentiveness and central mechanisms involved in pain transmission use identical neural networks (i.e., the anterior cingulate cor

Electroconvulsive therapy (ECT) is a well-established treatment for psychiatric disorders. Recent reports show that ECT improves motor deficits in Parkinson's disease (PD), while the mechanism of action remains unclear. To investigate the effects of ECT in PD, we produced partial dopaminergic depletion by unilateral striatal injection of 6-OHDA. After three weeks, behavioral testing was performed using the open field and corridor test. Animals with a lateralized phenotype were randomized into ECT or sham treatment. After a two-week treatment interval with daily ECT, behavioral testing was repe

1-Methyl-4-phenyl-pyridinium (MPP+) and 6-hydroxydopamine (6-OHDA) are the predominant neurotoxic agents used in the research of Parkinson's disease (PD). The mTORC2 is a significant signaling pathway whose specific functions and mechanisms remain partially elusive, especially in the context of PD-related oxidative stress. We aimed to determine the interconnection between mTORC2 and oxidative stress in MPP+ and 6-OHDA neurotoxic models of PD. All experiments were performed on the human neuroblastoma cell line, SH-SY5Y. Cells were divided into two groups: control (consists of control cells and

Parkinson's disease is a neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons, leading to a spectrum of motor and non-motor symptoms. While motor deficits serve as the primary criteria for diagnosis, emerging evidence suggests that non-motor symptoms may also significantly contribute to the disease's progression. In this study, our aim was to investigate the potential impact of IGF-1 on the progression of emotional-like behavioral deficits in a rat model of neurotoxicity induced by 6-OHDA infusion into the dorsolateral striatum. We evaluated behavioral chang

Aims: L-DOPA-induced dyskinesias (LID) cause disability in Parkinson’s disease patients undergoing L-DOPA treatment. It is known that maladaptive plastic changes in both pre-and post-synaptic components of striatal network contribute to LID. However, the possible role of perineuronal nets (PNN), a member of the tetrapartite synaptic unit, is still elusive. We aimed to investigate alterations in PNN structure mainly encapsulating parvalbumin positive interneurons (PV-IN) in a rat model of LID.Methods: 6-OHDA toxin-injected hemiparkinsonian, sham-operated, and naïve Wistar male rats received eit

Parkinson's disease (PD) is a complex neurodegenerative movement disorder. The central pathological feature of PD is the progressive loss of dopaminergic neurons in the substantia nigra pars compacta, that project to the dorsal striatum. The resulting dopamine deficiency in this area dysregulates the striatal neural net, causing the motor deficits of PD patients. However, the process leading dopamine's depletion into neural deficits and how it can reflect on cortical activity is still largely unknown. This project's goal is to investigate the electrophysiological and functional changes affecti

Parkinson's disease (PD) is the second most common neurodegenerative disease, manifested by the loss of dopaminergic neurons. It has been shown that oxidative stress and apoptosis play a major role in the pathology of PD. One of the most commonly used models for in vitro investigation of PD is the SH-SY5Y neuroblastoma cell line and application of hydroxydopamine (6-OHDA). The 6-OHDA exerts its cytotoxicity by generating reactive oxygen species (ROS) such as hydrogen peroxide, superoxide anion and hydroxyl-radical, leading to oxidative stress by disrupting the mitochondrial membrane integrity,

Parkinson’s disease (PD) is characterized by the loss of dopamine in the basal ganglia (BG), particularly in the striatum, leading to aberrant activity patterns in BG neuronal circuits. The external globus pallidus (GPe) is a central nucleus in the BG and plays a pivotal role in the function of the indirect pathway. two populations of GPe cells were described, the prototypic and arkypallidal neurons, which are distinct developmentally, anatomically and electrophysiologically. Additionally, they have been shown to be involved in sensory processing, mediated by different input pathways. How dopa

This research project investigates the role of lipid droplets (LDs) in neuronal survival and dysfunction, focussing on two human in vitro models of neurodegenerative diseases (NDs): neuroblastoma SH-SY5Y cell line exposed to 6-OHDA for Parkinson’s, and primary human fibroblasts from Alzheimer’s disease (AD) patients.Valid and reliable experimental tools for LDs detection and quantification were set up in SH-SY5Y. Confocal laser scanning microscopy was combined with image analysis, allowing an automatic and objective quantification of LDs in basal conditions, and in response to LDs modulation a