We have examined the adaptive modifications of brain monoamine receptors in response to pathophysiological processes in animal disease models: 6-OHDA lesioned and spontaneously hypertensive rats (SHR). The two models share a similar increase in D-1 receptor densities, while noradrenergic receptors are affected in different way: alpha-1 and beta are supersensitive in 6-OHDA lesioned rats and only alpha-2 are increased in SHR. S-1 receptors too are up-regulated in SHR. We must notice that though receptor hypersensitivity in the 6-OHDA model is linked to massive decreases in neurotransmitter levels, this mechanism seems not to exist in the SHR model.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.3109/10799898809048980 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Drug Development.
Alzheimers Dement
December 2024
National Institute on Aging, NIH, Baltimore, MD, USA.
Background: Epidemiological studies report an elevated risk of neurodegenerative disorders, particularly Parkinson's disease (PD), in patients with type 2 diabetes mellitus (T2DM) that is mitigated in those prescribed incretin mimetics or dipeptidyl peptidase 4 inhibitors (DPP-4Is). Incretin mimetic repurposing appears promising in human PD and Alzheimer's disease (AD) clinical trials. DPP-4Is are yet to be evaluated in PD or AD human studies.
View Article and Find Full Text PDFSystemically circulating 17β-estradiol enhances the neuroprotective effect of the smoking cessation drug cytisine in female parkinsonian mice.
NPJ Parkinsons Dis
January 2025
Department of Neuroscience & Experimental Therapeutics, Texas A&M University College of Medicine, 8447 John Sharp Pkwy, Bryan, TX, 77807-3260, USA.
The smoking cessation drug cytisine exerts neuroprotection in substantia nigra pars compacta (SNc) dopaminergic (DA) neurons of female but not male 6-hydroxydopamine (6-OHDA) lesioned parkinsonian mice. To address the important question of whether circulating 17β-estradiol mediates this effect, we employ two mouse models aimed at depleting systemically circulating 17β-estradiol: (i) bilateral ovariectomy (OVX), and (ii) aromatase inhibition with systemically administered letrozole. In both models, depleting systemically circulating 17β-estradiol in female 6-OHDA lesioned parkinsonian mice results in the loss of cytisine-mediated neuroprotection as measured using apomorphine-induced contralateral rotations and SNc DA neurodegeneration.
View Article and Find Full Text PDFPramipexole decreases allodynia and hyperalgesia via NF-κB in astrocytes in rats with Parkinson's disease.
Pharmacol Biochem Behav
December 2024
Departamento de Neurobiología del Desarrollo y Neurofisiología, Instituto de Neurobiología, Universidad Nacional Autónoma de México, Campus Juriquilla, Boulevard Juriquilla, No. 3001, C.P. 76230, Querétaro, Mexico.
Pain is one of the principal non-motor symptoms of Parkinson's disease (PD), negatively impacting the patient's quality of life. This study aimed to demonstrate whether an effective dose of pramipexole (PPX) can modulate the NF-κB/p-p65 activation in glial cells (astrocytes and microglia) and diminish the hypersensitivity (allodynia and hyperalgesia) in male Wistar rats with PD. For this, 2 μl of 6-hydroxydopamine (6-OHDA, 8 μg/μL/0.
View Article and Find Full Text PDFThe effects of chemogenetic targeting of serotonin-projecting pathways on L-DOPA-induced dyskinesia and psychosis in a bilateral rat model of Parkinson's disease.
Front Neural Circuits
December 2024
Department of Psychology, Binghamton University, Binghamton, NY, United States.
Introduction: Parkinson's disease (PD) is commonly characterized by severe dopamine (DA) depletion within the substantia nigra (SN) leading to a myriad of motor and non-motor symptoms. One underappreciated and prevalent non-motor symptom, Parkinson's disease-associated psychosis (PDAP), significantly erodes patient and caregiver quality of life yet remains vastly understudied. While the gold standard pharmacotherapy for motor symptoms Levodopa (LD) is initially highly effective, it can lead to motor fluctuations like LD-induced dyskinesia (LID) and non-motor fluctuations such as intermittent PDAP.
View Article and Find Full Text PDFEAAT2 Activation Regulates Glutamate Excitotoxicity and Reduces Impulsivity in a Rodent Model of Parkinson's Disease.
Mol Neurobiol
December 2024
Department of Microbiology and Immunology, Drexel University College of Medicine, Philadelphia, PA, 19129, USA.
Article Synopsis
- - Parkinson's disease involves the loss of dopamine-producing neurons, leading to disrupted brain circuitry that negatively impacts both cognitive function and decision-making behavior due to elevated glutamate levels.
- - The study investigates GTS467, a drug that activates an important transporter responsible for clearing excess glutamate, hypothesizing it could mitigate cognitive deficits without increasing impulsivity in PD patients.
- - Chronic treatment with GTS467 in rat models showed improved task performance and reduced impulsive actions, alongside beneficial changes in glutamate levels and gene expression related to brain health, supporting its potential as a therapeutic option for PD.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!