AI Article Synopsis
- Chronic administration of haloperidol to male Sprague Dawley rats causes oral dyskinesias, which serve as a model for studying tardive dyskinesia in humans.
- Co-administration of the GABA agonist tiagabine significantly reduces the severity of these dyskinesias by inhibiting vacuous chewing movements.
- The findings suggest that using GABA-mimetics like tiagabine alongside haloperidol could offer potential strategies for treating and preventing tardive dyskinesia in human patients.
Article Abstract
Chronic administration of haloperidol to male Sprague Dawley rats for 6 months at a dosage of 1.5 mg/kg/day produces oral dyskinesias in a significant percent of the treated group. This has been used as an animal model of tardive dyskinesia in several laboratories, because the rat movements display characteristics reminiscent of the human dyskinetic condition. Previously, we have reported a reduction in these haloperidol-induced oral dyskinesias with the coadministration of a direct acting GABA agonist progabide. Here, we have tested an indirect acting GABA agonist, tiagabine, coadministered with haloperidol, for its effect on the oral dyskinesias. At a dosage of 75 mg/kg/day tiagabine significantly inhibited the onset of vacuous chewing movements (VCMs), decreasing the average movement severity from 11.2 +/- 2.0 to 4.4 +/- 1.4, compared with a placebo rate of 1.3 +/- 0.5 (VCMs/5 min). These data support the proposition that an effective, potent GABAmimetic coadministered with haloperidol, will block the onset of rat oral dyskinesias. This conclusion has important implications for the treatment and prevention of tardive dyskinesia in humans.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1007/BF01283031 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Functional Neuroanatomy of Tics: A Brain Network Perspective.
Psychiatr Clin North Am
March 2025
Department of Neurology, Washington University School of Medicine, 4444 Forest Park Avenue, Campus Box 8514, St. Louis, MO 63108, USA.
Tourette syndrome is defined by motor and vocal tics, yet our understanding of the pathophysiology of tics remains limited. Functional MRI (fMRI) can localize brain function related to the clinical phenomenology of tics. Here, we review extant fMRI studies examining brain activity during the premonitory urge, tic release, and tic suppression.
View Article and Find Full Text PDFThe Role of CBGTC Synaptic Neurotransmission in the Pathophysiology of Tics.
Psychiatr Clin North Am
March 2025
Department of Neurology, Johns Hopkins University School of Medicine, Kennedy Krieger Institute, Baltimore, MD, USA.
The pathophysiology of tic disorders involves an alteration in the transmission of messages through the cortico-basal ganglia-thalamo-cortical circuit. A major requirement for the passage of a message through this circuit is an intact chemically mediated synaptic neurotransmitter system (ie, neurotransmitters and second messengers). This article reviews the scientific evidence supporting the involvement of a variety of neurotransmitters (ie, dopamine, glutamate, gamma-aminobutyric acid, serotonin, acetylcholine, and the opioid system).
View Article and Find Full Text PDFWhen It's Not Tics: Functional Tic-Like Behaviors.
Psychiatr Clin North Am
March 2025
Kennedy Krieger Institute, Department of Child Psychiatry, 707 North Broadway, Baltimore, MD 21205, USA; Johns Hopkins School of Medicine, Department of Child and Adolescent Psychiatry, 600 North Wolfe Street, Baltimore, MD 21205, USA.
Functional tic-like behaviors (FTLBs) are a manifestation of functional neurologic disorder that can be mistaken for neurodevelopmental tic disorders like Tourette syndrome. Much information was gained about FTLBs because of an outbreak of FTLBs spreading among adolescents and young adults via social media during the coronavirus disease 2019 pandemic. In comparison to neurodevelopmental tic disorders, FTLBs have an older age of onset, more abrupt symptom onset, and more complex tics as well as other features that would be atypical of Tourette syndrome.
View Article and Find Full Text PDFThe Pathophysiology of Tics: An Anatomic Review.
Psychiatr Clin North Am
March 2025
Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA; Kennedy Krieger Institute, Baltimore, MD, USA.
The underlying pathophysiology of tics in Tourette syndrome is a topic of major scientific interest. To date, there is an absence of consensus among researchers regarding the precise anatomic location responsible for tics. The goal of this article is to review the current understanding of these brain circuits and data supporting specific anatomic regions.
View Article and Find Full Text PDFCARP VIII antibody-related autoimmune cerebellar ataxia in a child after infection: a case report.
Front Immunol
January 2025
First Department of Pediatrics, Weifang People's Hospital Affiliated to Shandong Second Medical University, Weifang, China.
Autoimmune cerebellar ataxia (ACA) is a cerebellar syndrome induced by autoimmune reactions and its onset is induced by malignant tumors, prodromic infection, and gluten allergy. Its clinical symptoms include gait disorder, limb ataxia, dysarthria, and dysphagia. According to , the diagnosis of ACA is based on the following points: 1.
View Article and Find Full Text PDFWant 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!