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At least 181 records · Page 10Linked to original sources
PubMed1998

Quinpirole induces compulsive checking behavior in rats: a potential animal model of obsessive-compulsive disorder (OCD).

Rats treated chronically with the dopamine agonist quinpirole (0.5 mg/kg, twice weekly x 10) met 5 criteria for performance of compulsive checking. Specifically, in a large open-field with single small objects in 4 of 25 locales, quinpirole rats revisited two places/objects excessively often and rapidly, compared with other locations in the environment or saline controls. They performed a ritual-like set of behavioral acts at these two places/objects and stopped in relatively few locales before returning to the preferred places/objects. Finally, they shifted their behavior to a new location when the object was moved there. Clomipramine (10 mg/kg, daily) postponed but did not prevent the development of the quinpirole effect. Quinpirole-induced compulsive checking may be an exaggeration of normal checking of home site in rats. Results suggest an animal model of obsessive-compulsive disorder and a role for dopamine in this disorder.

Animals↗
PubMed2000

TS+OCD-like neuropotentiated mice are supersensitive to seizure induction.

Seizures can be induced by systemic dopamine D1 receptor agonists or by cortical-limbic neurostimulation non-selectively. Seizures are also often associated with tics and compulsions, which likewise involve cortical-limbic hyperactivity. To determine if selective potentiation of cortical-limbic D1 receptor-expressing (D1+) neurons increases seizure susceptibility, we administered pentylenetetrazole (PTZ) to mice that express a neuropotentiating transgene only in a glutamatergic, cortical-limbic subset of D1+ neurons (D1CT-7 line). These mice exhibited increased PTZ-dependent seizure incidence, onset rate and intensity. Because D1CT-7 mice also exhibit tic+compulsion-like behaviors, this implies that glutamatergic hyperactivity induced by cortical-limbic D1+ neuropotentiation facilitates not only epilepsy but also tics and compulsions. This suggests a dopamine-regulated glutamatergic basis for all three states and may explain why they often co-exist in humans.

Animals↗
PubMed1996

A putative poststreptococcal case of OCD with chronic tic disorder, not otherwise specified.

A 12-year-old girl presented with an atypical, recurrent, increasingly treatment-resistant case of obsessive-compulsive disorder and chronic tic disorder associated with profound separation anxiety, learning difficulty, and intermittent upper respiratory symptoms. In addition to detailed reviews of history and findings from many clinical caretakers from the prior 7 years, current pediatric, psychiatric, neuropsychological, neuroimaging, and clinical laboratory data were also available. Treatment options were considered from multiple perspectives: psychoanalytically oriented psychotherapy, conventional pharmacotherapy, family interventions, cognitive-behavioral therapy, and learning-supportive strategies. Psychological, neuropsychiatric, and neuroimmunological formulations of etiology were considered. Subsequent treatments included supportive psychotherapy, neuroleptic augmentation of selective serotonin reuptake inhibitors, prophylactic penicillin, and a course of six sessions of plasmapheresis over a 2-week period. The case raises questions for ongoing consideration that juxtapose dynamic, neuropsychiatric, and neuroimmunological perspectives.

Antibiotic Prophylaxis↗