Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Circling behavior is one of the best understood behaviors in animals. It is, for the most part, dopaminergically mediated and related to asymmetry in dopaminergic activity between the left and right basal ganglia or left and right frontal cortex. As a rule, animals rotate toward the hemisphere with lower striatal dopaminergic activity. A direct technique to find human analogs of circling behavior was not available. We have developed an automated rotometer with which we can apply the circling rodent model to humans. Left-prone circling behavior (neglect of right-sided turning) was found in 10 unmedicated schizophrenic patients, whereas 85 normal controls demonstrated almost equal right and left turning. These preliminary results may suggest the presence of a dopaminergic asymmetry in some unmedicated schizophrenic patients; that is, right anterior subcortical or cortical structures of the brain may manifest a relative dopaminergic overactivity compared to left anterior structures in at least some unmedicated patients with schizophrenia.
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PMID:Asymmetric rotational (circling) behavior, a dopamine-related asymmetry: preliminary findings in unmedicated and never-medicated schizophrenic patients. 360 40

Phospholipase A2 (PLA2) is a key enzyme in the phospholipid metabolism. In the CNS intracellular PLA2 plays an essential role in signal transduction by affecting both dopamine (DA) release and DA-receptor sensitivity. In schizophrenia a disordered phospholipid metabolism and increased activity of PLA2 have been reported. In this study we investigated the effects of intracerebral PLA2 injections on dopaminergic neurotransmission in rats using Ungerstedt's model of rotational behavior. Circling behavior induced by the DA agonist apomorphine after unilateral PLA2 injections into the substantia nigra pars compacta was recorded. Seven and 21 days after intranigral PLA2 injection, apomorphine induced an ipsilateral rotation indicating a long-lasting inhibition of ipsilateral nigrostriatal dopaminergic pathway by PLA2 application. In schizophrenia a reduced dopaminergic activity in the frontal cortex has been hypothesized. Recent spectroscopy studies reported on an accelerated break-down of membrane phospholipids in the frontal cortex from schizophrenics. The present findings suggest that increased PLA2 activity in schizophrenia could accelerate the breakdown of membrane phospholipids and thus contribute to a hypodopaminergy in the frontal cortex of schizophrenic patients.
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PMID:Intracerebral injection of phospholipase A2 inhibits dopamine-mediated behavior in rats: possible implications for schizophrenia. 877 14

Circling or rotational behavior is the most studied indicator of cerebral asymmetry in the rat. In humans, disturbances in cerebral asymmetry are involved in the etiology of several psychiatric disorders, including schizophrenia, Tourette syndrome and attention-deficit hyperactivity disorder. Abnormal rotational behavior in rodents is indicative of either an imbalance of forebrain dopamine systems, particularly an imbalance of nigrostriatal function, or an inner ear disease affecting the vestibular (balance) system. Abnormally enhanced circling behavior has been described in several mutant rat and mouse strains both with and without defects of the vestibular system. However, the relationship between vestibular defects and lateralized circling in rodents is only incompletely understood. In this review, we describe and discuss various spontaneous mutations associated with abnormal circling behavior in different rat strains and their potential relevance to model specific brain dysfunctions. The circling rat mutants described in this review illustrate how genetic animal models may serve to study multifaceted brain functions and dysfunctions, including disorders of the basal ganglia and vestibular system.
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PMID:Abnormal circling behavior in rat mutants and its relevance to model specific brain dysfunctions. 1960 57