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At least 1,009 records · Page 56Linked to original sources
PubMed1984

Methylphenidate, apomorphine, THIP, and diazepam in monkeys: dopamine-GABA behavior related to psychoses and tardive dyskinesia.

In eight monkeys (Cercopithecus aethiops), previously treated with haloperidol for 4-14 months, we have examined the behavioral effect of: (1) methylphenidate vs apomorphine; (2) 4,5,6,7-tetrahydroisoxazolo-(5,4-c)-pyridin-3-ol(THIP, a GABA agonist) vs diazepam; and (3) THIP and diazepam in methylphenidate-induced behavior. Methylphenidate (0.5-5.0 mg/kg) and apomorphine (0.1-0.5 mg/kg) both increased locomotion, but otherwise exhibited different behavioral profiles. Methylphenidate induced repetitive movements of head, limbs, and trunk, and hallucinatory-like behavior, but not oral hyperkinesia (licking and gnawing), whereas apomorphine preferentially caused oral hyperkinesia. THIP produced a syndrome of bradykinesia, dystonia, ataxia, myoclonus, sedation, and decreased responsiveness, whereas diazepam produced only bradykinesia, ataxia, sedation, and decreased responsiveness, but not dystonia and myoclonus. Methylphenidate-induced locomotion and repetitive movements were reduced by THIP and diazepam, whereas hallucinatory-like behavior was markedly aggravated by THIP, but not by diazepam.

Animals↗
PubMed1991

A cerebral computed tomography study of patients with drug-induced psychoses.

Twelve male patients with chronic drug consumption including cannabis (ICD = 304.3) and morphine (ICD = 304.7), who required inpatient treatment for drug-induced paranoid hallucinatory states (ICD = 292.1) were investigated using computed tomography for macroscopic structural changes in the brain. The findings were compared with those in a control group of schizophrenic patients who did not consume drugs. The brain scans were measured and not show any significant morphological differences between the two groups.

Adolescent↗
PubMed1999

GABA-ergic neurons and the neurobiology of schizophrenia and other psychoses.

There are a number of disorders in the Diagnostic and Statistical Manual of Mental Disorders (DSM IV) that are characterised by having psychotic symptoms as the defining feature [17]. The narrowest definition of psychosis is restricted to delusions or prominent hallucinations, with the hallucinations occurring in the absence of insight into their pathological nature. Schizophrenia is the most prevalent form of psychosis, but this may also occur due to other medical conditions (e.g., Prader-Willi syndrome, epilepsy), in the early post-partum period, at menopause, and as a result of drug use. This article attempts to draw together an underlying causation across the various forms of psychotic disorder and, by integrating this with what is known about the genetics, neuroanatomy and neuropharmacology of the positive symptoms in schizophrenia, produce a broader understanding. At the cellular level, gamma-aminobutyric acid (GABA)-ergic interneurons are a common feature in psychotic states, and are a principal focus for serotonin and dopamine innervations, as well as playing an important role in cortical development. At the systems level, prefrontal and medial temporal cortices are implicated with activity levels out of synchrony in schizophrenics. How these vast areas of disparately functioning cortical networks are "bound" together to provide coherent conscious experiences is again a function of GABA-ergic interneurons. These interneurons have highly divergent inhibitory projections to large numbers of pyramidal neurons and are themselves synchronised by the ascending dopamine and serotonin innervations.

Animals↗