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)

Hyponatremia occurs often in mental illness. The frequency was not noticed because of the uncharacteristic symptoms of mild hyponatremia. Of the 1,114 psychiatric inpatients retrospectively surveyed, 10.5% had hyponatremia. Not only patients with schizophrenia, but also patients with other mental illness, especially with epilepsy, having hyponatremia were confirmed. An early onset, a long duration of psychiatric disorder and a prolonged admission were statistically significant factors. Nicotine abuse was not a significant factor. It was suggested that the pathogenesis of hyponatremia in psychiatric patients might be involved in a chronic course of psychiatric disorders and poor response to psychopharmacotherapy.
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PMID:An epidemiological study on hyponatremia in psychiatric patients in mental hospitals in Nara Prefecture. 130 13

Diminished gating of the P50 auditory evoked response to repeated stimuli is a psychophysiological feature of schizophrenia, that is also present in many relatives of patients. Animal models of auditory sensory gating indicate that nicotinic cholinergic neurotransmission is a critical neuronal substrate. The aim of this experiment was to determine if the deficit in sensory gating could be reversed by nicotine administration. Nonsmoking relatives of schizophrenics with abnormal sensory gating were selected as subjects for this initial double-blind trial, to avoid effects of psychotropic medications that might complicate trials in schizophrenic patients themselves. Nicotine-containing gum increased P50 sensory gating to near normal levels within 30 min of administration. The effect was transient; the gating of P50 returned to baseline levels within 1 hr. There was no change observed after placebo administration. In one of the subjects, the anticholinesterase inhibitor physostigmine similarly normalized P50 gating. The results are consistent with the hypothesis that nicotinic cholinergic neurotransmission may mediate a familial psychophysiological deficit in schizophrenia.
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PMID:Normalization by nicotine of deficient auditory sensory gating in the relatives of schizophrenics. 145 Feb 87

Nicotine potentiates the catalepsy produced by haloperidol. Furthermore, nicotine as an adjunct to haloperidol produces a remarkable improvement in motor tics in Tourette's syndrome (TS) patients. The present experiments (1) compared the ability of nicotine to potentiate the catalepsy produced by haloperidol or the selective D1 dopamine receptor antagonist SCH 23390 and (2) examined the effects of various doses of nicotine (0.1, 0.2, or 0.3 mg/kg) on haloperidol-induced (0.1, 0.2, or 0.4 mg/kg) catalepsy and locomotor hypoactivity. In the first experiment, nicotine produced a five-fold increase in catalepsy following haloperidol but had no effect on the catalepsy produced by SCH 23390. In the second experiment, nicotine potentiated the cataleptic effects of both the 0.2 and 0.4 but not the 0.1 mg/kg dose of haloperidol. Haloperidol (0.1 and 0.4 mg/kg) also produced a dose-related decrease in locomotion that was significantly potentiated by nicotine (0.1 mg/kg). Nicotine alone did not produce catalepsy or any significant changes in locomotion. These results indicated that nicotine's potentiation of haloperidol-induced catalepsy is likely related to striatal D2 receptor mechanisms. Nicotine potentiated the locomotor effects of doses of haloperidol that were previously found to be subcataleptic, indicating that catalepsy testing may actually underestimate the behavioral interaction between haloperidol and nicotine. Nicotine may prove useful for treating neuroleptic responsive disorders such as TS, schizophrenia, and Huntington's disease.
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PMID:Nicotine potentiates the behavioral effects of haloperidol. 177 13

Nicotine was found to potentiate the catalepsy and reduced locomotion following the administration of haloperidol. The ability of various doses of nicotine (0.1, 0.2, or 0.3 mg/kg) to potentiate the catalepsy produced by haloperidol (0.1, 0.2 or 0.4 mg/kg) was investigated. Nicotine potentiated the cataleptic effects of both the 0.2 and 0.4 mg/kg doses of haloperidol, but had no effect following the lowest (0.1 mg/kg) dose of haloperidol. The nicotine potentiation of catalepsy produced by the highest dose of haloperidol was independent of the dose of nicotine used. Nicotine alone did not produce catalepsy. A second experiment evaluated the ability of nicotine to potentiate the decreases in spontaneous locomotor activity produced by haloperidol. Animals received nicotine (0.1 mg/kg) alone or in conjunction with haloperidol (0.1 or 0.4 mg/kg) and were tested in Digiscan Animal Monitors. Haloperidol produced a dose-related decrease in locomotion. Nicotine significantly potentiated the hypoactivity produced by both doses of haloperidol. These results indicated that: 1) nicotine produces a significant potentiation of both the catalepsy and locomotor decreases following haloperidol and 2) the Digiscam Animal Activity Monitors may provide a more sensitive assessment of the interaction between nicotine and haloperidol than the catalepsy bat test. These data suggest that adjunct treatment with nicotine may prove useful for treating neuroleptic responsive disorders such as Tourette Syndrome, schizophrenia and Huntington's disease.
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PMID:Nicotine potentiates haloperidol-induced catalepsy and locomotor hypoactivity. 187 Dec

Nicotine was found to markedly potentiate haloperidol-induced hypokinesia in rats. Nicotine alone was without effect. Subsequently, concurrent administration of 2 mg nicotine gum to 10 Tourette syndrome patients being treated with haloperidol produced a substantial decrease in tics and improvement of concentration and attention span. Nicotine gum alone was without effect. While 80% of children showed improvement with nicotine gum, 70% completely discontinued the gum because of side-effects, primarily involving nausea and bitter taste. Nicotine may prove useful for treating other neuroleptic responsive disorders, such as schizophrenia and Huntington's disease.
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PMID:Nicotine potentiates the effects of haloperidol in animals and in patients with Tourette syndrome. 273 Sep 49

The proceedings of the inaugural scientific meeting of the Society for Research on Nicotine and Tobacco (SRNT) are summarized. The primary objective of the meeting was to foster the exchange of information on the effects of nicotine and tobacco use, as well as factors which influence their use, drawing from biological, behavioral and social sciences. Much of this research can be viewed as a tale of "two" drugs--nicotine as a key to an important public health problem, and nicotine as a classical tool of physiological and pharmacological research. A historical overview of research on "both" drugs is provided first. Public policy alternatives for reducing the prevalence of tobacco use have been derived in part from basic and clinical research results and are briefly outlined. Evidence for genetic determinants on nicotine use and effects is presented using data from twin studies and from molecular genetic research with humans and animals. Consistent with this research, there is evidence of individual differences in pharmacokinetics and effects of nicotine, which could account for differences in smoking behavior and nicotine dependence. Finally, recent developments in the therapeutic uses of nicotine and novel nicotinic agonists with schizophrenia, Alzheimer's disease, Parkinson's disease, Tourette's syndrome and ulcerative colitis are presented. Overall, the research presented at the meeting demonstrated the vast diversity of areas of study involving nicotine and tobacco, as well as the rich opportunities for cross-communication among researchers from different disciplines.
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PMID:Society for Research on Nicotine and Tobacco. 882 21

Chronic nicotine (NIC) pretreatment has been shown to enhance NIC-induced locomotor stimulation, an effect that seems critically dependent on activation of brain dopamine (DA) systems. In the present study the effects of chronic, intermittent NIC treatment were examined in the rat to establish whether such behavioral sensitization is associated with specific, regional changes in brain dopaminergic activity. Male rats received daily injections in their home cage with either saline (SAL) or NIC (0.5 mg/kg, s.c.) for 12 days. Twenty-four hours later, the locomotor activity of the animals subjected to NIC challenge as well as the functional responsiveness of the mesolimbocortical dopaminergic system were assessed. To this end, microdialysis experiments were performed in awake animals, measuring extracellular concentrations of DA and its metabolites in the prefrontal cortex (PFC) and the nucleus accumbens (NAC). Extracellular single cell recordings from DA neurons in the ventral tegmental area (VTA) were also performed in anesthetized animals. NIC (0.5 mg/kg, s.c.) increased all measured parameters of locomotor activity, with the exception of rearing, in SAL-pretreated animals; these effects were substantially enhanced after pretreatment with NIC. Nicotine (0.5 mg/kg, s.c.) increased DA release in both the PFC and the NAC in SAL-treated animals. Nicotine pretreatment significantly enhanced this effect in the PFC, whereas it did not affect the response in the NAC. Low doses of intravenously administered NIC dose-dependently increased burst activity, starting at 12 micrograms/kg in the SAL pretreated animals and at 6 micrograms/kg in the NIC-pretreated animals, and also dose-dependently increased firing rate in SAL as well as NIC-pretreated animals, although starting at a higher dose level, i.e., 25 micrograms/kg. These results demonstrate that behavioral sensitization after chronic NIC treatment is accompanied by an enhanced dopamine release specifically within the PFC. This phenomenon may be highly significant for the dependence-producing effects of NIC, particularly in association with major psychiatric disorder, such as schizophrenia.
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PMID:Condition-independent sensitization of locomotor stimulation and mesocortical dopamine release following chronic nicotine treatment in the rat. 886 31

Latent inhibition (LI) is a phenomenon in which repeated non-reinforced exposure to a stimulus retards subsequent conditioning to that stimulus; it reflects a process whereby irrelevant stimuli become ignored, and has been the subject of study concerning attentional abnormalities in schizophrenia. Low doses of the indirect dopamine (DA) agonists, amphetamine and nicotine, disrupt LI in the rat. These drugs are believed to disrupt LI via DA release in the nucleus accumbens; LI in amphetamine- and nicotine-treated rats is reinstated by administration of the DA antagonist haloperidol. In human subjects, low doses of amphetamine abolish LI, and more recently haloperidol has been shown to potentiate LI. The present study investigated the effects of nicotine on LI in human subjects, and also attempted to replicate the abolition of LI by amphetamine. Nicotine failed to affect LI when administered either subcutaneously or by cigarette smoking. LI was, however, abolished in a group of subjects given 5 mg amphetamine 90 min before testing. Supplementary analyses of the data pooled from all three experiments showed that, in contrast to an earlier report, LI was no weaker in smokers than in nonsmokers.
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PMID:Effects of nicotine and amphetamine on latent inhibition in human subjects. 888 83

Nearly 90% of schizophrenics smoke cigarettes, considerably higher than the general population's rate of 25%. There is some indication that schizophrenics may smoke as a form of self-medication. Nicotine has a variety of pharmacologic effects that may both counteract some of the cognitive deficits of schizophrenia and counteract some of the adverse side effects of antipsychotic drugs. In the current study, we assessed the interactions of haloperidol and nicotine on cognitive performance of a group of schizophrenics. These patients were in a double-blind study, randomly assigning them to low, moderate, and high dose levels of haloperidol. The subjects, all smokers, came to the laboratory on four different mornings after overnight deprivation from cigarettes. In a double-blind fashion, they were administered placebo, low (7 mg/day), medium (14 mg/day), or high (21 mg/day) dose nicotine skin patches. Three hours after administration of the skin patch, the subjects were given a computerized cognitive test battery including: simple reaction time, complex reaction time (spatial rotation), delayed matching to sample, the Sternberg memory test, and the Conners continuous performance test (CPT). With the placebo nicotine patch, there was a haloperidol dose-related impairment in delayed matching to sample choice accuracy and an increase in response time on the complex reaction time task. Nicotine caused a dose-related reversal of the haloperidol-induced impairments in memory performance and complex reaction time. In the CPT, nicotine reduced the variability in response that is associated with attentional deficit. These results demonstrate the effects of nicotine in reversing some of the adverse side effects of haloperidol and improving cognitive performance in schizophrenia.
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PMID:Nicotine-haloperidol interactions and cognitive performance in schizophrenics. 891 15

Angiotensin (ANG)-containing axons, terminals, and receptors have been found in the hippocampus. When angiotensin II (ANG II) is administered to the dentate gyrus, long-term potentiation (LTP) induction, in response to medial perforant path stimulation, is inhibited and it can be blocked by losartan, an ANG II AT1 receptor antagonist. ANG II has been shown to mediate impairment of the retention of an inhibitory shock avoidance response and to be involved in ethanol and diazepam inhibition of dentate gyrus LTP, all of which can be blocked by losartan. Nicotine acetylcholine receptors are found in the hippocampus and nicotine is involved in the enhancement of complex and important psychological functions that are mediated by the hippocampus; therefore, the possibility that nicotine prevents the ANG II inhibition of dentate granule cell LTP was examined. Nicotine pretreatment reduced ANG II inhibition of LTP induction in a dose-dependent manner. Mecamylamine blocked the nicotine antagonism of ANG II-induced LTP inhibition and normal LTP occurred, whereas hexamethonium was ineffective in blocking these central effects of nicotine. Nicotine by itself did not affect normal LTP under these conditions. Nicotinic blocking of the ANG II inhibition of a frequency dependent type of synaptic plasticity provides a function for central nicotinic receptors and a possible mechanism of action a) to explain the enhancement of learning and memory by nicotine, b) an explanation for tobacco smoking while drinking alcohol, and c) a possible basis for the excessive use of tobacco in depression and schizophrenia that supports a possible therapeutic use of nicotine in some mental disorders.
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PMID:Nicotine blocks angiotensin II inhibition of LTP in the dentate gyrus. 895 46


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