Elevated neuronal nitric oxide synthase expression in chronic haloperidol-treated rats

Lau, Yuen-Sum; Petroske, Elizabeth; Meredith, Gloria E.; Wang, John Q.

doi:10.1016/s0028-3908(03)00314-9

Cited by 33 publications

(23 citation statements)

References 43 publications

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“…As all of our patients have been treated with typical antipsychotics, we can thus not exclude the possibility of drug-induced neuronal abnormalities, especially when methodological problems comparing animal studies with human data are taken into account. Most interestingly, a recent study demonstrated that haloperidol-induced tardive dyskinesia was associated with decreased NOS activity in an animal model, yet enzyme expression or neuronal morphology have not been assessed [20][21][22] . Thus, if the reduction of NOS-positive neurons is due to treatment with typical neuroleptics and not connected to schizophrenia per se, it might however contribute to the pathophysiology of extrapyramidal side effects.…”

Section: Discussionmentioning

confidence: 99%

Morphological Abnormalities in Nitric-Oxide-Synthase-Positive Striatal Interneurons of Schizophrenic Patients

Lauer¹,

Johannes²,

Fritzen³

et al. 2005

Neuropsychobiology

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Schizophrenia has been suggested to be a neurodevelopmental disorder, and nitric-oxide-synthase (NOS)-positive neurons were shown to be involved in distorted cortical development in schizophrenia. Here we investigated whether nitrinergic neurons in the striatum of schizophrenic patients also display abnormalities regarding distribution or morphology. To do so, postmortem putaminal sections of schizophrenic subjects were examined by means of nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd) staining and NOS immunohistochemistry. NOS-positive neurons were counted and analyzed morphologically. Abnormalities regarding morphology or number of NOS-containing neurons could be found in the putamen of schizophrenics (n = 3), but not controls (n = 5). Neurons were either of abnormal size and branching pattern, or they were markedly reduced (130 ± 44 vs. 54 ± 62 NADPHd-positive somata/mm³ putamen; p < 0.0001). Striatal nitrinergic interneurons might thus be involved in the pathogenesis of at least some forms of schizophrenia. Studies on larger samples are however needed to further corroborate this finding.

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Section: Discussionmentioning

confidence: 99%

Morphological Abnormalities in Nitric-Oxide-Synthase-Positive Striatal Interneurons of Schizophrenic Patients

Lauer¹,

Johannes²,

Fritzen³

et al. 2005

Neuropsychobiology

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“…Schizophrenia is a multifactorial psychiatric disorder that affects about 1 % of the population in the world and involves genetic factors, neurochemical and development changes in the nervous system (Weiss and Feldon 2001;Lau et al 2003). The main pathophysiological hypothesis of schizophrenia is based, at least in part, on drug responses.…”

Section: Introductionmentioning

confidence: 99%

Cannabidiol effects in the prepulse inhibition disruption induced by amphetamine

et al. 2015

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“…12 Histochemical studies have also shown that the striatum contains the enzyme for NO synthesis, nitric oxide synthase (NOS). 13 In addition, recent studies showed that NOS neurons in rat striatum express more NMDA receptor mRNA than non-NOS neurons.…”

Section: Introductionmentioning

confidence: 99%

Glutamate modulates sodium‐potassium‐ATPase through cyclic GMP and cyclic GMP‐dependent protein kinase in rat striatum

Munhoz

Kawamoto

Lima

et al. 2004

Cell Biochemistry & Function

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Excessive excitatory action of glutamate and nitric oxide (NO) has been implicated in degeneration of striatal neurons. Evidence had been provided that Na+K+-ATPase might be involved in this process. Here we investigated whether glutamate-regulated messengers, such as NO and cyclic GMP, could modulate the activity of membrane Na+K+-ATPase. Our results demonstrated that NO donors sodium nitroprusside (SNP at 30 and 300 microM) and S-nitroso-N-acetylpenicillamine (SNAP at 200 microM) increased alpha2,3Na+K+-ATPase activity which was blocked by the NO chelator, haemoglobin and was independent of [Na+]. This regulation was associated with cGMP synthesis and mimicked by glutamate (300 microM) and 8-Br-cyclic GMP (4 mM). 8-Br-cGMP-induced stimulation of Na+K+-ATPase activity could be blocked by KT5823 (an inhibitor of cGMP-dependent protein kinase, PKG), but not by KT5720 (an inhibitor of cAMP-dependent protein kinase, PKA). N-Methyl-D-aspartate (NMDA) receptors appeared to be involved in the effect of glutamate, since MK-801 (NMDA receptor antagonist) produced a partial reduction in glutamate-induced activation of the enzyme. MK-801 was not synergistic to L-NAME (NOS inhibitor), suggesting that glutamate stimulates the NMDA-NOS pathway to activate alpha2,3 Na+K+-ATPase in rat striatum. This regulation was associated with cyclic GMP (but not cyclic AMP) synthesis. These data indicate the existence, in vitro, of a regulatory pathway by which glutamate, acting through NO and cGMP, can cause alterations in striatal alpha2,3 Na+K+-ATPase activity.

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Elevated neuronal nitric oxide synthase expression in chronic haloperidol-treated rats

Cited by 33 publications

References 43 publications

Morphological Abnormalities in Nitric-Oxide-Synthase-Positive Striatal Interneurons of Schizophrenic Patients

Morphological Abnormalities in Nitric-Oxide-Synthase-Positive Striatal Interneurons of Schizophrenic Patients

Cannabidiol effects in the prepulse inhibition disruption induced by amphetamine

Glutamate modulates sodium‐potassium‐ATPase through cyclic GMP and cyclic GMP‐dependent protein kinase in rat striatum

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